Министерство здравоохранения Республики Беларусь

УЧРЕЖДЕНИЕ ОБРАЗОВАНИЯ
«ГРОДНЕНСКИЙ ГОСУДАРСТВЕННЫЙ МЕДИЦИНСКИЙ
УНИВЕРСИТЕТ»

Кафедра дерматовенерологии

А. А. БЕЛАЗАРОВИЧ
А. И. НОВОСЕЛЕЦКАЯ

ДЕРМАТОЛОГИЯ
Рекомендовано учебно-методическим объединением
по высшему медицинскому, фармацевтическому образованию в
качестве пособия для студентов учреждений высшего образования,
обучающихся по специальности 1-79 01 01 «Лечебное дело»

Anastasiya BELAZAROVICH
Aliavtsina NOVASIALETSKAYA

DERMATOLOGY
Manual for the Faculty of International Students
(English medium)

Гродно
ГрГМУ
2019
1
УДК 16.5+616.97(075.8)=111
ББК 55.8я73
Б43

Авторы: доц. каф. дерматовенерологии учреждения образования

«Гродненский государственный медицинский университет»,
канд. мед. наук А. А. Белазарович;
доц. каф. дерматовенерологии учреждения образования
«Гродненский государственный медицинский университет»,
канд. мед. наук А. И. Новоселецкая.

Рецензент: зав. каф. дерматовенерологии и косметологии

ГУО «БелМАПО, проф., д-р мед. наук О. В. Панкратов;
зав. каф. кожных и венерических болезней УО «БГМУ»,
доц., канд. мед. наук А. П. Музыченко.

Белазарович, А. А.
Б43 Дерматология : пособие для студентов учреждений
высшего образования, обучающихся по специальности
1-79 01 01 «Лечебное дело» [на англ. яз.] = Dermatology :
manual for the Faculty of International Students (English
medium) / А. А. Белазарович, А. И. Новоселецкая. – Гродно:
ГрГМУ, 2019. – 256 с.
ISBN 978-985-595-164-4.

Данное учебное пособие предназначено для студентов

факультета иностранных учащихся, обучающихся на
английском языке, для помощи в изучении основных разделов
цикла дерматологии.

УДК 16.5+616.97(075.8)=111
ББК 55.8я73

ISBN 978-985-595-164-4 © Белазарович А. А.,

Новоселецкая А. И., 2019
© ГрГМУ, 2019

2
CONTENTS
PREFACE .............................................................................................. 6
CHAPTER I ANATOMY AND HISTOLOGY OF NORMAL
SKIN ...................................................................................................... 7
Unit 1 Epidermis ................................................................................. 8
Unit 2 Dermis.................................................................................... 12
Unit 3 Subcutaneous Layer............................................................... 14
Unit 4 Skin Appendages ................................................................... 14
Unit 5 Other Structures in the Skin and theirFunctions
Nerve Supply .................................................................................... 22
Unit 6 Functions of the Skin ............................................................. 23
CHAPTER II DERMATOPATHOLOGICAL PROCESSES ............ 27
Unit 1 Exudative Processes in the Skin ............................................ 27
Unit 2 Keratinization Disorders ........................................................ 28
Unit 3 Proliferative Processes in the Skin ........................................ 28
CHAPTER III PRINCIPLES OF THERAPY IN
DERMATOLOGY .............................................................................. 30
Unit 1 Review of Systemic Therapy ................................................ 30
Unit 2 Principles of Topical Dermatologic Therapy ........................ 31
Unit 3 Other Treatments ................................................................... 34
CHAPTER IV TYPES OF LESIONS ................................................. 36
Unit 1 Primary Skin Lesions ............................................................ 36
Unit 2 Secondary Skin Lesions ........................................................ 38
CHAPTER V BACTERIAL INFECTIONS OF THE SKIN.............. 40
Unit 1 Etiology.................................................................................. 40
Unit 2 Pathogenesis .......................................................................... 41
Unit 3 Classification ......................................................................... 42
Unit 4 Staphyloderma ....................................................................... 43
Unit 5 Streptoderma .......................................................................... 45
Unit 6 Strepto-Staphyloderma .......................................................... 46
Unit 7 Diagnosis and Treatment ....................................................... 47
CHAPTER VI DESEASES OF NEWBORN’S SKIN ....................... 50
Unit 1 Omphalitis ............................................................................. 50
Unit 2 Intertrigo ................................................................................ 51
Unit 3 Other Diseases of the Newborn ............................................. 52

3
CHAPTER VII PARASITIC DISEASES OF THE SKIN ................. 54
Unit 1 Scabies ................................................................................... 54
Unit 2 Pediculosis ............................................................................. 61
CHAPTER VIII BULLOUS DERMATOSES .................................... 70
Unit 1 Pemphigus ............................................................................. 70
Unit 2 Pemphigoid ............................................................................ 75
Unit 3 Dermatitis Herpetiformis ....................................................... 77
CHAPTER VIII DISEASES OF SKIN APPENDAGES ................... 81
Unit 1 Seborrheic Dermatitis ............................................................ 81
Unit 2 Acne ....................................................................................... 85
Unit 3 Rosacea .................................................................................. 93
CHAPTER X CONNECTIVE TISSUE DISEASES .......................... 96
Unit 1 Lupus Erythematosus ............................................................ 96
Unit 2 Scleroderma ......................................................................... 106
CHAPTER XI ALLERGIC SKIN DISEASES ................................. 111
Unit 1 Allergic Contact Dermatitis ................................................. 111
Unit 2 Eczema ................................................................................. 113
Unit 3 Toxicoderma ........................................................................ 122
Unit 4 Toxic epidermal necrolysis (Lyell's syndrome) .................. 127
CHAPTER XII NEURODERMATITIS ........................................... 131
Unit 1 Atopic Dermatitis ................................................................ 131
Unit 2 Skin Itch (Pruritus) .............................................................. 138
Unit 3 Urticaria ............................................................................... 140
Unit 4 Prurigo ................................................................................. 146
CHAPTER XIII PAPULOSQUAMOUS DISEASES ..................... 150
Unit 1 Psoriasis ............................................................................... 150
Unit 2 Lichen Planus ...................................................................... 159
Unit 3 Pityriasis Rosea.................................................................... 161
CHAPTER XIV VIRAL INFECTIONS OF THE SKIN .................. 164
Unit 1 Herpes simplex .................................................................... 164
Unit 2 Herpes Zoster ....................................................................... 170
Unit 3 Warts .................................................................................... 174
Unit 4 Molluscum Contagiosum .................................................... 179
CHAPTER XV MYCOBACTERIAL INFECTIONS ...................... 184
Unit 1 Leprosy ................................................................................ 184
Unit 2 Cutaneous Tuberculosis....................................................... 188
Exogenous cutaneous tuberculosis ................................................. 190
Endogenous Cutaneous Tuberculosis Forms ................................. 192
Tuberculids ..................................................................................... 194
4
 Cutaneous Tuberculosis Secondary to BCG Vaccination.............. 196
CHAPTER XVI FUNGAL INFECTIONS ....................................... 199
Unit 1 Tinea corporis ...................................................................... 199
Unit 2 Tinea Capitis ........................................................................ 201
Unit 3 Tinea Pedis .......................................................................... 206
Unit 4 Onychomycosis ................................................................... 208
Unit 5 Candidiasis........................................................................... 211
CHAPTER XVII ALLERGIC VASCULITIS AND REACTIVE
ERYTHEMAS ................................................................................... 215
Unit 1 Erythema nodosum .............................................................. 216
Unit 2 Henoch-Schonlein purpura .................................................. 218
CHAPTER XVIII SKIN TUMOURS ............................................... 223
Unit 1 Actinic Keratosis ................................................................. 223
Unit 2 Keratoacanthoma ................................................................. 227
Unit 3 Bowen's Disease .................................................................. 229
Unit 4 Sebaceous Naevus ............................................................... 231
Unit 5 Malignant melanoma ........................................................... 232
Unit 6 Squamous Cell Carcinoma of the Skin ............................... 236
Unit 7 Basal Cell Carcinoma .......................................................... 240
CHAPTER XIX GENODERMATOSIS ........................................... 245
Unit 1 Ichthyosis ............................................................................. 245
Unit 2 Epidermolysis Bullosa ......................................................... 247
REFERENCES .................................................................................. 253

5
PREFACE
The Manual "Dermatology" is written to facilitate the assimilation
of the material in the studying dermatology by English speaking
students. The Manual includes 19 Chapters composing of Units. They
describe general and particular dermatology. The description begins
with the anatomy and histology of the intact skin. Further attention is
paid to pathological processes in the skin, primary and secondary skin
lesions, without knowledge of which the study of the skin diseases
will be impossible. There is a Chapter devoted to the principles of
treatment of skin diseases. In each Unit there is a part devoted to the
principles of the skin diseases treatment.
The Manual describes more than 40 skin diseases known in the
world. The skin diseases description includes various etiology,
pathogenesis and clinical manifestations of the diseases. They are one
of the serious social and psychological problems. Their social
significance is determined by a high prevalence, rise in morbidity and
a chronic course. There is a group of skin diseases that are transmitted
by contact and are contagious.
The authors hope that this Manual on Dermatology will help to
enrich information as well as obtain deep knowledge on the skin
diseases by foreign students in this field of clinical medicine.

6
CHAPTER I
ANATOMY AND HISTOLOGY OF
NORMAL SKIN
Introduction to the Structure of the Skin
The skin is considered the largest organ of the people’s body. It
has a surface area of 1.8-2 square meters in adults, and makes up
approximately 16% of the total body weight (5 kilograms).
The thickness of the skin varies throughout the body. It depends
on how much we use this area. It varies from 0.5mm thick on the
eyelids to 4.0 mm thick on the heels of feet.
Three layers of the skin (Fig.1.1):
1. Epidermis.
2. Derma.
3. Subcutaneous tissue.
The skin also has some appendages:
x Sebaceous glands.
x Eccrine sweat glands.
x Apocrine sweat glands.
x Hair follicles.
x Nails.

Fig. 1.1. – Layers and Structure of the Skin

7
 Unit 1
Epidermis
The epidermis is the most superficial layer of the skin derived
from ectoderm and provides the first barrier of protection from
invasion of foreign substances into the body. The principal cell of the
epidermis is called a keratinocyte.
The epidermis is subdivided into five layers or strata:
x Stratum basale (a basal cell layer).
x Stratum spinosum (a prickle cell layer).
x Stratum granulosum (a granular cell layer).
x Stratum lucidum.
x Stratum corneum (a horny layer) in which a keratinocyte
gradually migrates to the surface and is sloughed off in the process
called desquamation.
The bottom layer, the stratum basale, provides the germinal
cells necessary for the regeneration of the layers of the epidermis.
These germinal cells are separated from the dermis by a thin layer of a
basement membrane - a multilayered structure with anchoring fibrils
extending into the superficial dermis. After a mitotic division a newly
formed cell will undergo progressive maturation called keratinization
as it migrates to the surface. Interspersed amongst the basal cells are
melanocytes, large dendritic cells responsible for melanin pigment
production.
Stratum spinosum
Spinous layer consists of living keratinocytes with the
eosinophylic cytoplasma. The cells that divide in the statum
germinativum soon begin to accumulate many desmosomes
(intercellular bridges) on their outer surface which provide the
characteristic «prickles» (seen on a closer view) of the stratum
spinosum, which is often called a prickle-cell layer.
Scattered throughout the prickle cell layer are numbers of
dendritic cells called Langerhan`s cells. Like macrophages,
Langerhan`s cells originate in the bone marrow and have an antigen-
presenting capacity.
Stratum granulosum
Progressive maturation of a keratinocyte is characterized by
accumulation of keratin, called keratinization. The cells of stratum
granulosum accumulate dense basophilic keratohyalin granules (seen
8
on a closer view). Also present in the cytoplasm of cells in the
granular layer organelles known as lamellar granules (Odland bodies).
These granules contain lipids, which along with the desmosome
connections help to form a waterproof barrier that functions to prevent
fluid loss from the body.
Stratum lucidum
Epidermis varies in thickness throughout the body depending
mainly on frictional forces and is thickest on the palms of the hands
and soles of the feet. The stratum lucidum is normally only well seen
in thick epidermis and represents a transition from the stratum
granulosum to the stratum corneum.
Stratum corneum
As a cell accumulates keratinohyalin granules, it is thought that
rupture of lysosomal membranes release lysosomal enzymes that
eventually cause cell death. The dead and dying cells filled with
mature keratin form the stratum corneum. It acts as a major physical
barrier in the epidermis. The deeper cells of stratum corneum retain
their desmosomal junctions, but as they are pushed to the surface by
newly formed cells of the stratum basale, the dead cells gradually
break apart and are lost every 2 weeks. This process is called
desquamation. There is a gradual differentiation from basal layer
to the horny layer that takes about 70 days. The rate of cell
production in the germinative compartment of the epidermis must be
balanced by the rate of cell loss at the surface of the stratum corneum.
The epidermis has three main types of cells:
x Keratinocytes (85% of cells in epidermis).
x Melanocytes (pigment-producing cells).
x Langerhans cells (immune cells).
Merkel’s cell is a fourth, less visible, epidermal cell.
The epidermis forms undulating appearance, with intermittent
regular protrusions of the epidermis layer (rete pegs) into the upper
layers of the underlying dermis. In some areas of the body such as the
palms and soles, the rete pegs are less pronounced. The pillars of
dermis next to the rete pegs form rete ridges. The small area of
epidermis between rete pegs is called a suprapapillary plate.
Keratinocytes
Keratinocytes are present in all layers of the skin. The
keratinocytes become more mature or differentiated and accumulate
keratin as they move outwards. They eventually form four distinct
9
layers, from the most superficial to the deepest described in the table
below (Table 1).

Table 1

Layer Cell type

Stratum corneum x Called corneocytes or
(a horny layer) squames.
x Dead, dried-out hard cells
without nuclei.
Stratum granulosum x Cells contain basophilic
(a granular layer) granules.
x Waxy material is secreted
into the intercellular spaces.
Stratum spinulosum x Intercellular bridges called
(a spinous, spiny or prickle cell desmosomes link the cells
layer) together.
x The cells become
increasingly flattened as they
move upward.
Stratum basale (basal layer) x Columnar (tall) regenerative
cells.
x As a basal cell divides, a
daughter cell migrates upwards
to replenish the layer above.

Dermo-epidermal junction
The structures of the dermo-epidermal junction provide good
mechanical support, adhesion and growth of the basal layer unless it is
diseased. Just below the epidermis is a basement membrane, a
specialized structure that lies between the epidermis and dermis. It
includes various protein structures linking the basal layer of
keratinocytes to the basement membrane (hemidesmosomes) and the
basement membrane to the underlying dermis (anchoring fibrils). The
10
basement membrane has an important role in making sure the
epidermis sticks tightly to the underlying dermis.
The epidermis gives rise to a number of specialized appendages
also called adnexal structures or adnexa. Hair and nails are such
examples, i.e. they are specialized structures formed by direct
extension of the epidermis. The hair follicles are associated with
sebaceous (oil) glands and arrector pili smooth muscle. This muscle is
responsible for goose bumps appearing on the skin in response to cold.
The epidermis also gives rise to eccrine (sweat) glands, a tangle
of tubules deep within the dermis that secretes a watery salt solution
into a duct that ends on the skin surface. Larger apocrine sweat glands
are found in the armpits and groin.
Different areas of the body have different proportions of the
adnexal and hair follicle structures. For example:
x dense hair on the scalp and none on the palms;
x intense sweating from armpits, palms and soles as compared
with other sites.
Melanocytes
Melanocytes are found in the basal layer of the epidermis. These
cells produce pigment called melanin, which is responsible for
different skin color. Melanin is packaged into small parcels (or
melanosomes), which are then transferred to keratinocytes.
Langerhans cells
Langerhans cells (800 per sq mm) are immune cells found in the
epidermis, and are responsible for helping the body learn and later
recognize new ‘allergens’ (material foreign to the body). It is the first
that reacts at the effect of the antigens. Langerhans cells break the
allergen into smaller pieces then migrate from the epidermis into the
dermis. They find their way to lymphatic and blood vessels before
eventual reaching the lymph nodes. Here they present the allergen to
immune cells called lymphocytes.
Once the allergen is successfully ‘presented’, the lymphocytes
initiate a sequence of events to initiate an immune reaction to destroy
the material, and stimulate proliferation of more lymphocytes that
recognize and remember the allergen in the future.
Merkel cells are cells found in the basal layer of epidermis. Their
exact role and function is not well understood.
A Merkel cell has a lobulated nucleus and characteristic granules;
it is embedded in the basal layer of epidermal cells, with which it has
11
desmosomal connections; it contains intermediate filaments composed
of low molecular weight keratin rather than neurofilament protein.

Unit 2
Dermis
The dermis assumes some important functions of
thermoregulation and supports the vascular network to supply the
avascular epidermis with nutrients.
The dermis is typically subdivided into two zones, a papillary
dermis and a reticular layer. The dermis contains mostly fibroblasts
which are responsible for secreting collagen, elastin and ground
substance that give the support and elasticity to the skin. Immune cells
that are involved in defense against foreign invaders passing through
the epidermis are present as well.
1. Papillary dermis
A papillary dermis contains vascular networks that have two
important functions. The first function is to support an avascular
epidermis with vital nutrients and the second one - to provide a
network for thermoregulation. The vasculature is organized so that by
increasing or decreasing blood flow, heat can either be conserved or
dissipated. The vasculature interdigitates into the areas called dermal
papillae (DP). The papillary dermis also contains certain free sensory
nerve endings and structures called Meissner`s corpuscles in the
highly sensitive areas.
2. Reticular dermis
A reticular layer of the dermis consists of a dense irregular
connective tissue, which differs from a papillary layer that is made up
of mainly a loose connective tissue (note the difference in the number
of cells). The reticular layer of the dermis is important in giving the
skin its overall strength and elasticity, as well as housing other
important epithelial derived structures such as glands and hair
follicles.
The dermis is a fibrous connective tissue or supportive layer of
the skin.
The major fibers are as follows:
x Collagen fibers which predominate in the dermis. Collagen
fibers have enormous tensile strength and provide the skin with
strength and toughness. Collagen bundles are small in the upper or

12
papillary dermis, and form thicker bundles in the deeper or reticular
dermis.
x Elastin which provides the properties of elasticity and
pliability to the skin.
The collagen and elastin fibers are bound together by ground
substance, a mucopolysaccharide gel in which nutrients and wastes
can diffuse to and from other tissue components. The dermis also
contains nerves, blood vessels, epidermal adnexal structures (as
described above), and cells.
Normal cells in the dermis include:
Mast cells which contain granules packed with histamine and
other chemicals, released when the cell is disturbed.
Vascular smooth muscle cells which allow blood vessels to
contract and dilate are required to control body temperature.
Specialized muscle cells are for example, myoepithelial cells
which are found around sweat glands and contract to expel sweat.
Fibroblasts which produce and deposit collagen and other
elements of the dermis as required for growth or to repair wounds. A
resting fibroblast has a very little cytoplasm as compared with an
active cell and appears to have a ‘naked’ nucleus.
Immune cells have many types, for example, histiocytes,
lymphocytes and etc. The role of tissue macrophages (histiocytes) is
to remove and digest foreign or degraded material (this is known as
phagocytosis). There are also small numbers of lymphocytes in the
normal dermis.
Transient inflammatory cells or leukocytes are white cells that
leave the blood vessels to heal wounds, destroy infections or cause
disease.
They include:
x Neutrophils (polymorphs) which have segmented nuclei, and
are the first white blood cells to enter tissue during acute
inflammation.
x T and B Lymphocytes which are small inflammatory cells
having many subtypes. They arrive later but persist longer in the
inflammatory skin conditions and are important in the regulation of
immune response. Plasma cells are specialized lymphocytes that
produce antibodies.
x Eosinophils which have bilobed nuclei and a pink cytoplasm
on H&E stain.
13
 x Monocytes which form macrophages.
Derma is the thickest at the palms, soles and back (3 mm) and
least thick at the eyelids (0.3 mm) and penis.

Unit 3
Subcutaneous Layer
The subcutaneous layer lies between the dermis and the
underlying fascia covering muscle. This layer is made of groups of
adipocytes (fat cells) that are separated by fibrous septa. It has three
functions: to insulate the body from cold, to absorb trauma and
cushion deeper tissues, and to act as storage for the body’s fuel
reserve. The size of this layer varies throughout the body and from
person to person. It is absent in the eyelids and the male genitalia. It
has abundant blood and lymphatic supplies.

Unit 4
Skin Appendages
The skin contains a variety of appendages, mainly, hair follicles,
sweat glands and sebaceous glands, which are all embryonically
epidermal in origin.

Hair Follicles
Hair is simple in structure, but has important functions in social
functioning. Hair helps transmit sensory information and creates
gender identity. Hair is made of keratin, the same substance that forms
nails and the top layer of the epidermis (stratum corneum). Hair is a
derivative of the epidermis and consists of two distinct parts: the
follicle – the living part located under the skin and the hair shaft-fully
keratinized nonliving part above the skin surface (Fig. 1.2).

14
 Fig. 1.2. – Hair

The follicle is a stocking-like structure that contains several layers

with different jobs. At the base of the follicle is a projection – papilla
that contains capillaries, or tiny blood vessels, that feed the cells. The
living part of the hair is bottom part of the stocking surrounding the

15
papilla called the bulb. This bottom part is the only part fed by the
capillaries. The cells in the bulb divide every 23 to 72 hours, faster
than any other cells in the body.
The follicle is surrounded by two sheaths – an inner and outer
sheath. These sheaths protect and mold the growing hair shaft. The
hair shaft consists of a cortex and cuticle cells, and a medulla for some
types of hairs.
The arrector pili muscle lies between the hair bulge area and
dermoepidermal junction. Above the insertion of an arrector pili
muscle, sebaceous glands and, in some certain regions, apocrine
glands open into the follicle.
The hair shaft is made up of dead, hard protein called keratin in
three layers. The inner layer is called the medulla and may not be
present. The next layer is the cortex and the outer layer is the cuticle.
The cortex makes up the majority of the hair shaft. The cuticle is
formed by tightly packed scales in an overlapping structure similar to
roof shingles.
A hair follicle has continuous growth and rest sequence named
hair cycle. (Fig.1.3) The duration of growth and rest cycle is
coordinated by many endocrine, vascular and neural stimuli and
depends not only on localization of the hair but also on various
factors, like age and nutritional habits.

Fig. 1.3. – Hair growth cycle

Humans have approximately 5 million hair follicles and 100,000

of them are located on the scalp (Table 2).

16
 Table 2

Total count Almost 5,000,000

Scalp hair count 80,000–150,000
Hair cycle ratios of scalp hair Anagen: 85–90%
Catagen: 1%
Telogen: 10–15%
Duration of hair cycle phase Anagen: 2–6 years
Catagen: 2–3 weeks
Telogen: 3 months
Physiologic hair shedding rate ~100–200/day
(scalp)

Different pigment cells located in the root of the hair make

keratin and melanin which gives its color to hair.
Humans have two types of hair:
x vellus (light and fine)
x terminal (dark and thick).
A sebaceous gland secretes an oily substance called sebum that
drains into the canal of a hair follicle to reach the surface of the skin.
Together, a hair follicle and its associated sebaceous gland are called a
pilosebaceous unit.
Hair follicles are distributed everywhere on the body except the
palms, soles and mucosal regions of lips and external genitalia. In
humans, hair is largely decorative, but it also has a protective function.
Eyebrows and eyelashes protect eyes from dust and sunlight, while the
nasal hairs block out foreign bodies from your nose. The scalp hair
provides some temperature insulation.
Nails
Nails are the only skin appendages that are not located in the
dermis but instead are located at the ends of fingers and toes. They are
used to grasp and pinch objects and, like hair, have a growing
decorative function in our society. The nail acts as a protective
covering to the end of the digit.
The nail structure is divided into six parts: root, nail bed, nail
plate, eponychium (cuticle), paronychiu and hyponychium (Fig.1.4).

17
 Fig. 1.4. – The nail structure

Nail folds
Folds of normal skin surround the nail plate. These folds form the
nail grooves, the slits or furrows on the sides of the nail on which it
moves as it grows.
Classification of nail fold:
x Paronychium, a lateral nail fold, is the soft tissue border
around the nail
x Eponychium, a proximal nail fold, is the extension of the
cuticle at the base of the nail body that partly overlaps the lunula.
The proximal nail fold is similar in structure to the adjacent skin
but is normally devoid of dermatoglyphic markings and sebaceous
glands. The cuticle (eponychium) is composed of modified stratum
corneum and serves to protect the structures at the base of the nail,
particularly a germinative matrix, from environmental insults such as
irritants, allergens and bacterial and fungal pathogens.
Nail matrix
The matrix, sometimes called the matrix unguis, keratogenous
membrane, nail matrix, or onychostroma, is the tissue (or germinal
matrix) which the nail protects.
The nail’s matrix is the tissue under the nail that it rests on; it
extends under the nail root, and contains blood vessels and nerves. It
is the part of the nail bed that is beneath the nail and contains nerves,
lymph and blood vessels.
18
 The proximal (dorsal) and distal (intermediate) matrix produces
new keratinocytes that eventually become the nail plate. The nail
matrix keratinocytes mature and keratinize without keratohyalin
(granular layer) formation. The length, thickness, and overall size of
the matrix will determine the width and thickness of the nail plate
above. So provided it is receiving adequate nutrition and is kept in a
healthy condition, the nail matrix will continue to grow and keep a
healthy nail plate above it. As the previously mentioned cells are
created, they push forward the old nail plate cells as they emerge,
which is how your nail “grows”. These new cells start out white, but
as they push forward more they become translucent, and then appear
to be pink as they are “back lit” by the capillaries in the nail bed
underneath.
The lunula is the visible part of the matrix, the whitish crescent-
shaped base of the visible nail. The lunula can best be seen in the
thumb and may not be visible in the little finger.
Nail bed
The nail bed is the place beneath the nail plate.
It consists of an epidermal part and an underlying dermal part
closely opposed to the periosteum of the distal phalanx. There is no
subcutaneous fat layer in the nail bed, although scattered dermal fat
cells may be visible microscopically. The epidermal layer is usually
no more than two or three cells thick.
Collectively, the nail bed (sterile matrix), nail fold, eponychium,
paronychium, and hyponychium are referred to as the perionychium.
Nail plate
This is the most visible part of the nail. The nail plate is made of
dead keratin, which forms a hard protective structure about 0.3-0.65 mm
thick. Keratin is formed in the nail matrix by dividing epidermal cells.
The nail plate is composed of three horizontal layers: a thin dorsal
lamina, a thicker intermediate lamina and a ventral layer from the nail
bed.
Free edge extends over tip of finger or toe.
The free margin (margo liber) or distal edge is the anterior margin
of the nail plate corresponding to the abrasive or cutting edge of the nail.
Hyponychium
The hyponychium is the thickened stratum corneum of the
epidermis located beneath the nail plate at the junction between the
free edge and the skin of the fingertip. It forms a seal that protects the
19
nail bed.
Nail growth
x Nails grow at an average rate of 0.1 mm per day (average
growth is 1/8” per month).
x Nail growth is influenced by nutrition, general health, and
disease.
x Nail grows forward, starting at the matrix and extending over
the digit tip.
x Nails grow in a variety of shapes.
x Growth is faster in summer than in winter.
x Children’s nails grow faster than adults’ nails.
x Middle fingernail grows fastest.
x Thumbnail grows slowest.
x Toenails grow slower than fingernails, but are harder and
thicker.

Glands of the Skin

Sweat Glands
They, also known as sudoriferous or sudoriparous glands, from
Latin sudor, meaning 'sweat', are a type of exocrine gland, which are
glands that produce and secrete substances onto an epithelial surface
by way of a duct.
Human skin possesses two kinds of sweat glands that differ in
their structure, function, secretion, mechanism of excretion, anatomic
distribution, and distribution across species:
Eccrine sweat glands
The release of sweat from eccrine glands is the body’s cooling
process. Sweat is produced in a coiled tubule in the dermis and is
transported by a sweat duct through the epidermis to be secreted.
Eccrine sweat glands are distributed almost all over the human
body surface, in varying densities, with the highest density in palms
and soles, then on the head, but much less on the trunk and the
extremities.
Glands can produce up to 10 L of sweat per day. In addition to the
secretion of water and electrolytes, the sweat glands serve as excretory
organ for heavy metals, organic compounds, and macromolecules.
The sweat is composed of 99% water, electrolytes, lactate (provides
an acidic pH to resist infection), urea, ammonia, proteolytic enzymes,
20
and other substances.
Apocrine Sweat Glands
In humans, apocrine sweat glands have an unknown function and
are regarded as vestigial glands perhaps useful to our ancestors. They
are located mainly in the underarm and perianal areas areas.
Like eccrine sweat, apocrine one is also produced in the coiled
tubules of the dermis, but the apocrine duct drains sweat into a hair
follicle from which it reaches the skins surface. Contrary to popular
belief, the sweat from the apocrine glands is odorless. The action of
normal skin bacteria on excreted apocrine sweat is responsible for
body odor.
Ceruminous glands (which produce ear wax), mammary glands
(which produce milk), and ciliary glands in the eyelids are modified
apocrine sweat glands.
Sebaceous Glands
These exocrine glands produce an oily substance called sebum, to
lubricate and waterproof the skin and hair. They are most prominent in
the skin of the scalp, face, and upper trunk and are absent in the palms
and soles.
The type of secretion of the sebaceous glands is referred to as
holocrine. As a part of the pilosebaceous unit, sebaceous glands
secrete sebum that drains into the follicular canal and eventually onto
the surface of the skin.
The sebaceous glands increase in size and produce more sebum in
response to increased hormone levels, specifically androgen during
adolescence. They play an important role in the development of acne
(Fig. 1.5).

21
 Fig. 1.5. – Glands of the Skin

Unit 5
Other Structures in the Skin and theirFunctions
Nerve Supply
The skin is richly innervated, the highest density of nerves being
found in the areas such as hands, face and genitalia. All nerves
supplying the skin have their cell bodies in the dorsal root ganglia.
There are both myelinated and nonmyelinated fibers. The nerves
contain neuropeptides.
Free sensory nerve endings are seen in the dermis and also
encroaching upon the epidermis where they may abut on Merkel cells.
These nerve endings detect a pain, itch and temperature. Certain
specialized corpuscular receptors are distributed in the dermis, such as
Pacinian corpuscle (detecting pressure and vibration) and touch-
sensitive Meissner's corpuscles which are mainly seen in the dermal
papillae of your feet and hands.
The Pacinian corpuscle is one of the encapsulated receptors. It is
22
an ovoid structure about 1mm in length, which is lamellated in cross-
section like an onion, and is innervated by a myelinated sensory axon
which loses its sheath as it traverses the core.
The Golgi-Mazzoni corpuscle found in the subcutaneous tissue of
the human finger is similarly laminate but of much simpler
organization. These receptors are movement and vibration detectors.
The Krause end bulb is an encapsulated swelling on myelinated
fibers situated in the superficial layers of the dermis. Ruffini endings
in the human digits have several expanded endings branching from a
single myelinated afferent fiber; the endings are directly related to
collagen fibrils; they are stretch receptors.
'Free nerve endings', which appear to be derived from non-
myelinated fibers occur in the superficial dermis and in the overlying
epidermis; they are receptors for pain, touch, pressure and
temperature. Hair follicles have fine nerve filaments running parallel
to and encircling the follicles; each group of axons is surrounded by
Schwann cells; they mediate touch sensation.
Blood and Lymphatic Vessels
The skin also has a rich and adaptive blood supply. Arteries in the
subcutis branch ascend forming a superficial plexus at the
papillary/reticular dermal boundary. The branches extend to the
dermal papillae, each of which has a single loop of capillary vessels,
one arterial and one venous. Veins drain from the venous side of this
loop to form mid-dermal and subcutaneous venous networks. In the
reticular and papillary dermis there are arteriovenous anastomoses
which are well innervated and concerned with thermoregulation.
The lymphatic drainage of the skin is important, and abundant
meshes of lymphatics originate in the papillae and assemble into
larger vessels which ultimately drain into the regional lymph nodes.

Unit 6
Functions of the Skin
The skin is a multifunctional organ. What does the skin do?
x Protective Function (barrier function)
The healthy skin acts as a barrier between the outside world and
the inside of the body. The epidermis and subcutaneous fat play their
roles in the protective functions. The mechanical properties of the skin
depend mainly on the dermis. It protects the penetration of harmful

23
substances and bacterial invasions as well as protects against sunlight
by synthesis of melanin pigment.
x Immunological Function
The skin is in the front line of the defense of the body. In essence
the defenses involve production of an antibody-complex, multi hair
proteins, which bind with the offensive antigens. Langerhans’s cells
probably play a crucial role in connect sensitization, immune
surveillance against viral infections and neoplasms.
x Sensory Functions
The skin is richly supplied with nerves and various types of
specialized sensory endings – organs which provide information
regarding environment changes, so that body can then adjust its
activities accordingly. In some animals hair under certain situations
have specialized sensory receptors located at the bases of the hair
follicles which serve to enhance sensory appreciation.
x Secretion and Excretion
The skin possesses various types of glands, which pour secretions
on the surface. The more important glands are sweat and the
sebaceous glands. The endocrine glands which are scattered all over
the body surface secrete a thin transparent watery fluid known as true
sweat, while the apocrine glands secrete a thicker rather milky and
odoriferous solution. Sweat consists of 1.2% solids and 98.8% water.
The substances excreted in it are Sodium Chloride, Sodium
Phosphate, Sodium Bicarbonate, Keratin and small amount of Urea.
The skin can also excrete drugs administered to the individual (e.g.,
mercury, arsenic, iodine etc.) The sebaceous glands of the skin secrete
sebum which is composed of fatty acids, cholesterol, alcohol, etc.
Fatty acids have a mild fungistatic activity. Sebum acts as a lubricant
for some drying effects of the atmosphere.
x Synthesis of Vitamin ‘D’
Vitamin ‘D’ is synthesized in the skin as a result of exposure to
ultra violet ‘B’ (UVB) radiation and since it is carried in the blood
attached to a binding protein to exercise a specific effect at different
sites. Vitamin D5 is essential for skeletal development and it contains
antirachitic properties. Vitamin D3 is formed principally in the
stratum spinosum and the stratum barale, from precursor 7 dehydro
cholesterol by way of a provitamin D3.
x Body Heat Regulation
The skin plays the most important role in the regulation of heat
24
loss. It losses heat to the external environment in three ways by
conduction, by radiation and by evaporation, Heat loss by the first two
mechanisms takes place when the environmental temperature is lower
than that of the skin. Heat loss by evaporation mainly means the
amount of heat spent by the body to evaporate the sweat from the
surface of the skin. About 90% of the total loss of the body is
regulated by the skin.
The heat loss through the skin in regulated by various
physiological mechanisms, which include:
- reaction of the cutaneous vessels;
- reaction of the smooth muscle fibers of the skin;
- perspiration.
x Endocrine Functions
Hair follicles and sebaceous glands are target for the organic
steroids secreted by the gonads the adrenal cortex and melanocytes are
directly are directly influenced by polypeptide hormones of the
pituitary.
x Storage Function of the Skin
Blood is stored in the rich sub papillary plexuses of the dermis,
about one liter. The skin is also a good storehouse of ergosterol which
is irradiated by ultra violet light of the sun and converted into vitamin
‘D’. The junction between dermis and hypodermis has a considerable
capacity for storing fat and permanent store of subcutaneous adipose
tissue. Certain substances like glucose and chloride may also be stored
in the skin temperately. The cornfield layer also acts as a reservoir for
topically applied corticosteroids (or) other hormones, which are
absorbed slowly for many days from the surface.
x Absorption
The skin can absorb substances dissolved in fatty solvents like
vitamins and hormones. The information greatly increases the skin
permeability. The substances that are completely insoluble in water
and lipids do not penetrate.
x Gaseous Exchange through the Skin
A small amount of gaseous exchange occurs through the skin. In
man the amount of CO exchange through the skin is negligible as
compared to the amount exhaled from the lungs.

25
 Checkup Questions
1. What is the body's largest organ? How much surface area does
it cover?
2. What layers is the epidermis divided into?
3. What types of hair do you know?
4. How is thermoregulation performed?
5. What skin appendages do you know?
6. What are the main parts of the nail?

26
CHAPTER II
DERMATOPATHOLOGICAL
PROCESSES
Unit 1
Exudative Processes in the Skin
Acantholysis
x The keratinocytes are seen ‘floating apart’ from each other
because of loss of desmosome cell connections (intercellular bridges)
leading to intraepidermal blisters.
x Different conditions have unique patterns of acantholysis, for
example, in pemphigus vulgaris, acantholysis is just above the basal
layer of the epidermis (suprabasilar acantholysis or suprabasilar
clefting) but the basal layer remains intact (tombstone appearance). In
contrast, in pemphigus foliaceus, acantholysis is higher, just below the
stratum corneum.
Ballooning degeneration
x Intracellular edema with cellular swelling.
x Destruction of cells because of increased intracellular fluid in
response to cell injury (often seen with herpes virus infections).
Spongiosis (or intercellular edema)
x Abnormal accumulation of fluid between keratinocytes in the
spinous layer.
x Spaces between keratinocytes are more apparent than normal.
x Excessive spongiosis can lead to intraepidermal vesicles
(eczematous dermatitis).
x Eosinophilic spongiosis is the term used when eosinophils
predominate in inflammation, for example in atopic eczema,
pemphigus and pemphigoid.
Vacuolar Degeneration:
x Cell damage by the formation of intercellular vacuoles, most
common in cells of basal layer with inflammation at dermal-epidermal
junction, usually followed by cell death.

27
 Unit 2
Keratinization Disorders
Hyperkeratosis
x Increased thickness of stratum corneum, whether by normal or
abnormal keratinocytes.
x It can result from normal use of corns, calluses, chronic
inflammation (eczema) or genetic disorders (X-linked ichthyosis,
ichthyosis vulgaris).
x Keratinization associated with hair follicles is called follicular
keratosis.
Parakeratosis
x Process of incomplete keratinization in which keratinocytes
retain their nuclei in the stratum corneum.
x Parakeratosis indicates that the epidermis is inflamed or
injured.
x In the normal skin, keratinocytes denucleate when reach the
horny cell layer; however, keratinocyte formation in inflammatory
diseases such as psoriasis vulgaris or in tumorous diseases such as
actinic keratosis and Bowen`s disease takes place so quickly that most
of nuclei remain in the horny cell layer.
Dyskeratosis: occurs when some keratinocytes keratinize
abnormally before they reach the horny cell layer. The keratinocytes
become apoptotic and necrotic. The nuclei shrink and contain
eosinophilic cytoplasm. Since intercellular btidges between the
peripheral keratinocytes are lost, the cells become round.
Dyskeratosis is often found with inflammatory disease and
malignant tumours. It is termed «grains» in Darier`s disease and
«individual cell keratinizations» in Bowen`s disease.

Unit 3
Proliferative Processes in the Skin
Acanthosis
x It is thickening of a spinous layer of the epidermis, which may
be papillomatous or psoriasiform.
x One can distinguish between broad-based acanthosis as in
chronic dermatitis and psoriasiform acanthosis with elongated rete
ridges as in psoriasis.
28
 x It may be associated with enlargement of rete pegs.
Hypergranulosis – increase in thickness of the granular layer,
especially common in inflammatory disorders (lichen planus) and in
human papilloma virus infections.
Papillomatosis – enlargement of the dermal papillae leading to
finger-like projections of the epidermis and papillary dermis (also
called church spires). A typical example is a common wart.

Checkup Questions
1. What pathological processes are exudative?
2. What skin disease does acantholysis occur in?
3. With what pathological process do warts form?
4. What are the pathological processes related to keratinization
disorders?
5. What changes develop in the skin with hypergranulosis?

29
CHAPTER III
PRINCIPLES OF THERAPY IN
DERMATOLOGY
Treatment must be individualized to suit every patient. Skin is a
superficial and being an ectodermal structure takes time to heal.
Hence, great care should be exercised in prescribing the right topical
remedy and in its mode of application.
Many skin disorders are treatable. The treatment of skin diseases
includes topical, systemic, intralesional, radiation and surgical
modalities.
Topical drugs (drugs applied directly to the skin) are a mainstay
of treating skin disorders. Systemic drugs are taken by mouth or given
by injection and are distributed throughout the body.
Rarely, when a high concentration of a drug is required to the
affected area, a doctor injects the drug just under the skin (an
intradermal injection).
Principles of dermatological management:
x Proper diagnosis, definition of the cause and sincere attempts
to eliminate or correct causes;
x Encouragement of the patient and relatives so as to allay their
anxiety about infectivity, severity, scarring and chances of recovery;
x Specific and palliative treatment:
- general measures-diet, rest, environments;
- internal-systemic drugs;
- local-topical measures;
- physical treatment and surgery.

Unit 1
Review of Systemic Therapy
It is used particularly for more severe conditions and infections
(Table 3).

30
 Unit 2
Principles of Topical Dermatologic Therapy
Appropriately selected topical therapy will lead to preservation or
restoration of the normal physiologic state of the skin. Topical therapy
offers the possibility of delivering an optimal dose of a desired
medication to the exact site where it is needed, while minimizing
systemic drug effects.
There are five components to the successful use of topical
therapies:
x Propert diagnosis
x Type of the lesion being treated
x Medication
x Vehicle (the base in which the active medication is delivered)
x Route used to apply medication
Topical dermatologic treatments are grouped according to their
therapeutic functions and include:
x Cleansing agents
x Absorbent dressings (eg, hydrocolloid patches or powder) and
super-absorbent powders
x Anti-infective agents
x Anti-inflammatory agent
x Astringents (drying agents that precipitate protein and shrink
and contract the skin)
x Drying agents
x Moisturizing agents (emollients, skin hydrators, and softeners)
x Keratolytics (agents that soften, loosen, and facilitate
exfoliation of the squamous cells of the epidermis)
x Antipruritics

31
 Table 3

Group Drug Indications

Corticosteroids Prednisolone Bullous disorders, connective
usually tissue disease, vasculitis
Cytotoxics Methotrexate Psoriasis, sarcoidosis
Hydroxyurea Psoriasis
Azathioprine Bullous disorders, chronic actinic
dermatitis, atopic eczema
Immunosup- Ciclosporin Psoriasis, atopic eczema, pyoderma
pressants gangrenosum
Gold Bullous disorders, lupus
erythematosus
Immunomodu- Inosine Viral warts (genital), herpes
lators pranobex simplex (genital)
Retinoids Acitretin Psoriasis, other keratinization
disorders
Isotretinoin Acne
Antifungals Griseofulvin, Fungal infection, candidiasis
terbinafine,
ketoconazole,
itraconazole,
fluconazole
Antibiotics Various Skin sepsis, acne, rosacea
Antivirals Aciclovir, Herpes simplex, herpes zoster
valaciclovir
Famciclovir Herpes zoster, genital herpes
simplex
Antihistamines H 1 blockers Urticaria, eczema
Antiandrogens Cyproterone Acne (females only)
Antimalarials Hydroxychlo- Lupus erythematosus, porphyria
roquine cutanea tarda
Antileprotic Dapsone Dermatitis herpetiformis, leprosy,
vasculitis

Topical treatments are usually consist of a vehicle an an active

ingredient.

32
 Pharmacokinetics
The ability of a drug to penetrate the epidermis depends on
several factors. They include:
x Drug's molecular structure.
x Vehicle.
x The site on the body (absorption is greatest through the eyelid
and genitalia).
x Condition of the skin (whether the skin is diseased or intact).
Classes of Topical Medications
Topical solutions are of low viscosity and often use water or
alcohol in the base. The solution can cause drying the skin if alcohol is
used in the base. These are usually a powder dissolved in water,
alcohol, and sometimes in oil. Alcohol in topical steroids can
frequently cause drying if it is used as a base ingredient. There is a
significant variability between generic brands and name brands. There
is a risk of irritation depending on the preservatives and fragrances
used in the base.
Lotions are similar to solutions but are thicker and tend to be
more emollient in nature than solutions. They are usually oil mixed
with water, and more often than not have less alcohol than solutions.
They are easily applied to hairy skin. Lotions cool and dry acute
inflammatory and exudative lesions.
Shake lotions are a mixture that separates into two or three parts
after certain time. Frequently oil is mixed with a water-based solution.
This lotion needs to be shaken into suspension before use.
Creams are semi-solid emulsions of oil and water in
approximately equal proportions; contains a preservative to prevent
overgrowth of micro-organisms. They penetrate well into the stratum
corneum outer layer of the skin. They are used for moisturizing and
cooling and when exudation is present. They vanish when rubbed into
skin.
Creams are not greasy and are easy to remove. They are often
used for dry skin lesions. Creams are more superficial as compared
with ointments.
Ointments are homogeneous, viscous, semi-solid preparations,
most commonly greasy, thick oil (oil – 80%, water – 20%) with high
viscosity that is intended for external application to the skin or
mucous membranes. They are used as emollients or for application of
active ingredients to the skin with protective, therapeutic or
33
prophylactic purposes and where a certain degree of occlusion is
required.
Ointments are used topically on a variety of body surfaces. These
include the skin and the mucous membranes of the eyes (an eye
ointment), vagina, anus, and nose. An ointment may or may not be
medicated.
Ointments are usually very moisturizing and good for the dry
skin. They have a low risk of sensitization due to having few
ingredients beyond the base oil or fat, and low irritation risk.
Ointments are optimal lubricants and increase drug penetration
because of their occlusive nature; a given concentration of drug is
typically more potent in an ointment. They are preferred for
lichenified lesions and lesions with thick crusts or heaped-up scales,
including psoriasis and lichen simplex chronicus. Ointments are less
irritating than creams for erosions or ulcers. They are usually best
applied after bathing or dampening the skin with water.
Gel is a semi-solid transparent non-greasy emulsion. Gels are
thicker than solutions; they are frequently a semisolid emulsion in the
alcohol base and due to alcohol have a drying and stinging effect.
Some of them will melt at body temperature.
Powder is a pure drug (talcum powder) or is made of the drug
mixed in (with) a carrier such as corn starch or corn cob powder.
Powders should be used only on dry lesions since oozing will change
the powder into a hard mass which will irritate the inflamed skin.
Powders soothe the skin, and protect it from externalirritation and
friction and so are useful in prickly heat and intertrigo. Ordinary
powder contains talcum, starch or chaik with boric acid added to it as
an antiseptic.
Paste combines three agents – oil, water and powder. It is an
ointment in which a powder is suspended. Pastes can be applied to
well-demarcated lesions. Due to its ointment base, they are difficult to
remove.

Unit 3
Other Treatments
A wide variety of other, more specialized treatments exists for
specific skin conditions. Corticosteroids are sometimes injected
directly into lesions (e.g. to treat keloids). Certain disorders are

34
responsive to ultraviolet B or photochemotherapy.
In the past X-ray irradiation was used to treat a range of skin
conditions including psoriasis, acne, tinea capitis, skin tuberculosis
and hand eczema. There are now very few indications for X-ray
treatment of non-malignant diseases, although irradiation is of great
value in several types of skin tumors.
Cryotherapy, in which liquid nitrogen is applied to the skin, is
currently widely used in dermatology. Liquid nitrogen (-196°C) is
delivered by cotton wool bud or spray gun and injures cells by ice
formation. It is mainly employed for the treatment of benign or pre-
malignant skin tumors, warts.
A laser is a device that emits light through a process of optical
amplification based on the stimulated emission of electromagnetic
radiation. The term "laser" originated as an acronym for "Light
Amplification by Stimulated Emission of Radiation".
Uses for lasers are including: port wine stain nevi, telangiectasia,
viral warts, some tumors, and tattoos.

Checkup Questions
1. What antileprotic drug do you know?
2. What is the difference between ointment and cream?
3. What diseases can laser treatment be used for?
4. What are the components of a paste?
5. When will powder be used?

35
CHAPTER IV
TYPES OF LESIONS
The most fundamental and important methods of medical
examination for skin diseases are visual inspection and palpation.
The recent development of biochemical and immune system
examination methods has made diagnosis more accurate.
However, naked-eye and dermoscopy inspection and palpation
are always the most important in acquiring information on the nature
of skin lesions, including their distribution, form, color, shape and
firmness.
A skin lesion is generally called an eruption. Skin lesions come in
many different forms and can be the symptoms of a variety of diseases
and underlying issues.
There are 2 main categories of skin lesions: primary and
secondary.
Primary skin lesions are formed due to a disease or infection.
They are various in color or texture that may be present at birth as
moles or birthmarks, or may be acquired during a person's lifetime and
be associated with infectious diseases (e.g. warts, acne, or psoriasis),
allergic reactions (e.g. hives or contact dermatitis), or environmental
agents (e.g. sunburn, pressure, or temperature extremes).
Secondary skin lesions are those changes in the skin that result
from primary skin lesions, either as natural progression or as a result
of person’s manipulating (e.g. scratching or picking) at a primary
lesion.

Unit 1
Primary Skin Lesions
Macule (from Latin "macula" meaning "spot") is a small-sized,
not raised, circular, flat lesion less than 2/5 inches (1 cm) in diameter.
The color of a macule is not the same as that of the nearby skin.
There are two types of macules:
x Erythematous (macular syphilide, erythema multiforme,
ezanthema).

36
 x Pigmentary:
- hyperpigmentary macules (Lentigines, naevi, chloasma);
- depigmentation (Vitiligo);
- hypopigmentation (Tinea versicolor, leprosy, pityriasis Alba).
A macule more than 2/5 inches (1 cm) in diameter is called a
patch; it has an irregular shape (Fig. 2).

Fig. 2. – Macule and patch

Vesicle is a raised circumscribed, serum- or plasma-containing
lesion less than 1/5 inches (5 mm) across. The vesicles that are more
than 1/5 in (5 mm) across are called bullae or blisters. The common
causes of vesicles are: herpes simplex, eczema and chickenpox.
Pustule is a raised, circumscribed, palpable encapsulated lesion
filled with pus. A pustule is usually a result of certain infection, such
as acne, impetigo, or boils.
Papule is a solid, elevated, raised lesion less than 2/5 inches (1
cm) across. A patch of closely grouped papules more than 2/5 inches
(1 cm) across is called a plaque. Papules and plaques can be rough in
texture and red, pink or brown in color. They may be acuminate
(pointed), dome-shaped (rounded), filiform (thread-like), flat-topped,
oval or round, pedunculated (with a stalk), sessile (without a stalk),
umbilicated (with a central depression), verrucous (warty). Papules are
associated with such conditions as warts, syphilis, psoriasis,
seborrheic and actinic keratoses, lichen planus, and skin cancer.
Wheal is a skin elevation caused by swelling that can be itchy
and usually disappears soon after erupting. Wheals are generally
associated with an allergic reaction, such as to a drug or an insect bite.
Nodule or tubercle is a solid lesion that has distinct edges and is
usually more deeply rooted than a papule. Doctors often describe a
37
nodule as "palpable," meaning that, when examined by touch, it can
be felt as a hard mass distinct from the tissue surrounding it.
A nodule more than 2 cm in diameter is called a tumor. Nodules
are associated with keratinous cysts, lipomas, fibromas, and some
types of lymphomas (Table 4).
Table 4

Unit 2
Secondary Skin Lesions
Ulcer is a lesion that involves loss of the upper portion of the skin
(epidermis) and part of the lower portion (dermis). Ulcers can result
from acute conditions such as bacterial infection or trauma, or from
more chronic conditions, such as scleroderma or disorders involving
peripheral veins and arteries. An ulcer that appears as a deep crack
extending to the dermis is called a fissure.
Scale is a dry, horny build-up of dead skin cells that often flakes
off the surface of the skin. Diseases that promote scale include fungal
infections, psoriasis, and seborrheic dermatitis.
Crust is a dried collection of blood, serum, or pus. Also called a
scab, a crust is often part of the normal healing process of many
infectious lesions.
Erosion is a lesion that involves loss of the epidermis.
38
 Excoriation is a hollow, crusted area caused by scratching or
picking at a primary lesion.
Scar is a discolored, fibrous tissue that permanently replaces the
normal skin after destruction of the dermis. A very thick and raised
scar is called a keloid.
Lichenification is a rough, thick epidermis with exaggerated skin
lines. This is often a typical feature of scratch dermatitis and atopic
dermatitis.
Vegetation is a growth of pathological tissue consisting of
multiple closely set papillary masses.
Atrophy is an area of the skin that has become very thin and
wrinkled; it is normally seen in eldly individuals and people who are
using very strong topical corticosteroid medications.
Causes and symptoms
Skin lesions can be caused by a wide variety of conditions and
diseases. A tendency toward developing moles, freckles, or birthmarks
may be inherited. Infection of the skin itself precipitated by bacteria,
viruses, fungi, or parasites is the most common cause of skin lesions.
Acne, athlete's foot (tinea pedis), warts, and scabies are examples of skin
infections that cause lesions. Allergic reactions and sensitivity to outside
environmental factors can also lead to the formation of skin lesions.
Underlying conditions can also precipitate the appearance of skin
lesions. For example, the decreased sensitivity and poor circulation that
accompanies diabetes mellitus can contribute to the formation of
extensive ulcers on the extremities such as the feet. Infections of body's
entire system can cause a sudden onset of skin lesions. For example,
skin lesions are a hallmark symptom of such diseases as chicken pox,
herpes, and small pox. Cancers affecting the skin, including basal cell
carcinoma, squamous cell carcinoma, malignant melanoma, and
Kaposi's sarcoma are recognized by their lesions.

Checkup Questions
1. How many types of macules do you know?
2. What is an example of a disease with the formation of
vesicles?
3. What is the difference between a vesicle and bullae?
4. What is the evolution of the pustule over time?
5. What are the types of papules?
6. How does a wheal develop?
39
CHAPTER V
BACTERIAL INFECTIONS OF
THE SKIN
Pyodermas (synonym: pustular skin diseases) are a group of skin
diseases caused by pyogenic microorganisms, mainly staphylococci,
streptococci and other less often (pseudomonas infection, etc.).
The onset of the disease is usually acute, sometimes subsequently
taking a chronic relapsing course. In economically developed
countries, patients with pyoderma are 1/3 among patients suffering
from infectious diseases. In childhood, the incidence is higher than in
adults, and is 25-60% of the total number of dermatosis diseases at
this age.

Unit 1
Etiology
Normal skin has a resident flora of usually harmless
microorganisms, including bacteria, yeasts and mites. The bacteria are
mostly staphylococci (e.g. Staph. epidermidis), micrococci,
corynebacteria (diphtheroids) and propionibacteria. They cluster in the
stratum corneum or hair follicles, and their number varies between
individuals and between different sites on the body Micrococci, for
example, number 0.5 million per cm2 in the axilla but only 60 per cm:
on the forearm.
The main causative agents of pyoderma are:
x Staphylococcus.
x Streptococcus.
x Proteus vulgaris.
x Pseudomonas.
x Escherichia coli.
Staphylococcus and streptococci themselves cause skin lesions.
Purulent inflammation occurs with staphylococcal infection, with
streptococcal infection – serous. Other bacteria are more likely to
cause skin damage in association with each other, as well as with
other anaerobic microorganisms and fungi.
Staphylococcus aureus is gram-positive anaerobic cocci. It
40
produces two enzymes – catalase and coagulase, the analysis of which
is used to identify the pathogenic properties of the pathogen.
Staphylococcus is commensal and usually exists on the skin,
especially in the area of large folds and on the nasal mucosa, without
causing disease. Staphylococcus has many pathogenic factors:
mucopeptides; coagulase; protein A; fibronectin; collagenase;
enterotoxins; epidermolytic toxin; hemolysin and leukocidin and
others.
The source of infection is patients with chronic purulent infection
of the upper respiratory tract, the gastrointestinal tract, the female
genital tract, with a surgical infection, as well as patients with
pyoderma. Often there are recurrent forms that occur as a result of
autoinoculation of the pathogen from the foci of chronic purulent
infection. The path of infection is usually contact with hands, clothing
and contaminated objects.
Streptococcus pyogenes – gram-positive anaerobic cocci. Has
the form of grape-like chains. It has hemolytic properties. Catalazo-
negative. Constantly found on the mucous membrane of the upper
respiratory tract and skin.
Streptococcus is spread by direct contact and airborne. It can
survive in the dust. The pathogenicity of streptococcus is determined
by the properties of its enzymes and toxins, as a result of which the
skin lesions develop. The enzymes cause tissue necrosis, damage the
DNA of cells and promote the spread of infection.

Unit 2
Pathogenesis
Local and general antibacterial resistance of the macroorganism
plays a role in the development of pustular skin diseases. There are
factors that prevent the penetration of microorganisms through the
skin.
The horny layer of the skin has a high density and strength. The
desquamation of the upper layers of the epidermis and the mechanical
removal of microorganisms constantly occur. High concentration of
hydrogen ions (pH 3.5–6.7), bactericidal, bacteriostatic properties of
the tissue fluid and secretions of sweat and sebaceous glands have an
adverse effect on the growth and reproduction of the pyococci.
The bactericidal function of the skin is reduced as a result of the

41
widespread irrational use of antibiotics. This leads to the displacement
of normal microflora from the body and contributes to the
reproduction of pathogenic microorganisms on the skin and mucous
membranes. As a result, conditions are created for the penetration of
microorganisms into deep tissues.
The “entrance gate” for the infection is a microtrauma of the skin.
Their occurrence is promoted by maceration and thinning of the
stratum corneum. Adverse factors are overcooling and overheating of
the body. They disrupt the metabolic processes in the skin. The
composition and amount of tissue fluid, sweat and sebum vary. Their
antibacterial properties are reduced. Contribute to pyoderma: diseases
of the central and vegetative nervous systems, starvation, malnutrition
(lack of proteins, vitamins and salts), X-ray irradiation, treatment with
corticosteroids and immunosuppressive drugs. Some patients indicate
that their relatives have had various purulent skin diseases for a long
time. In patients with pustular skin diseases, often comorbid diseases
are detected: periodontal disease, gingivitis, caries, chronic tonsillitis
and pharyngitis, diabetes and obesity, etc. More than half of patients
(52%) with chronic pyoderma consume a lot of carbohydrates. The
emergence and chronic course of pyoderma often contributes to the
high content of sugar in the blood and skin.

Unit 3
Classification
I Superficial.
II Deep.
1. Staphyloderma:
x Ostiofolliculitis.
x Folliculitis: superficial folliculitis and deep folliculitis.
x Furuncle.
x Superficial furunculosis.
x Carbuncle.
x Sycosis Barbae.
x Hydradenitis.
2. Streptoderma:
x Streptococcal impetigo.
x Ecthyma.
x Dry streptoderma.
42
 3. Strepto-staphyloderma:
x Impetigo vulgaris.
x Chronic ulcerative pyoderma.

Unit 4
Staphyloderma
Clinical Presentation
Folliculitis – purulent inflammation of the hair follicle. There are
ostiofolliculitis, superficial and deep folliculitis.
Ostiofolliculitis (syn. staphylococcal impetigo) is characterized
by small (miliary) follicular superficial conical pustules with purulent
heads. Pustules are localized in the hair follicles, penetrated by a hair.
On the periphery of the pustules there is a pink rim. Rashes are
localized on the face, trunk, and limbs. After 3-5 days, the contents of
the pustules are dried in crusts, which fall off without leaving a trace.
Superficial folliculitis differs only in somewhat larger sizes (0.5–
0.7 cm in diameter) and in depth of damage (up to 2/3 of the hair
follicle). The erythematous zone around the abscess is 2–3 mm.
Pustule is tense, its tire is tight. The pus is thick, yellowish-green. In
the places of rashes patients there is pain, which disappears after the
opening of the pustules and the separation of pus. The general
condition of the patient does not suffer.
Deep folliculitis is characterized by large pustules (1–1.5 cm in
diameter), which affect the entire hair follicle. The rash is sharply
painful, but the necrotic stem is absent, unlike the furuncle. With a
common process, the patient’s general condition worsens: subfebrile
and febrile fever, headaches, leukocytosis and accelerated ESR are
observed in the blood.
Diagnosis
Diagnosis is based on the patient's medical history and
observations. Laboratory analysis of the substance drained from a
pustule can be used to distinguish bacterial folliculitis from fungal
folliculitis.
Treatment
Bacterial folliculitis may disappear without treatment, but is
likely to recur. Non-prescription topical antibiotics like Bacitracin,
Mycitracin or Neomycin, gently rubbed on to affected areas three or
four times a day, can clear up a small number of bacterial folliculitis
43
pustules. Oral antibiotics such as erythromycin may be prescribed if
the infection is widespread.
Furuncle, furunculosis is a deep staphyloderma characterized by
purulent-necrotic inflammation of the hair follicle and the surrounding
tissue with a self-limiting nature of the process due to granulation
tissue.
Furuncles are more often located on the face, neck, shoulders,
thighs, or buttocks. At the beginning, mildly limited redness occurs in
the region of the hair follicle. Gradually, the focus turns into a nodus
with a diameter of 3–5 cm. A “necrotic rod” is formed in the central
part of the nodus in 3–4 days. The discharge of pus occurs after the
opening of the furuncle within 3-4 days. The formed ulcer gradually
(within 4–5 days) is performed by granulations and heals with scar
formation. The furuncle evolution takes an average of 2 weeks.
Chronic recurrent process may occur for several months or years.
Furuncles are in different stages of development and periodically new
elements appear (furunculosis), which is determined by a weakening
of the immune status. Systemic factors that lower resistance
commonly are detectable, including: diabetes, obesity, and
hematologic disorders.
The general condition of the patient with a single furuncle usually
does not suffer. Fever, malaise, headaches, leukocytosis in the blood,
increased ESR can occur with multiple furuncles and furunculosis.
Patients with localization of furuncles on the face, lips and nose
require special attention and urgent treatment due to the possibility of
purulent thrombophlebitis of the facial veins, meningitis, sepsis or
septicopyemia with the formation of multiple abscesses in various
organs and tissues, which can lead to death of the patient.
Carbuncle – purulent-necrotic inflammation of several hair
follicles with the formation of confluent inflammatory infiltrate,
localized in the dermis and subcutaneous tissue.
The size of the carbuncle is larger than the furuncle. It can be 5-
10 cm in diameter. The purple-blue, almost black color, dense to the
touch, sharply painful infiltrate slowly (within 10–14 days) softens,
forming several fistulous openings through which liquid bloody pus is
released. At the bottom of the ulcer, multiple necrotic rods are visible,
after rejection of which a wide and deep defect occurs. The ulcer
gradually heals with extensive retracted scar. Temperature rises more
often and higher (up to 40–41°C) with carbuncles than with furuncle.
44
Pain in the eruption site more pronounced, stronger manifestations of
intoxication, septic complications.
Sycosis Barbae is a common subacute or chronic pyogenic
infection of the hair follicles of the beard. It occurs only in males after
puberty. Most cases begin in the third or fourth decade but the
disorder may arise in the post-pubertal teenage years.
The essential lesion is an oedematous, red, follicular papule or
pustule centred on a hair. Individual papules remain discrete, but can
combine to form raised plaques. In the common subacute forms the
lesions may be scattered irregularly over the beard or grouped
especially on the upper lip and below the angles of the jaw. Attacks of
varying duration occur at irregular intervals over months or years.
In more chronic forms the lesions are typically clustered into
plaques, especially on the upper lip and chin, and may persist for very
long periods, even up to twenty years in some cases. There is often
some crusting or scaling but the hairs are retained and there is no
evident scarring.
Hydradenitis is a purulent inflammation of the apocrine sweat
glands caused by staphylococci, penetrating into the glands through
their ducts, small skin injuries, often occurring when shaving the
axillary folds. The disease develops slowly, occurs after puberty,
equally often in men and women.
The process is localized more often in the armpits, more rarely –
near the nipples of the mammary glands, around the anus, i.e. in those
places where functioning apocrine sweat glands are located. The
formation of hydradenitis begins with a painful node in the thickness
of the skin the size of a pea. After 2-3 days, the nodus increases to 1-2
cm in diameter, becoming purple-red. At the same time, new nodes
appear nearby. They form a tight, painful infiltration. Nodes open and
pus is released from the holes. The general condition is violated. The
temperature rises. The malaise is marked. Scarring occurs after
7-10 days.

Unit 5
Streptoderma
Streptococcal impetigo is a highly contagious disease that occurs
more often in women and children who have more tender skin and a
thin stratum corneum. It is a superficial non-follicular cystic element

45
filled with serous-purulent contents. The surface of the blister is
sluggish. On the periphery, there may be a small edematous
hyperemic border, indicating a tendency toward peripheral growth.
The process tends to spread rapidly as a result of autoinoculation. The
diameter of the blister is from 2 to 10 mm. Localization – mainly on
the face, less often affects the skin of the trunk and extremities.
Ecthyma vulgaris is an ulcerative, deep form of streptoderma.
The disease begins with the appearance of deep epidermal pustules
against the background of inflammatory infiltrate. Pustule quickly
dries into a crust. An ulcer defect forms deep under the crust. The
ulcer has a rounded or oval shape, steeply hyperemic, swollen edges, a
bleeding bottom with granulations and mucopurulent discharge. The
ulcer is painful. Ecthyma heals for a long time with a deep scar. With
an unfavorable course of the process, gangrenization is observed in
the ulcer area or extensive disintegration of the underlying tissues.
The most frequent localization of ecthyma is the skin of the legs.
Usually elements of ecthyma are single (no more than 10 elements are
described). Less commonly, ecthymes are located on the buttocks,
thighs, and body.
Dry streptoderma occurs, as a rule, in children and adolescents,
often in individuals visiting pools (due to a shift in the pH of the skin
in an alkaline environment). The disease may be endemic in children's
groups, especially in the spring. The clinical picture: one or several
pink-red spots covered with whitish small scales appear on the skin of
the extensor surfaces of the limbs, sometimes the body. Macula 3-4
cm in diameter, have a tendency to peripheral growth. Patients are
worried about a slight itching, dry skin in the lesions, a cosmetic
defect. Secondary depigmented macules (pseudoleukoderma) remain
at the site of the lesions. Chronic, recurrent course of the disease is
possible.

Unit 6
Strepto-Staphyloderma
Impetigo vulgar, a form of pyoderma is a highly contagious
disease (especially in children's groups). Clinically, it is characterized
by manifestations typical of impetigo streptococcal, ostiofolliculitis
and folliculitis. Blisters, osteofolliculitis and folliculitis, surrounded
by hyperemia occur on the inflamed, hyperemic skin. Erosion (round

46
and irregular in shape with a pink-red slightly bleeding bottom) and
thick, rough, yellow crusts form during the development of a
pathological process on the skin. Foci of vulgar impetigo are prone to
peripheral growth, may merge with each other, occupying large areas
of the skin, and become disseminated. In such cases, possible painful
swelling of the lymph nodes, increased ESR, leukocytosis.
Localization – the face, open areas of the limbs. The prognosis of the
disease is usually favorable: on the 5–7th day the crusts disappear,
leaving a secondary, erythematous, slightly scaly macula that
disappears without a trace. In severe cases, children may have a
complication in the form of acute nephritis.
Chronic ulcerative pyoderma occurs at any age, but more often
in people from 40 to 60 years. The development of the process is
promoted by severe immunodeficiency associated with comorbidities,
intoxication (ulcerative colitis, malignant tumors of the internal
organs, lymphomas, alcoholism, drug addiction), leading to a
deficiency of T- and B-cellular immune systems.
For the clinical picture of the disease is characterized by the
development of ulcerated plaques of a bluish-red color of soft
consistency, sharply delimited from the surrounding healthy skin,
having irregular round or oval contours. The surface of the plaques is
fully or partially ulcerated. The skin around the ulcers is inflamed, on
it you can see the follicular and non-follicular superficial pustules,
sometimes merging into continuous lesions, covered with purulent
crusts, from which serous-purulent exudate is separated. The process
is spreading and capturing new areas of the skin. It is accompanied by
pain, limitation of movement in the limb. The course of chronic
ulcerative pyoderma is very long (months and even years), with
periods of attenuation and exacerbation.

Unit 7
Diagnosis and Treatment
Diagnosis
Diagnosis is based on the clinical picture, laboratory tests. In
doubtful cases, conduct bacteriological and histological studies.
Differential Diagnostics
Folliculitis is differentiated from acne, eosinophilic folliculitis (in
HIV- infected), drug toxicidermia (bromine preparations,

47
corticosteroids, lithium), follicular lichen planus, ingrown hair. When
the process is localized in the armpits folliculitis is differentiated with
hydradenitis.
Furuncle and furunculosis differentiate with carbuncle and
hydradenitis.
A carbuncle is differentiated from a furuncle (that has one
necrotic rod) and an abscess.
Hydradenitis is with lymphadenitis, tuberculosis which affects the
lymph nodes.
Impetigo is with eczema, pemphigus, candidal lesions of skin
folds.
Dry streptoderma – with fungal skin lesions using studies on
pathogenic fungi.
Ecthyma is with a furuncle and syphilitic ecthyma.
Treatment
A patient with pyoderma needs rational skin care. In case of
localized forms of the disease, it is not recommended to wash the skin
in the lesion and near it, and in the disseminated process, washing is
prohibited altogether. Hair in the area of pyodermic rashes should be
cut (do not shave!). Unaffected skin is treated, especially carefully
around the circumference of the lesion, with disinfecting solutions (1–
2% alcohol solution of salicylic acid, 0.1% aqueous solution of
potassium permanganate, etc.).
Topical therapy
x Antiseptics.
x Topical corticosteroids (For the topical therapy of some forms
of pyoderma corticosteroids are used in combination with antiseptics,
antibiotics in the form of ointments and creams.)
x Proteolytic enzymes (trypsin, chemotrypsin) (They are used to
accelerate the purification of ulcers from necrotic masses.)
x Combined antibacterial drugs
Systemic therapy
x Antibiotics
x Sulfanilamides
x Quinolines
x Immunotherap

48
Checkup Questions
1. What is pyoderma?
2. What is a causative agent of pyoderma?
3. What typical clinical picture of staphyloderma develops?
4. What clinical manifestations are observed in streptoderma?
5. What is the clinical picture of strepto-staphyloderma?
6. What methods of diagnosis are used to define pyoderma?
7. How is pyoderma treated?

49
CHAPTER VI
DESEASES OF NEWBORN’S SKIN
Unit 1
Omphalitis
Omphalitis is inflammation of the skin around the remains of the
umbilical cord. Normally, the remaining umbilical cord disappears by
the end of the 1st week. The remaining umbilical wound
epithelializes, granulates and forms a scar by the end of the 2nd
beginning of the 3rd week of life. The healing of the umbilical wound
is delayed when it is infected.
Catarrhal omphalitis is an inflammatory process with a serous
discharge which dries in crusts. After rejection of crusts, a wound with
a bleeding surface is exposed. There is redness at the edges. This is a
relatively easy inflammatory process. The general condition of the
child is not disturbed, the appetite is good, the temperature remains
normal.
Treatment
In case of catarrhal omphalitis, the umbilical wound is washed
daily with a 3% hydrogen peroxide solution. Then the wound is
treated with 1-2% solution of brilliant green, or 5% solution of
potassium permanganate, or 2-5% solution of silver nitrate. Processed
1-2 times a day.
It is necessary to bathe the baby in a non-concentrated solution of
potassium permanganate. The newborn should have its own bath,
which after each use should be washed. To heal a wound, a child
should have an «air bath» every day. It is very important that the edge
of the diaper does not come into contact with this area.
At the discretion of the physician, physiotherapy can be
prescribed.
Purulent omphalitis is a significant umbilical hyperemic,
edematous and infiltrated protrusion. Thin blue strips (dilated veins)
depart radially from the umbilical wound. Often, red stripes are visible
near the blue stripes due to the attachment of lymphangitis. The
general condition of the child is disturbed, he eats poorly, becomes
restless. Breathing becomes superficial, rapid. The legs are brought to
50
the stomach, the temperature rises moderately (37.2-37.5°C). With a
mild course of the disease comes complete recovery. Peritonitis and
sepsis is possible in severe cases.
Treatment
General treatment is carried out along with local, if the
inflammatory process extends to the surrounding tissues and in depth,
and the temperature rises. Prescribe injections of antibiotics and 2-3
injections of anti-staphylococcal gamma globulin or polyglobulin (1-2
times a week). Consult with a surgeon. Mothers who breastfeed a
baby should receive vit. A, C, complex B, PP.
Prevention of Omphalitis
The umbilical wound is treated first with 3% hydrogen peroxide
solution, and then with 5% potassium permanganate solution or 1%
alcohol solution of aniline dyes. Do it daily until healing.

Unit 2
Intertrigo
Diaper rash (Intertrigo) is impaired skin integrity due to
improper care of the newborn. Localization: buttocks, inner thighs,
folds, behind the ears.
Degree of diaper rash:
I – moderate hyperemia of the skin without visible violation of its
integrity;
II – bright hyperemia with large erosion;
III – bright skin hyperemia, weeping as a result of merged
erosions.
Erosion can become infected.
Principles of treatment of diaper rash:
x Washout after bowel movements
x Thorough drying of the skin after bathing
x Treatment of skin folds with baby oil, cream
x Hygienic bath
x UFO of affected skin
Stage 1 – cream "Bepanten", creams with zinc.
Stage 2 – agitated solutions with drying substances such as zinc
oxide, talc. Pustules are treated with brilliant green.
Stage 3 – emulsions with antibiotics.

51
 Unit 3
Other Diseases of the Newborn
Miliaria appears more often in obese children when they are
overheated. Its certain types are distinguished:
x Crystalline miliaria – vesicles with transparent contents appear
on the skin;
x Red miliaria – papules appear with vesicles on the top, around
them hyperemia;
x White miliaria – vesicles with purulent contents.
Subcutaneous adiponecrosis occurs at 1-2 weeks of life in large
children with difficult childbirth as a result of tissue compression.
Localization - the skin of the trunk and limbs. There are nodes the size
of a pea to children's palm. The skin over them is cyanotic, in 3-4
months they spontaneously dissolve. Treatment: Solux, UHF,
phonophoresis, magnetic therapy.
Scleredema appears on the 2-4 day of the child's life, more often
in premature babies. Clinic: on the skin of the leg and thighs – a seal
with swelling of the skin. It spreads over the entire skin. When
pressed, the fossa remains. Treatment: corticosteroids, vitamins A, C,
E, warming the baby and ointment with glucocorticoids.
Sclerema develops in premature babies with hypotrophy for 3-4
days of life. Clinic: begins with the leg and buttocks extends to the
entire skin. Diffuse compaction of the skin and subcutaneous tissue
develops. When pressing, the recesses do not remain. On palpation,
the skin is cold; the skin is not going to fold. The face is masklike.
The joints of the lower jaw are fixed. Unlike scleredema, the soles,
palms, scrotum and penis are not affected. Treatment: glucocorticoids,
antibiotics, vitamins C, B2, B6, B15, E, topical ointments with
glucocorticoids.
Pseudofurunculosis is an inflammation of the sweat glands.
Localization: scalp, neck, back, buttocks. Clinical manifestations:
there are multiple nodes, purple-bluish color, painful. A fluctuation
appears in the center, an abscess is opened with the discharge of pus.
The general condition is extremely serious.
Leiner’s disease
This is a severe toxic condition caused by staphylococcus.
Manifestation: skin lesions, enterocolitis, and change in blood picture.
Skin lesions: the skin is hyperemic, multiple erosion and sero-purulent
52
crusts are noted. The general condition is severe: diarrhea, vomiting,
pneumonia, sepsis. Staphylococcus, anemia, hypoalbuminemia is
found in the blood.
Treatment
Antibiotics, corticosteroids, vitamins, antistaphylococcal plasma
are used. Locally: antibiotic ointment.

Checkup Questions
1. What diseases are related to the skin diseases of newborns?
2. What are the causes of omphalitis, diaper rash and miliaria?
3. What is the clinical picture of omphalitis, diaper rash and
miliaria?
4. What clinical signs are characteristic of subcutaneous
adiponecrosis, scleredema and sclerema?
5. How do pseudofurunculosis and Leiner’s disease l manifest
clinically?

53
CHAPTER VII
PARASITIC DISEASES OF THE
SKIN
A parasitic disease, also known as parasitosis, is an infectious
disease caused or transmitted by a parasite.
Parasites – the creatures living on the nutrients derived from the
host organism. Skin parasites can live on the skin (lice) and under the
skin (scabies mites).

Unit 1
Scabies
Scabies is a contagious, extremely itchy, skin disorder that leads
to a rash. It is caused by an infestation with a parasite - the scabies
mite. The mite lives on the skin and burrows into it. Scabies is spread
to others through close skin-to-skin contact.
Scabies is caused by the arachnid mite (like a tiny insect) called
Sarcoptes scabiei var hominis. The mite is a parasite, meaning it
lives off the host (a human) with no benefit to the host. Scabies mites
are tiny. They have a cream-colored body, bristles and spines on their
back, and four pairs of legs. The female mite is bigger (about 0.4 mm
x 0.3 mm) compared with the male (0.2 mm x 0.15 mm).
Pathophysiology
The mite, S. scabies, spreads disease through direct and
prolonged contact with the host. The mite remains viable for 2−5 days
on inanimate objects; therefore, transmission through fomites, such as
infected bedding or clothing, is possible, but less likely. The female
mites tunnel into the skin and lay eggs. About 40-50 eggs are laid in
the lifetime of a mite. The eggs hatch into larvae after 3-4 days; these
then grow into adults within 10-15 days. The larvae leave the burrow
to mature on the skin. Less than one in 10 eggs becomes an adult
scabies mite (Fig. 3.1).

54
 Fig. 3.1. – Life cycle of the scabies mite

Most of the symptoms of scabies infestation are due to the

immune system response to the mites themselves, their saliva, their
eggs or their faeces. A delayed type IV hypersensitivity reaction to the
mites, their eggs, or scybala (packets of feces) occurs approximately
30 days after infestation.
This reaction is responsible for the intense pruritus, which is the
hallmark of the disease. Individuals who are already sensitized from a
prior infestation can develop symptoms within hours.
The average number of mites on an infected person is 12.
Neglected children with scabies in underprivileged communities may
have 100s of mites.
Scabies is more common in urban (town) areas, in women and
children (probably due to close contact), in the winter (again when
people spend more time closer together), and in the North of the
country.
How do you get scabies?
Close skin-to-skin contact with an infected person causes scabies.
This is because the scabies mite cannot jump or fly.
Most cases of scabies are probably caught from prolonged hand-
holding with an infected person. The hand is the most common site to
be first affected.
55
 Close skin-to-skin contact when having sex is another common
way of catching scabies.
The skin-to-skin contact needs to be for a reasonable time to catch
the mite. Therefore, you are unlikely to catch scabies from an infected
person by casual short contact such as a handshake or a hug. The rate
of transmission (spread) is higher the greater the number of mites. The
mites live in skin and can survive away from the host human for about
24-36 hours. You are unlikely to catch scabies from bedding and
towels unless you use them immediately after being used by someone
with scabies. However, due to the potential risk, it is best to treat
bedding and towels by hot washing (described later). Sometimes
outbreaks of scabies occur in places such as nurseries and residential
homes, where people are in regular close contact.
Clinical Presentation
Mite tunnels (burrows). These may be seen on the skin as fine,
irregular, dark, or silvery lines about 2-10 mm long. They most
commonly occur in the loose skin between the fingers (the web
spaces), the inner surface of the wrists, and the hands. In infants,
burrows are commonly located on the palms and soles. However, they
can occur on any part of the skin. You may not notice the burrows
until rash or itch develops. A black dot may be seen at one end of the
burrow, indicating the presence of a mite.
Itching. This is often severe and at first tends to be in one place
(often on the hands), and then spreads to other areas. Itch is usually
present in the palms, interdigital areas, axillae (armpits), gluteal and
abdominal regions, (stomach), but can be generalized. In grown-ups
the rash usually doesn`t affect the face and neck However, in infants
and young children, the lesions are localized on the face, neck, trunk,
palms, and soles. Patients with crusted scabies may itch only 50% of
the time. The itch is generally worse at night and after hot bath. You
can have widespread itching, even with only a few mites.
Rash. The rash usually appears soon after the itch starts. It is
typically a blotchy, lumpy red rash that can appear anywhere on the
body. The rash is often most obvious on the inner side of the thighs,
parts of the abdomen and buttocks, armpits, and around the nipples in
women. The appearance of the rash is often typical. However, some
people develop unusual rash which may be confused with other skin
conditions. Vesicles and papules usually pared can be seen near
burrows or alone. Vesicles appear as discrete lesions filled with serous
56
rather than purulent fluid.
Secondary elements are usually the result of excessive
scratching. Characteristic findings include excoriations,
postinflammatory hyperpigmentation, generalized eczematous
dermatitis, erythroderma, prurigo like lesions, and pyoderma.
Specific additional symptoms of scabies:
• Gorchakov`s symptom – hemorrhagic crusts in the area of the
elbows.
• Ardi symptom – impetigo-like elements around elbow area.
• Triangular symptom – crusts, excoriations, papular-pustular
elements in the glutea and sacral areas.
Scratching. Scratching due to intense itching can cause minor
skin damage. In some cases the damaged skin becomes infected by
bacteria – a secondary skin infection develops. If the skin becomes
infected with bacteria it becomes red, inflamed, hot, and tender.
Aggravation of pre-existing skin conditions
Scabies can worsen the symptoms of other skin conditions,
particularly itchy skin problems such as eczema, or problems such as
psoriasis. Scabies can be more difficult to diagnose in these situations too.
Diagnosis
Scabies tends to be diagnosed clinically. This means on the basis
of typical symptoms and the typical appearance of the skin rash.
Often, a doctor will find one or more mite burrows on the skin to
confirm the diagnosis.
It is sometimes difficult to see the difference between the rash
caused by scabies and some other skin conditions. Therefore, a
scraping from the skin is sometimes sent to the laboratory to look for
mites under the microscope if there is doubt about the diagnosis. A
definitive diagnosis is made if the scraping contains a mite, larvae,
eggs, or fecal pellets.
If itching and a rash develop in several people who live in the
same home at about the same time, then scabies is a likely cause.
Treatment
Who should be treated?
Scabies will persist indefinitely if not treated.
Treatment is needed for:
x Anybody who has scabies.
x All household members, close contacts, and sleeping/sexual
partners of the affected person – even if they have no symptoms. This
57
is because it can take up to six weeks to develop symptoms after you
become infected. Close contacts may be infected, but have no
symptoms, and may pass on the mite.
Note: everyone who is treated should be treated at the same time
– that is, on the same day.
Scabies is curable. The usual scabies treatment is with permethrin
5% dermal cream (Lyclear). Permethrin is an insecticide that kills the
mites. If permethrin cannot be used, an alternative is to use a Prioderm
Malathion Lotion 0.5% (some people may be allergic to permethrin),
Crotamiton (Eurax), 25% benzyl benzoate ointment (Ascabiol) and
10% sulphur ointment.
5% permethrin cream is a standard therapy for scabies in adults
and children over five years of age. Permethrin is a synthetic
pyrethoid and potent insecticide. Permethrin is very effective against
mites with a low mammalian toxicity. Permethrin is absorbed
cutaneously only in small amounts, rapidly metabolized by skin
esterases, and excreted in urine. Adverse effects include itching and
stinging on application. After taking bath or shower, 5 % permethrin
cream is applied to the entire body starting from the neck and then
down across the body. The cream is washed off after eight to 14
hours. Unless new lesions develop within 10 days, retreatment is
unnecessary. 5 percent permethrin cream may be used in infants over
two months of age. In children under five years old, the cream must be
applied to the head and neck, as well as to the body.
Permethrin is a pregnancy category B drug and has been used
without apparent side-effects in pregnant women. Its safety in
breastfeeding women is unknown. When a nursing mother has to be
treated with permethrin, it would be appropriate for her to bottle-feed
her infant and discard pumped breast milk until residual cream has
been washed off thoroughly.
Previously, 1% lindane lotion was a standard treatment for usual
scabies. Although lindane is generally effective, treatment resistance
has occurred. The chief advantage of lindane is its low cost. The
primary disadvantage is a potential for neurotoxicity, if misused,
which may be increased in patients with major breaks (damages) in
their skin (e.g., those with crusted scabies) or in infants and little
children. Lindane lotion is applied like permethrin cream, but it is
washed off after six hours and reapplied one week later.
5 or 10% precipitated sulfur in petrolatum is effective. This
58
agent is inexpensive and can be made by a compounding pharmacy. It
should be applied to the entire body (including the head and neck in
newborns) for 24 hours and then reapplied every 24 hours for next
5−7 days. Bath should be taken before each application and 24 hours
after the last application. All clothes and bed linens should be changed
when treatment is completed. Environmental control is essential for
successful treatment. Sulphur is recommended as a safe alternative for
treatment of scabies in infants, children, and pregnant women.
Benzylbenzoate, an ester of benzoic acid and benzyl alcohol is
obtained from balsam of Peru and Tolu. Benzyl benzoate is neurotoxic
to the mites. It is used as a 25% emulsion and the contact period is 24
hours.
Benzyl benzoate should be applied below the neck three times
within 24 hours without an intervening bath. In young adults or
children, the dosage can be reduced to 12.5%. Benzyl benzoate is very
effective when used properly. If not properly applied, it may lead to
treatment failure. Moreover, it can also cause irritant dermatitis on the
face and scrotum. Repeated usage may lead to allergic dermatitis.
It is forbidden in pregnant and lactating women, infants, and
young children under 2 years old. Because of the side effects and
availability of less toxic agents, this scabicide had fallen into
disrepute. However, recent studies have found it to be effective in the
management of permethrin resistant crusted scabies and in
combination with ivermectin in patients with relapses after a single
treatment with ivermectin. In developing countries where the
resources are limited, it is used in the management of scabies as a
cheaper alternative.
Crotamiton (crotonyl-N-ethyl-o-toluidine) is used as 10% cream or
lotion. The success rate varies between 50% and 70%. The best results
have been obtained when applied twice daily for five consecutive days
after bathing and changing clothes. However, much stress has been put
on its antipruritic properties but recent studies have not revealed any
specific antipruritic effects. Some authors do not recommend crotamiton
because of the lack of efficacy and toxicity data.
Monosulfiram .The chemical name of monosulfiram is tetraethyl
thiuram monosulphide. Monosulfiram emulsion is applied all over the
body after bathing, and it should be rubbed in well once a day on two
or three consecutive days. Monosulfiram is chemically related to
antabuse and hence alcoholic beverages should be avoided during or
59
soon after treatment. Soaps containing monosulfiram have been used
in the past as a prophylactic measure in infected communities.
Atypical Forms of Scabies
Crusted scabies (Norwegian scabies)
This type of scabies is unusual, and most people who develop
scabies do not suffer from Norwegian scabies.
It is more severe form of scabies with a hyperinfestation of
scabies mites. This means that there are thousands or millions of the
mites, causing excessive flaking of the skin. As there are so many
mites, and because the skin is flaking off, it is very contagious. The
rash is crusting and looks a bit like psoriasis. It can be very extensive
and can, if severe, lead to serious secondary bacterial skin infections.
Crusted scabies mainly occurs in people who are
immunocompromised (i.e. have a poor immune system). They include
people with HIV/AIDS, people having chemotherapy and frail people
who are elderly or ill with other diseases. Other people at risk are
those who are malnourished; have learning difficulties (i.e. they
cannot comprehend or respond to the itch) or nerve-related problems
(i.e. they cannot feel the itch).
Crusted scabies is more easily transmitted through contact with
towels, bedding and upholstery. In crusted scabies, the mites can
survive for a week. Even minimally exposed people, such as cleaners
and laundry personnel, are at risk from crusted scabies and need
insecticide treatment if they are working in an institution with an
outbreak of this infection. An outbreak in the institution with many
vulnerable people, such as a nursing home, can be extremely
challenging. It is likely that all residents and all staff would require
treatment.
A healthy person with a normal immune system would develop
'normal' scabies if infested with the scabies mite following contact
with someone who had crusted scabies.
Crusted scabies may be impossible to eradicate in people with
HIV infection, and recurrences are common.
Nodular scabies occurs in 7−10% of patients with scabies.
Nodular scabies is a chronic form of scabies characterized by pink,
tan, brown, or red nodules on the covered parts of the body
particularly on the male genitalia, groin, and axillary region. They
range from 2−20 millimeters in diameter
Scabies without a burrow can develop in patients who wash
60
hands often. In such cases the clinics can be not so prominent.
Scabies developed during use of corticosteroids.
Corticosteroids that are used for the treatment of other diseases may
prevent the development of the inflammation and make the diagnosis
more difficult.
Scabies of the animal`s mites. The acarus from cats and dogs
rarely attack the human skin, as man is not a suitable host. Human
infestation with animal scabies is known to be self-limiting, and,
clinically burrows are often absent. Cases have been documented of
transmission from horses, cattle, goats, camels, llamas, sheep and
foxes. The affection in such cases is usually transient.

Unit 2
Pediculosis
Pediculosis is a human parasitic infection that has been
widespread and known for thousands of years. Pediculosis means an
infestation with lice in humans. Overcrowding encourages the spread
of lice. The body louse is the vector of typhus, trench fever, and
relapsing fever.
The disease is spread from person to person by close physical
contact or through fomites (e.g., combs, clothes, hats, linens). Lice are
blood-sucking insects and specific parasites of human beings.
Pathophysiology
Lice are 1-3 mm long and have three pairs of legs that end in
powerful claws. Pubic lice are slightly smaller than head lice and body
lice. The female lives for 1-3 months but dies when separated from the
host.
The female louse lays up to 300 eggs, called nits, during her
lifetime. The nits are less than 1 mm in diameter and, when viable, are
opalescent. The nits hatch 6-10 days after laying, giving rise to
nymphs that become adults in 10 days (Fig. 3.2).

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 Fig. 3.2. – Life cycle of the lice

3 species of lice have adapted to live on humans:

x Head louse (Pediculus humanus variety capitis) is responsible
for head lice.
x Body louse (Pediculus humanus variety corporis) giving body
lice, which were very common during the First World War and are
now seen in a precarious situation (homeless, migrants).
x Crab (or pubic) louse (Phtirus pubis) is responsible for pubic
phthiriasis, colonization by “pubic hair”, which is most often to be
considered a sexually transmitted disease.
Head Lice
Cause
Head lice are still common, affecting up to 10% of children even
in the smartest schools. All socioeconomic classes are affected. Girls
are more commonly infested, but hair length or personal hygiene is
not predictive factors. Due to unique hair characteristics, African
Americans are less commonly bothered by head lice.
Head-lice transmission is most commonly via direct head-to-head
contact. Sharing pillows, caps, headphones, and combs/brushes are
notorious ways to transmit head lice. Since the head louse dies due to
dehydration within two days if not feeding on their human host,
contact with carpeting and couches is less commonly seen as a route
of transmission.
The head louse is a grey-white animal about 2 mm-3 mm in
length (about the size of a sesame seed), and often rather hard to find.
The life span of the female louse is about one month. During this time,
she will produce seven to 10 eggs ("nits") per day. After six to 10
62
days, the oval-shaped nits hatch as nymphs and become adults in 10
days. However, its egg cases (nits) can be seen easily enough, firmly
stuck to the hair shafts. These grayish-white nits, which resemble
dandruff, are attached with a cement-like, water-insoluble substance that
makes them difficult to remove. Spread from person to person is
achieved by head-to-head contact, and perhaps by shared combs or hats.
Clinical Presentation
Most lice infestations are asymptomatic (meaning they cause no
symptoms). However, if symptoms are present, itching of the scalp,
neck, and behind the ears are the most common complaints. Intense
scratching may lead to secondary skin infections (for example,
impetigo) and associated enlargement of the lymph nodes of the neck
and scalp regions. Head lice are found most often on the back of the
head and neck and behind the ears. Eyelashes may be involved. Adult
body lice and nits are found in clothing seams.
The main symptom is itching, at first around the sides and back of
the scalp and then more generally over it. Itching occurs, most
commonly at night, scratching may cause inflammation and a
secondary bacterial infection. Uninfected bites present as
erythematous papules, 2-4 mm in diameter, with an erythematous
base. Scratching and secondary infection soon follow and, in heavy
infestations, the hair becomes matted and smelly.
Complications
x Secondary bacterial infection may be severe enough to make
the child listless and feverish.
x Blepharitis, conjunctivitis, or corneal epithelial keratitis when
the eyelashes are affected may develop.
Differential diagnosis
All patients with recurrent impetigo or crusted eczema on their
scalps should be carefully examined for the presence of nits.
Investigations
None are usually required. The diagnosis is made by
demonstration of the adult lice or nits. Nits are more easily seen when
examined using a Wood's light ("black light") that causes them to
fluoresce as pale blue objects attached to the hair shafts near the scalp.
A fine-tooth comb run through the hair will also demonstrate adult
lice and nits.

63
 Treatment
Head lice have been found on hats, scarves, brushes, combs, hair
accessories, linens, towels, and stuffed animals. Since exposure to
these fomites could result in infestation, it is recommended that such
items used by the infested person within 2 days prior to pediculicide
treatment be machine washed with hot water and dried with hot air
since the lice and eggs are killed after 5 minutes of exposure to
temperatures greater than 53.5°C (128.3°F). Items that cannot be
laundered can be dry-cleaned or sealed in a plastic bag for 2 weeks.
The floors and furniture should be vacuumed in order to remove hairs
from an infested individual, which might have been shed with viable
nits attached. Children should also be educated not to share combs,
brushes, hair accessories, and towels.
Malathion, carbaryl and permethrin preparations are probably the
treatments of choice now. They kill lice and eggs effectively;
Malathion has the extra value of sticking to the hair and so protecting
against reinfection for 6 weeks.
Lotions should remain on the scalp for at least 12 hours, and they
are more effective than shampoos. The application should be repeated
after 1 week so that any lice that survive the first application and hatch
out in that interval can be killed. Other members of the family and
school mates should be checked. A toothcomb helps to remove nits
but occasionally matting is so severe that the hair has to be clipped
short.
Pubic Louse
Cause
The pubic louse ("crab louse") is distinct morphologically
(somewhat rounded with three pairs of legs on either side of the body
from which it takes its descriptive name) from the head and body
louse. The pubic louse (Pthirus pubis) is 'crab'-shaped, grey-brown in
colour, and about 2 mm in length. The female life span is slightly
shorter (three weeks), and it produces fewer eggs per day (three) than
her counterparts. The eggs attach to the base of the pubic hair shaft for
approximately six to eight days before hatching. The female louse lays
eggs (smaller than a pinhead) on the hair shaft, near to the body. The
eggs hatch after about 6-10 days. The empty eggshells (nits) are
tightly attached to the hair. The female louse lives for 1-3 months.
Eradication of pubic lice from the body is unlikely unless treated.

64
 Clinical Presentation
They are common among young adults.
Pubic lice are transmitted by close body contact, which can be
from sexual contact or from close family contact (e.g. from an infested
beard or chest). Pubic lice in children may be an indication of sexual
abuse but most children with pubic lice infestation have probably
acquired this innocently. Transmission by bed linens and infested
clothing is less likely and doubted by some. Contrary to popular
thinking, pubic lice are not spread by toilet seats.
The incubation period is usually between 5 days and several weeks.
Pubic hair is the most common site of the pubic lice. Pubic lice
may spread to hair around the anus, abdomen, axillae, and chest. Risk
factors include overcrowding, poor hygiene, debilitated and
malnourished individuals, sexual promiscuity. Pubic lice are readily
transmitted sexually. Perhaps they occasionally may be transmitted
through contaminated clothing or towels, although this is
controversial. Intense itching of the pubic area is characteristic. Itchy
red papules are the most common presentation. Itching takes 1-3
weeks to develop after the first infestation, but may occur immediately
following reinfestation. Itching tends to be worse at night.
Blue macules may be visible at feeding sites.
The presence of pubic lice should prompt an evaluation for other
common sexually transmitted diseases, such as chlamydial infection
and gonorrhea.
Complications
Excoriation and skin infection are due to scratching. Blepharitis,
conjunctivitis, or corneal epithelial keratitis may develop when the
eyelashes are affected.
Differential Diagnosis
Nits: seborrheic scales, small crusts of scratched dermatitis, hair
muffs (secretions from the hair follicle that are wrapped round the hair
shaft). These can all be brushed off but nits are firmly attached to the hair.
Body (clothing) lice (Pediculus humanus), which are slightly
larger than pubic lice, are found only on clothes; head lice, which are
slightly larger than pubic ones, are found only on the scalp.
Itchy red papules: scabies.
Investigations
The diagnosis is based on finding adult lice or eggs. Pubic lice
live on coarse hair, especially in the pubic and perianal areas, but also
65
on the eyelashes, abdomen, back, axillae and on the head. Therefore,
all hairy parts of the body should be examined. A fine-toothed comb
may be useful for detection. Minute dark-brown specks of louse
excreta are sometimes seen on the skin and underwear.
Treatment
Treatment is the same as for head lice.
Any close contacts over the past 3 months should be examined for
pubic lice. Advise the individual to avoid close body contact until
they, and any current sexual partner, have been treated. Sexual
contacts also should be treated if infested.
For people with infestation of the eyelashes, treat the eyelashes
with an inert occlusive ophthalmic ointment (e.g. simple eye ointment
BP) or a topical insecticide (a cream rinse or shampoo should be
used). On the eyelashes, it is possible to apply a cream containing 1%
permethrin or in the absence of it – pure petrolatum. An inert
occlusive ophthalmic ointment should be used for people under the
age of 18 years, and for those who are pregnant or breast-feeding.
Pediculosis of the pubis is treated with the same products as that
of the scalp, i.e., by a lotion of insecticide (Malathion, Prioderm to
avoid before two years, pyrethrins: Para, Spray Pax). It is best to treat
all the hairy areas of the trunk and thighs but not the scalp. Hair
shaving is sometimes necessary in case of heavy nits and mowers,
razors, scissors, etc. must be removed by soaking them in water at
more than 65 ° C for at least 10 minutes. Clothing that has been in
contact with the infested area of the person for 3 days prior to
treatment is disinfected by washing at 60 ° C. Non washable textiles at
60°C must be insulated in a plastic bag for at least 3 days.
Treat the individual with a topical insecticide: two applications of
malathion – 0.5% aqueous lotion or permethrin -5% dermal cream, 7
days apart. All surfaces of the body should be treated, including the
scalp, neck, and face (paying particular attention to the eyebrows and
other facial hair). If pubic lice infestation is unresponsive to initial
insecticide treatment, repeat the previous treatment with the correct
technique (rather than switching to a different treatment).
If insecticide resistance is suspected, use an alternative insecticide
(Malathion or Permethrin).
When reinfestation occurs, repeat the previous treatment and
assess all close contacts for pubic lice and treat all positive cases
simultaneously.
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 Prevention
Shaving the infested areas does not provide protection from
reinfestation because pubic lice need only a minimal length of hair on
which to lay eggs.
Body Lice
Cause
Pediculosis is usually caused by contact with an infested person.
Body-lice infestation is a prominent public health problem in
communities with large populations dealing with poverty,
overcrowding, and poor personal hygiene. Reused mattresses and bed
linens as well as communal beds are risk factors. Body lice are most
often seen in cold climates, in poor sanitation and with overcrowding.
Body lice also occur mainly when clothes are not changed or washed
regularly. Therefore homeless populations are predominantly affected.
Pediculosis and scabies may coexist in the same individual.
Clinical Presentation
The body louse is slightly larger than the head louse but has the
same general appearance. Unlike the head louse, this lives on its
human host, the body louse lives in clothing (commonly in the seamed
areas) and then transfers to the human host to feed. The life cycle of
the head louse and the body louse are similar in character and
duration. An important difference, however, is the ability of the body
louse to survive for up to 30 days away from its human host.
Itching is the primary symptom of body-lice infestation. Areas
where seams of clothing are tightly adherent to the body are the most
likely areas of involvement. Waistband lines, and axillary and bra
strap regions are examples of where excoriation (crusts, abrasions, or
scabbing) from scratching is commonly noted.
Many lice infestations are asymptomatic.
Pruritus is accompanied by excoriations that can become infected
secondarily and papules are linked to bite reactions.
Complications
The body louse acts as a vector for trench fever, epidemic typhus
and relapsing fever.
Differential diagnosis
Unlike dandruff and hair root sheath casts, nits are stuck to the
hair and are difficult to remove. Nits are fluorescent under a Wood's
light.

67
 Investigations
Diagnosis is based on seeing eggs (nits), nymphs or mature lice.
Mature lice are 3-4 mm long. Nits are much smaller (about 1
mm). The pubic louse is about the same length as the head or body
louse but has a wider body.
Body lice can be found in any area of the body, although they
tend to avoid the scalp. Nits are laid in the host's clothing and are not
usually found on the hair as with head lice and pubic lice. Body lice
and their eggs are found in clothing seams.
Chronic infestation often leads to postinflammatory pigmentation.
Bedbugs are related to lice. They hide among sheets, blankets,
and in furniture and really do bite during the night when they seek a
warm body for a meal. They usually leave brown or black markings
on the bed linens and bite in rows, often leaving three or more linear
bite marks.
Treatment
Treatment includes improved hygiene and laundering in hot water
of all the infested clothing, bedding and linens. Drug treatment (e.g.
malathion or permethrin) is required in large-scale infestations.
Patients with body lice infestations should wash their entire body
thoroughly and then put on clean clothing. If the infestation is severe,
topically administered permethrin, pyrethrin, or malathion also may
help. Clothing and bedding should be decontaminated by hot-water
washing (60°C) and heated drying, or by dry cleaning. Body lice may
transmit typhus and trench fever.
Antibiotics are needed to treat louse-borne infectious diseases.
Treating clothing with permethrin may prevent infestation.
Treatments are very effective in killing nymphs and mature lice but
less effective in killing eggs.
Appropriate therapy cures in more than 90% of cases.
Prevention
To prevent reinfestation, treat contacts of the patient at the same
time as the patient. Washing combs and brushes reduces reinfestation.

Checkup Questions
1. What do you know about the scabies mite life cycle?
2. In which skin layer does a female scabies mite live?
3. What clinical picture is characteristic of scabies?
4. What is the Ardi symptom?
68
 5. How is the Gorchakov`s symptom desscribed?
6. What is the Triangular symptom?
7. What atypical forms of scabies can develop?
8. What principles of treatment are used for scabies?
9. What kinds of lice exist?
10. What are the clinical manifestations of head pediculosis?
11. What are the differences in the clinical manifestations of head
and pubic pediculosis?
12. What current methods of treatment forpediculosis do you
know?
13. Does the patient need to shave the hair when treating head
lice?

69
CHAPTER VIII
BULLOUS DERMATOSES
Unit 1
Pemphigus
Pemphigus is a rare group of blistering autoimmune, severe and
potentially fatal diseases affecting the skin and mucous membranes.
The etiology of pemphigus is unknown. There are infectious,
neurogenic, endocrine, enzymes and toxic theories of the development
of the disease.
Pathogenesis of pemphigus is autoimmune. In pemphigus,
autoantibodies against desmoglein form. Desmoglein forms the "glue"
that attaches adjacent epidermal cells via attachment points called
desmosomes.
When autoantibodies attack desmogleins, the cells become
separated from each other and the epidermis becomes "unglued", a
phenomenon called acantholysis. This leads to the formation of
intraepidermal blisters and erosions. In some cases, these blisters can
cover a significant area of the skin.
Classification
Pemphigus is a group of autoimmune blistering diseases that may
be classified into the following types:
x Pemphigus vulgaris.
x Pemphigus vegetans:
- Pemphigus vegetans of Hallopeau.
- Pemphigus vegetans of Neumann.
x Pemphigus foliaceus:
- Pemphigus erythematosus.
- Endemic pemphigus.
x Paraneoplastic pemphigus.
x IgA pemphigus:
- Subcorneal pustular dermatosis.
- Intraepidermal neutrophilic IgA dermatosis.
The most common form of the disorder is pemphigus vulgaris. It
is caused by autoantibodies against keratinocyte proteins desmoglein-
70
1 and desmoglein-3. Although pemphigus vulgaris may occur at any
age, it is the most common among people between the ages of 40 and
60.The disease begins on the mucous membrane of the mouth and lips
(more than 60% of cases), less often on the mucous membrane of the
larynx, the posterior pharyngeal wall, trachea, nasal mucosa, rectum
and genital mucosa. Erosions often occur in the mouth making eating
difficult and uncomfortable.
The disease spreads to the skin after 1-3 months or more. First,
the rash is monomorphic and localized on the head, chest, back and
limbs. It is located on the non-inflamed skin and is represented by
flaccid blisters with serous contents. Exudate becomes purulent when
pyococcal flora is added. Crusts appear over time. Epithelization of
erosion is slow. Secondary macules remain in the places of erosion
after epithelialization.
Nickolsky‘s sign is typical for pemphigus.
It has 2 forms:
x dislodging the epidermis by lateral finger pressure in the
vicinity of the lesions which leads to an erosion;
x pressure on the bulla leads to lateral extension of a blister.
Pemphigus vegetans is usually confined to the intertriginous
regions, perioral area, neck, and scalp. Granulomatous vegetating
purulent plaques extend centrifugally. The beginning does not differ
from the initial manifestations of pemphigus vulgaris. Blisters appear
on the apparently unchanged mucosa and skin. The progression of the
disease on the skin can occur in two types.
Type 1 (pemphigus vegetans of Neumann)
Flaccid blisters appear on the skin without hyperemia. Verruciform
growths develop inside the blisters and then open on the surface of
erosions. The plaques rising above the skin grow around the periphery
forming large verruciform grayish white surfaces. Serous-purulent
exudate releases from the surface of the rash. It has a fetid odor due to
the addition of a secondary infection, microbial and fungal (such as
Candida). The verruciform-hyperkeratotic plaques develop not only in
the intertriginous regions, but also outside them (on the head, limbs).
On their surface the crusts of dirty-gray color with painful fissura and
fetid odor are formed. Typical blisters may occur nearby.
Type 2 (pemphigus vegetans of Hallopeau)
The rash is usually localized in the intertriginous regions.
However, the primary skin lesions are represented as grouped
71
yellowish pustules (small acantholytic blisters with a large number of
eosinophilic leukocytes). The verruciform papillomatous growths
develop inside the pustules or on erosion surfaces. New pustules
appear on the edge of the lesions. The area of the lesion increases at
the periphery. Patient's condition worsens: intoxication, fever, poor
appetite, insomnia appears and sepsis joins.
Pemphigus foliaceus
Flabby flat blisters and some erosion appear in the seborrheic
zones (scalp, face, chest and back). They transform into layered
scales-crusts very quickly. Mucous membranes are not affected. A
characteristic clinical sign is appearance of new blisters on the ground
of the previous erosion under the crusts. Layers of yellowish-brownish
scale-crusts form in the places of affection. The lesions have a
tendency to peripheral growth and fusion. Without adequate therapy,
damage to the entire surface of the skin (exfoliative erythroderma)
develops. Nikolsky's symptom is positive.
The least common and most severe type of pemphigus is
paraneoplastic pemphigus. This disorder is a complication of cancer,
usually lymphoma and Castleman's disease. It may precede the
diagnosis of a tumor. Painful sores appear on the mouth, lips, and the
esophagus. In this variety of pemphigus, the disease process often
involves the lungs causing constrictive bronchiolitis. Complete
removal and/or cure of the tumor may improve the skin disease but
lung damage is generally irreversible.
Hailey-Hailey disease, also called familial benign pemphigus, is
an inherited (genetic) skin disease, not an autoimmune disease.
Therefore, it is not considered a part of the Pemphigus group of
diseases.
Diagnosis
Pemphigus is recognized by a dermatologist due to appearance
and distribution of the skin lesions. It is also commonly diagnosed by
specialists practicing otolaryngology (head and neck surgery),
periodontists, oral and maxillofacial surgeons and oculists as the
lesions can affect eyes and the mucous membrane of the oral cavity.
Intraorally it resembles more common diseases – lichen planus and
mucous membrane pemphigoid.
A definitive diagnosis requires examination of the skin or mucous
membrane biopsy by a dermatopathologist. The skin biopsy is taken
from the edge of a blister, prepared for histopathology and examined
72
under microscope. A pathologist looks for intraepidermal vesicles
caused by breaking apart epidermal cells (acantholysis).
A definitive diagnosis also requires demonstration of anti-
desmoglein autoantibodies by direct immunofluorescence on the skin
biopsy. These antibodies appear as IgG deposits along the
desmosomes between the epidermal cells, a pattern reminiscent of
chicken wire. Anti-desmoglein antibodies can also be detected in a
blood sample using the ELISA technique (enzyme-linked
immunosorbent assay). A half of pemphigus patients have oral lesions
alone during the first year but later develop skin lesions.
Main criteria for diagnosis:
x Specific clinical manifestations: blisters on apparently
unchanged skin, long-existing erosion on the skin and on the
apparently unaltered mucous membrane of the mouth, conjunctiva,
nasal mucosa, genitalia.
x Nickolsky‘s sign.
x Asboe-Hansen sign: lateral pressure on the edge of a blister
can spread the blister into clinically intact skin.
x Cytological diagnosis (Tzanck test): smears-prints taken
from the bottom of erosion are stained according to Romanovsky-
Giemsa. Acantholytic cells are found by microscopy. Acantholytic
cells or Tzanck cells are altered keratinocytes of the spinous layer of
the epidermis. They are round, small in size and fragmented. The
nuclei of the cells are intensely stained and enlarged. The cytoplasms
of the cells are light blue around the nuclei and dark blue around the
periphery.
x Biopsy: the biopsy sample will be processed in the laboratory
and examined under microscope. A part of the biopsy sample will be
examined by a technique known as direct immunofluorescence to
demonstrate the presence of pemphigus vulgaris autoantibodies (IgG)
and C3-complement deposition on desmosomes of the cells of the
spinous layer of the epidermis.
x Indirect immunofluorescence: pemphigus vulgaris
autoantibodies (IgG) against desmoglein-1 and desmoglein-3 which
develop can be measured in the blood.
Treatment
If not treated, pemphigus can be fatal because of joining a
secondary infection. Pemphigus vulgaris is usually treated first with

73
oral corticosteroids. Oral corticosteroids are effective and effect
quicker than most other remedies. The corticosteroids used are
synthetic versions of a natural hormone produced in smaller quantities
by the adrenal gland and effect by suppressing the immune system.
The side effects of corticosteroids may require administration of
so-called steroid-sparing or adjuvant drugs. Corticosteroids may be
prescribed as monotherapy or in combination with such cytostatics as
azathioprine or metatrexate, cyclophosphamide and cyclosporin A
(combined therapy). Cytostatics cannot completely replace
corticosteroids. With their help, it is possible to reduce the dose of
corticosteroids.
This treatment has 3 stages:
1. The use of "shock" daily doses (90-120 mg) of corticosteroids
at the beginning of treatment (duration 3-6 weeks before the cessation
of new blisters formation and the completion of skin erosion
epithelization.
2. A gradual slow reduction of a daily dose of corticosteroids to
maintenance one (the duration of the stage is about 4 months).
3. Long-term (whole life) treatment of the patient with
maintenance doses of corticosteroids.
A maintenance dose of corticosteroids is a minimum dose that
inhibits the appearance of blisters.
All these drugs may cause severe side effects, so the patient
should be carefully monitored by doctors. Any cases of
discontinuation of treatment lead to a relapse of the disease
If the skin lesions do become infected, antibiotic may be
prescribed. Local therapy of pemphigus does not make much sense. In
a local treatment the drug combination consisting of corticosteroids
and antibiotics or corticosteroids, antibiotics and antifungal
components is used.
The main complications of steroid therapy include:
x Exogenous (drug-induced) Itsenko-Cushing syndrome.
x Immunosuppressive state with the addition of a secondary
infection.
x Changes in water-salt balance of the body.
x Hypoproteinemia.
x Gastritis, esophagitis, gastric and duodenal ulcer.
x Diabetes.

74
 x Insomnia, euphoria, sometimes steroid psychosis.
x Muscle atrophy, purpura, steroid acne, etc.

Unit 2
Pemphigoid
Pemphigoid is a group of uncommon autoimmune blistering skin
diseases. As its name indicates, pemphigoid is similar to pemphigus
but unlike pemphigus, pemphigoid does not feature acantholysis.
Pemphigoid is more common than pemphigus, and is slightly
more common in women than in men. It is also more common in
people over 60 years old than in younger people.
Etiopathogenesis
IgG autoantibodies to bullous pemphigoid antigens in the
hemidesmosomes at the basement membrane zone bind complement
which induces inflammation and protease release, leading to
subepidermal bulla formation. IgG and C3 are detected by direct
immunofluorescence. Indirect methods demonstrate circulating
autoantibodies in 70% of cases.
Classificiation
There are several types:
x Pemphigoid gestationis (formerly called Herpes gestationis).
x Bullous pemphigoid. It rarely affects the mouth.
x Cicatricial pemphigoid, also known as mucous membrane
pemphigoid (no skin involvement).
Bullous and Cicatricial pemphigoids usually affect persons who
are over 60years old. Gestational pemphigoid occurs during
pregnancy, typically in the second or third trimester, and/or
immediately following pregnancy.
Pemphigoid is usually considered to be mediated by IgG, but
IgA-mediated forms have also been described. IgA pemphigoid rarely
affecst the mouth.
Clinical Presentation
Bullous pemphigoid usually affects the elderly. Tense large
blisters arise on the red or normal-looking skin, often of the limbs,
trunk and flexures. Oral lesions occur only in 10% of cases. The
blisters with bullous pemphigoid persist on the oral mucosa for several
days because of a large depth. When they are opened, painful, well-
defined erosions without fibrinous scurf are formed, which
75
epithelialize faster than with pemphigus. Very rarely, in addition to
the skin, the mucous membrane of the pharynx, larynx, genitalia and
eyes can be affected. An urticarial eruption may precede the onset of
blistering. Pemphigoid is sometimes localized on one site, often the
lower leg. The differential diagnosis of pemphigoid may include
dermatitis herpetiformis, linear IgA disease or pemphigus.
Immunofluorescence and histology may confirm the diagnosis.
Cicatritial pemphigoid mainly affects the ocular and oral
mucous membranes. Scarring results and this can cause serious eye
problems.
Pemphigoid (herpes) gestationis is a rare but characteristic
bullous eruption associated with pregnancy, which remits after the
delivery but can recur during subsequent pregnancies.
Diagnosis is made by the following criteria
x Characteristic clinical manifestations: tense large blisters on
the red or normal-looking skin.
x Nikolsky's sign is negative (but may be slightly positive with
bullous pemphigoid).
x Asboe-Hansen sign can be positive with bullous pemphigoid.
x Cytological diagnosis: a large number of eosinophils (20–
30% or more) are found in the smears from fresh erosion, akantolithic
cells being absent.
x Biopsy: a subepidermal cavity is found with numerous
eosinophils.
x Direct immunofluorescence: homogeneous strip-like
deposition of immunoglobulin G and C3-complement is detected in
the area of the basement membrane
x Indirect immunofluorescence: IgG antibodies to the protein,
which is part of the basement membrane (BP180, 230).
Treatment
Pemphigoid responds to the dose of steroids lower than
pemphigus: from 30-60 mg to lower than 10 mg within some weeks.
Azathioprine is sometimes prescribed too.
The disease is self-limiting in about 50% of cases, and steroids
can often be ceased in 2 years. Cicatricial pemphigoid does not
respond to treatment so well. In the cicatricial stage of the disease
surgery, followed by plastic surgery of the defect is necessary.
Pemphigoid gestationis is controlled by standard doses of steroids.

76
Steroid-induced side-effects may be a problem, especially in the
elderly. A local treatment is prescribed such as for pemphigus.
Corticosteroids are used on the lesions in the form of solutions (intra
focal injections), suspensions, gel or cream, depending on the stage
and localization of the lesion.

Unit 3
Dermatitis Herpetiformis
Dermatitis herpetiformis or Duhring's disease – is a rare
benign, chronically recurrent, polymorphic dermatosis with the
formation of typical herpetiform blisters, accompanied by itching and
burning, and associated with enteropathy in case of hypersensitivity to
gluten. In addition, patients with dermatitis herpetiformis have an
increased sensitivity to iodine salts.
Dermatitis herpetiformis was first described by Dr. Louis Duhring
in 1884. A connection between dermatitis herpetiformis and gluten
intolerance (coeliac disease) was recognized in 1967, although the
exact causal mechanism is not known.
The age of onset is usually about 15-40 years, but dermatitis
herpetiformis can also affect children and the elderly. Men and
women are equally affected. Estimations of dermatitis herpetiformis
prevalence vary from 1 in 400 to 1 in 10000 people.
Etiopathogenesis
Dermatitis herpetiformis is characterized by finding a granular
IgA in the dermal papillae on immunofluorescence, and by the
response of the skin lesions to a gluten-free diet.
Clinical Presentation
Dermatitis herpetiformis is characterized by intensely itchy,
chronic papulovesicular eruptions, usually distributed symmetrically
on the extensor surfaces (buttocks, back of the neck, scalp, elbows,
knees, back, hairline, groin and face). The blisters vary in size from
very small up to 1 cm across.
The condition is extremely itchy, and the desire to scratch can be
overwhelming. Intense itching or burning sensations are sometimes
felt before the blisters appear in a particular area.
Untreated, the severity of dermatitis herpetiformis can vary
significantly over time, in response to the amount of gluten ingested.
Dermatitis herpetiformis symptoms first typically appear in the

77
early years of adulthood between 20 and 30 years of age.
Although the first signs and symptoms of dermatitis herpetiformis
are intense itching and burning, the first visible signs are some small
papules or vesicles that usually look like red bumps or blisters.
Sometimes they appear on the face and along the hairline and, on
occasion, on the shoulders, the lower end of the spinal column and
within the mouth. Rash rarely occurs on the other mucous
membranes, except for the mouth or lips. The symptoms range in
severity from mild to serious, but they are likely to disappear if gluten
ingestion is avoided and appropriate treatment is administered.
Dermatitis herpetiformis symptoms are chronic, and they tend to
come and go, mostly in short periods of time. Sometimes, these
symptoms may be accompanied by the symptoms of coeliac disease,
commonly including abdominal tender bloating or loose stool and
fatigue.
The rash caused by dermatitis herpetiformis forms disappears in
three stages. In the first stage, a patient may notice a slight
discoloration of the skin at the site where the lesions appear. In the
next stage, the skin lesions transform into obvious vesicles and
papules that are likely to occur in groups. Healing of the lesions is the
last stage of the development of the symptoms, usually characterized
by a change in the skin color. This can result in the areas of the skin
turning darker or lighter than the color of the skin on the rest of the
body. Because of the intense itching, patients usually scratch, and this
can lead to the formation of crusts.
Diagnosis Criteria
x Characteristic clinical manifestations;
x Nikolsky's sign is negative;
x Asboe-Hansen sign is negative;
x Jadassohn skin test (a method of diagnosing dermatitis
herpetiformis, based on the increased sensitivity of patients to iodine
preparations; it consists of applying an ointment compress containing
potassium iodide to the skin site at which the patient has erythematous
and vesicular rash);
x Eosinophilia revealed in the blood by test;
x Biopsy of the small intestine finds changes in 70% of patients,
as in a celiac disease;
x Cytological diagnosis shows a large number of eosinophils

78
found in the smears from fresh erosion, akantolithic cells being absent.
x Skin biopsy finds subepidermally located blisters, in the
cavity of which numerous eosinophilic and neutrophilic leukocytes are
detected.
x Direct immunofluorescence shows IgA and C3-complement
deposits detected in the dermal papillae.
x Indirect immunofluorescence reveals IgA antibodies against
endomysium.
Indirect and direct immunofluorescence should be done before the
patient starts on a gluten-free diet, otherwise they might produce false
negatives.
Treatment
Dermatitis herpetiformis responds well to medication and changes
in diet.
A gluten-free diet is a treatment of choice, as it corrects both the
bowel and the skin lesions. In addition, foods rich in iodine salts (sea
fish, squids, crabs, shrimp, algae, various shellfish, etc.) and iodine-
containing medicines should be excluded.
Dapsone (50-200 mg daily) will control the eruption and is often
given until the gluten-free diet has its beneficial effect. A haemolytic
anemia may occur because of dapsone use. Regular blood counts are
necessary.

Checkup Questions
1. What are the forms of pemphigus? How is it classified?
2. What is a clinical picture of the most common form of
pemphigus?
3. What is Nikolsky's sign?
4. What clinical signs are characteristic of pemphigus vegetans,
pemphigus foliaceus and paraneoplastic pemphigus?
5. What methods are used to diagnose pemphigus?
6. What is Asboe-Hansen sign?
7. What are acantholytic cells (Tzanck cells)?
8. What is the basis of the treatment for pemphigus?
9. What complications of corticosteroid therapy can develop?
10. What forms of pemphigoid are distinguished?
11. What are the clinical manifestations of pemphigoid?
12. What methods are used to diagnose pemphigoid?

79
 13. How does dermatitis herpetiformis manifests clinically?
14. What diagnostic methods are used to define dermatitis
herpetiformis?
15. What does Jadassohn skin test consist of?
16. What are the main principles of treatment for dermatitis
herpetiformis?

80
CHAPTER VIII
DISEASES OF SKIN APPENDAGES
Unit 1
Seborrheic Dermatitis
Seborrheic dermatitis (Seborrhea) is a papulosquamous
disorder patterned on the sebum-rich areas of the scalp, face, and
trunk. In addition to sebum, this dermatitis is linked to Malassezia,
immunologic abnormalities, and activation of complement. It is
commonly aggravated by changes in humidity, changes in seasons,
trauma (e.g., scratching), or emotional stress. The severity varies from
mild dandruff to exfoliative erythroderma. People who have immune
system problems, such as HIV/AIDS and people with Parkinson's
disease, are more likely to develop seborrhoeic dermatitis. Also,
emotional stress is thought to aggravate the condition.
Seborrheic dermatitis causes bad dandruff and sometimes rash,
commonly on the face and upper body. It is sometimes called
seborrheic eczema. It mainly occurs in young adults with a peak
around the age of 40. This condition develops about 1 in 25 adults. It
is more common in men than women. Some babies have a similar
condition that usually clears within a few months which is sometimes
called cradle cap.
Pathogenesis
Seborrheic dermatitis is an inflammation of the skin caused by
increased allocation of qualitatively altered fat and active exposure to
microbial agents – Pitirosporum orbiculare and Pityrosporum ovale –
opportunistic fungi of the genus Malassezia furfur. Seborrheic
dermatitis is usually associated with normal levels of Malassezia but
an abnormal immune response. Helper T-cells, phytohemagglutinin
and concanaval in stimulation as well as antibody titers are depressed
as compared with those of control subjects. The effect of Malassezia
may be because of its lipase activity, i.e., releasing inflammatory free
fatty acids and due to its ability to activate the alternative complement
pathway.
However, it is not just a simple skin infection and it is not
contagious (you cannot catch this condition from others). The germ
81
lives in the sebum (oil) of the human skin in most adults. In most
people it does no harm. But some people may react to this yeast germ
in some way which causes the skin inflammation. This involves
exposed skin, densely populated sebaceous glands, the face (namely,
forehead, chin, nose, esomeone folds, scalp, chest (middle line), back
(interscapular region) and the region of the auricles. It is noticed that
the activity of these opportunistic fungi grows under adverse
conditions, such as immune and endocrine disorders, stress, and
various lesions of the nervous system. It is known that opportunistic
pathogenic fungi of the genus Malassezia are concentrated around the
mouths of the sebaceous glands to produce fatty acids, abundant
sebaceous saturating the secret. Thus, seborrhea changes the quality
and quantity of sebum promotes hyperactivation of the fungal
microflora: Pityrosporum ovale, a parasite mainly on the scalp and
Pityrosporum orbiculare, isotropic to the sebaceous glands chest and
back. Adverse factors to enhance the pathological process are
considered irritating alkaline detergents, excessive sweating and a
winter season.
Clinical Presentation
The areas of the body that tend to be affected are those where
there are the most skin glands which make sebum (seborrheic zones).
Therefore, the condition mainly affects the more greasy areas of the
skin such as the scalp, forehead and face around the eyebrow area and
on either side of the nose.
Other areas which are sometimes affected are the chest, the
armpits, and the area under the breasts, the groins and inside and
behind the ears. Some people also develop inflammation of the outer
ear canal and/or of the eyelids.
When seborrheic dermatitis skin lesion is gradual, slowly
progressive in nature and is accompanied by itching, often intense. On
the seborrheic areas on the background stains of red plaques appear
with fairly clear boundaries, formed by the merger of small papules of
yellowish-pink color, covered with greasy scales. The process of skin
lesions development is often symmetrical in nature and at the expense
of peripheral growth and resolution in the center of the plaque can be
purchased and getlangoptions annular shape.
The condition tends to flare up and down from time to time.
However, treatment can usually keep symptoms to a minimum.
In most cases, no investigations are needed and seborrheic
82
dermatitis is diagnosed by the typical symptoms and rash. However,
treatment can usually keep symptoms to a minimum.
Diagnosis of seborrheic dermatitis
In most cases, no investigations are needed and seborrheic
dermatitis is diagnosed by the typical symptoms and rash.
If the diagnosis of seborrheic dermatitis you need to eliminate
such skin diseases as atopic dermatitis, eczematid, psoriasis, fungal
infections (ringworm) and microbial infections of the skin. This
requires microscopic and mycological study of skin flakes pathogenic
fungi.
Sometimes it is useful to resort to diagnostic biopsy, which
together with multiple signs will record cells-neutrophils in the
composition of crusts and scales, and in the mouths of the hair
follicles.
When seborrheic dermatitis is torpedo, further research of the
patient’s hormonal status is necessary.
Treatment
Commonly used treatments include the following:
An antifungal (anti-yeast) shampoo such as ketoconazole is used
to treat the scalp, eyebrows and other hairy areas. This kills the fungal
germ and the skin then usually returns to normal. Use the shampoo
2-3 times a week (and use normal shampoo the rest of the time).
Leave the shampoo on for about five minutes before rinsing off.
Follow the instructions that come with the shampoo. Dandruff
responds to more frequent shampooing or a longer period of lathering.
Use of hair spray or hair pomades should be stopped.
Shampoos containing salicylic acid, tar, selenium, sulfur, or zinc
are effective and may be used in an alternating schedule.
An antifungal cream can be used to treat other areas. Apply the
cream to affected areas once or twice daily, depending on the type of
cream prescribed.
It often takes 2-4 weeks to clear the dandruff or rash completely.
Keep using the treatment for a few days after the dandruff or rash has
cleared. You should avoid using soap or shaving creams on your face
as they can add to the skin irritation. A non-greasy emollient soap
substitute can be used. Cosmetic products that contain alcohol should
also be avoided.
Other treatments which may be used are as follows:
x A normal anti-dandruff shampoo that contains zinc pyrithione
83
or coal tar may clear dandruff in mild cases, if used regularly.
x A scale softener is sometimes advised for the scalp to lift the
scale if dandruff is severe. This is in addition to the antifungal
shampoo.
x A mild steroid cream and/or steroid scalp lotion is sometimes
advised each day for a week or so in addition to an antifungal cream
or shampoo. This is used if the skin or scalp is badly inflamed. Steroid
creams and lotions dampen inflammation, that reduces the redness and
itch. However, you should not use steroid creams, ointments or lotions
long-term. See your doctor if the inflammation does not settle within a
week or so.
x Pimecrolimus cream (Elidel) or tacrolimus ointment may
sometimes be prescribed if skin inflammation is more severe.
x A course of antifungal tablets may be needed if the condition
affects many areas of skin, or does not clear with an antifungal cream.
x Phototherapy (light treatment) with ultraviolet B is sometimes
used in severe cases.
However, sebum is a natural place for the germ to live. In many
cases, the number of germs gradually rises again on the skin after
finishing a course of treatment. So, often, seborrheic dermatitis recurs
some weeks or months after finishing a course of treatment.
How can you prevent seborrheic dermatitis from recurrence?
Once the symptoms have gone with treatment, the following may
help to keep the condition from recurring:
For the scalp – use an antifungal shampoo such as ketoconazole
once every 1-2 weeks. Leave it on the scalp for five minutes before
rinsing. (Use a normal shampoo at other times.)
For the body – daily washing with soap and water helps to
remove the greasy sebum from the body. This helps to keep the
number of fungal germs to a minimum. This procedure combined with
using an antifungal shampoo every 1-2 weeks, and rubbing the
shampoo lather on your body as well as your scalp, may resolve the
condition. However, to keep the condition from recurrence, some
people need to use an antifungal cream 1-3 times a week on areas of
the skin usually affected.

84
 Unit 2
Acne
Acne is a very common polymorphic dermatosis of the
pilosebaceous unit with characteristic clinical features. The intensity
and duration of activity vary for each individual. The clinical
expression ranges from non-inflammatory closed and open comedones
to inflammatory papules, pustules, and nodules. Acne varies in
severity from a very distressing, socially disabling disorder to a state
that has been regarded by some authors as physiological. Acne has an
equal sex incidence and tends to affect women earlier than men,
although the peak age for clinical acne is 18 years in both sexes.
Acne is a chronic inflammation of the pilosebaceous units,
producing comedones, papules, pustules, cysts, and scars.
Causes
The most common trigger is puberty, namely:
x increased sebum excretion;
x pilosebaceous duct hyperkeratosis;
x colonization of the duct with Propionibacterium acnes;
x release of inflammatory mediators (including cytokines).
During puberty, surges in androgen stimulate sebum production
and hyperproliferation of keratinocytes. Propionibacterium acnes (a
normal human anaerobe) proliferate in sebum, and the follicular
epithelial lining becomes altered and forms plugs called comedones.
Excess sebum is also a key factor in the development of acne
vulgaris. The amount of sebum produced and the degree as well as
the severity of the acne are strongly correlated. Factors in sebum
induce comedones, and P. acnes initiates inflammation through
chemical mediators inducing enzymes (e.g. lipase) and
prostaglandins.
Other triggers include:
x Hormonal changes that occur with pregnancy or the menstrual
cycle. Sebum excretion is under hormonal control. Androgens
stimulate sebocyte differentiation and sebum production, whereas
estrogens have an inhibitory effect;
x Occlusive cosmetics, cleansers, lotions, and clothing;
x High humidity and sweating;
Some studies suggest a possible association with milk products
and high-glycemic diets.
85
 Acne may abate in summer months because of sunlight’s anti-
inflammatory effects.
Proposed associations between acne and hyperinsulinizm require
further investigation.
Some drugs and chemicals (e.g, corticosteroids, lithium,
phenytoin and isoniazid) worsen acne or cause acneiform eruptions.
Factors in sebum induce comedones, and P. acnes initiates
inflammation through chemical mediators inducing enzymes (e.g.
lipase) and prostaglandins.
Clinical Presentation
Acne lesions
These lesions can be described in 3 categories:
1. Noninflammatory lesions consist of open (blackheads –
dilated pores with black plugs of melanin-containing keratin) and
closed (whiteheads – small cream-colored, dome-shaped papules)
comedones. They appear at the age of about 12 years and evolve into
inflammatory lesions.
2. Inflammatory lesions are characterized by the presence of one
or more of the following types of lesions:
x papules;
x pustules;
x nodules (cysts).
Papules are less than 5 mm in diameter. Pustules have a visible
central core of purulent material. Nodules are greater than 5 mm in
diameter. Nodules may become suppurative or hemorrhagic.
Suppurative nodular lesions have been referred to as cysts because
of their resemblance to inflamed epidermal cysts.
For inflammatory acne lesions, the Consensus Panel proposes that
lesions should be classified as papulopustular and/or nodular. A
severity grade can be mild, moderate, or severe.
3. Scars
Recurring rupture and reepithelialization of cysts leads to
epithelial-lined sinus tracts, often accompanied by disfiguring scars.
Scars may follow healing, especially of cysts or abscesses. Scars may
be 'ice-pick', atrophic or keloidal.
Other factors in assessment of severity include ongoing scarring,
persistent purulent and/or serosanguineous drainage from the lesions,
and the presence of sinus tracts. The sites of predilection, namely, the
face, shoulders, back and upper chest - have many sebaceous glands.
86
 The severity of acne depends on its extent and the type of the
lesion, with the most destructive cysts. Acne usually persists until the
early 20s, although in a few patients, particularly women, the disease
continues into the 5th decade.
Types of Acne
Acne vulgaris is a common skin disease that affects 85-100% of
people at certain time during their lives. There are several types of
acne. They are:
x Comedonic acne.
x Papular pustular acne.
x Nodular acne.
It affects comedogenic areas and occurs mainly in puberty (in
boys more frequently than in girls.
Infantile acne is mostly found on the faces of male infants.
Cause: unknown. Acneiform lesions confined to the nose and cheeks
may be present at birth or may develop in early infancy. The lesions
clear without treatment as the large sebaceous glands stimulated by
maternal androgens become smaller and less active.
Severe nodulocystic acne includes localized cystic acne (few
cysts on the face, chest, or back), diffuse cystic acne (wide areas of the
face, chest, and back), pyoderma faciale (inflamed cysts localized on
the face in females), and acne conglobate (highly inflammatory, with
cysts that develop under the skin, abscesses, and burrowing sinus
tracts).
Cystic acne is a serious and sometimes devastating disease that
requires aggressive treatment. The face, chest, back, and upper arms
may be permanently mutilated by numerous atrophic or hypertrophic
scars. Patients are often embarrassed and preoccupied with their
disease. They may experience anxiety, depression, insecurity, psychic
suffering, and social isolation. The physical appearance may be so
unattractive that teenagers refuse to attend school and adults have fear
of going to work.
There are three less common variants of cystic acne:
xAcne conglobate is a chronic, highly inflammatory form of
cystic acne in which involved areas contain a mixture of double
comedones, papules, pustules, communicating cysts, abscesses, and
draining sinus tracts. The disease may linger for years, ending with
deep atrophic or keloidal scarring. Acne conglobata is a part of the
rare follicular occlusion triad syndrome of acne conglobata,
87
hidradenitis suppurativa, and dissecting cellulitis of the scalp.
Musculoskeletal symptoms have been reported in some of these
patients; 85% were black. There is no fever or weight loss as is seen in
acne fulminans.
xAcne fulminans is a rare ulcerative form of acne of unknown
etiology with an acute onset and systemic symptoms. It most
commonly affects adolescent white boys. A genetic predisposition is
suspected. Ulcerative, necrotic acne with systemic symptoms develops
rapidly. There are arthralgias or severe muscle pain, or both, that
accompany the acne flare. Painful bone lesions occur in approximately
40% of patients. Weight loss, fever, leukocytosis, and elevated
erythrocyte sedimentation rate (ESR) are common findings.
xPyoderma faciale is a distinctive variant of cystic acne that
remains confined to the face. It is a disease of adult women ranging in
age from the teens to the forties. They experience the rapid onset of
large, sore, erythematous-to-purple cysts, predominantly on the central
portion of the cheeks. Erythema may be intense. Purulent drainage
from cysts occurs spontaneously or with minor trauma. Comedones
are absent and scarring occurs in most cases. A traumatic emotional
experience has been associated with some cases. Many patients do not
have a history of acne. Cultures help to differentiate this condition
from gramnegative acne.
Occupational acne is an extensive, diffuse eruption of large
comedones and pustules that may occur in some individuals who are
exposed to certain industrial chemicals. These include chlorinated
hydrocarbons and other industrial solvents (e.g., chloracne is caused
by certain aromatic halogenated industrial chemicals), coal tar
derivatives, and oils. Lesions occur on the extremities and trunk where
clothing saturated with chemicals has been in prolonged close contact
with the skin. Patients predisposed to this form of acne must avoid
exposure to wearing protective clothing or must find other work.
Steroid acne is a sudden onset of follicular pustules and papules
which may occur in predisposed individuals 2 to 5 weeks after starting
oral corticosteroids. The lesions of steroid acne differ from those of
acne vulgaris by being of uniform size and symmetric distribution,
usually on the neck, chest, and back. They are 1- to 3-mm, flesh-
colored or pink-to-red, dome-shaped papules and pustules.
Comedones may form later. There is no scarring. Steroid-induced
acne is rare before puberty and in the elderly. There is no residual
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scarring. This drug eruption is not a contraindication to continued or
future use of oral corticosteroids.
Acne mechanica
Mechanical pressure may induce an acne form eruption. Common
causes include forehead guards and chin straps on sports helmets and
orthopedic braces.
Excoriated acne is broad, red erosions with adherent crusts
which are obvious signs of manipulation and can be differentiated
easily from resolved papules and pustules.
Most acne patients attempt to drain comedones and pustules with
moderate finger pressure. Occasionally, a young woman with little or
no acne develops several deep, linear erosions on the face. The skin
has been picked vigorously with the fingernail and eventually forms a
crust. This inappropriate attempt to eradicate lesions causes scarring
and brown hyperpigmentation. Women may deny or be oblivious to
their manipulation.
Cosmetic acne is pomade and cosmetic-induced
comedonal/papular acne (mainly seen in the USA).Closed and open
comedones, papules, and pustules may develop in postadolescent
women who regularly apply layers of cosmetics.
Diagnosis
For diagnosis visual inspection is enough, and for identifying the
causes the following tests will help:
x Assessment for contributing factors (e.g., hormonal,
mechanical, or drug related).
- Analysis of blood on hormones (free testosterone, FSH, LH,
estradiol, 5-testosterone and 5-androstendiol). Tests should pass on
an empty stomach for women at 5-7 day of their menstrual cycle, for
men it does not matter, preferably before 10 o’clock in the morning
with subsequent consultation with a gynecologist and
endocrinologist.
- Biochemical analysis of blood (especially to check blood
cholesterol, total bilirubin and fractions, triglycerides, ALT and
AST) are required in the treatment of systemic retinoids.
- Women’s fasting before ultrasound and also on the 5-7th day
of their menstrual cycle (to exclude cystic ovaries).
- The analysis on a dysbacteriosis of intestines; any changes to
the tests – it is necessary to consult a doctor (gynecologist,
gynecologist-endocrinologist, therapist, andrologist,
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gastroenterologist) to correct the condition.
- Clinical analysis of blood (whether there is inflammation.
because it will aggravate acne).
- In severe acne the isolation and identification of microbial
flora by culture content pustules with sensitivity sown flora to
antibiotics should be performed.
x Determination of severity (mild, moderate, severe).
x Assessment of psychosocial impact.
Differential diagnosis includes rosacea (in which no comedones
are seen), corticosteroid-induced acne (which lacks comedones and
in which pustules are usually in the same stage of development),
perioral dermatitis (usually with a more perioral and periorbital
distribution), and acne form drug eruptions.
Treatment
Treatment depends on the type and extent of acne and the
patient's psychological state.
Oral treatment with antibiotics, retinoids or hormones is
prescribed for moderate or severe acne, acne excoriee and in
depressed patients.
Treatment should be directed toward the known pathogenic
factors involved in acne. These include follicular hyperproliferation,
excess sebum, P. acnes, and inflammation. The grade and the severity
of acne help in determining which of the following treatments, alone
or in combination, are most appropriate.
Antibiotics (broad-spectrum) are aimed not only against
Propionbacterium acnes, and reducing the production of fat. The first-
line systemic antibiotic drug is tetracycline, 500 mg twice daily (taken
half an hour before food with water), given for a minimum of 4
months. Tetracyclines are contraindicated in children and in
pregnancy, and may cause C. albicans infection or photosensitivity.
Minocycline (Minocin, Aknemin, 100 mg daily) and doxycycline
(Vibramycin, 50 mg once daily) are alternative tetracyclines that are
better absorbed.These drugs are banned for use in the active period of
the sun, because they have a phototoxic effect, pregnant, lactating and
children under 13 years of age.
Erythromycin (500 mg twice daily) and trimethoprim are second-
choice antibiotics. Women on oral contraceptives who take an
antibiotic are advised that, if diarrhoea develops, additional
contraception is needed for the rest of the menstrual cycle.
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 Despite the fact that Propionbacterium acnes to erythromycin is
most often stable, the product can be used in pregnant, lactating and
children (500 mg 2 times daily-2 to 4 weeks).
Often shows the assignment of a staphylococcal vaccine.
Anti-androgen
To reduce the effect of androgens on the sebaceous glands to
women and girls with moderate to severe acne are assigned to
combined oral contraceptives. Most often used “GES”, “Diane-35”
assigned to for a long time, 6 months or more. The anti-androgen
suppresses sebum production.
Retinoid
The most effective is the purposes of systemic retinoids, which
reduces sebum excretion, inhibits P. acnes and are antiinflammatory.
Isotretinoin (Roaccutane, Accutane) is used if acne is severe or
unresponsive to conventional treatment, or if acne relapses quickly
once antibiotics are stopped. A course lasts 4 -6 months and requires
the monitoring of liver function and fasting lipids.There is a certain
approach to the administration of a daily dose of the drug, we select
exclusively individually (0.5-1 mg/kg).
Due to the presence of teratogenic and embryotoxic action
contraindication is established and planned pregnancy, and lactation.
To support the work of the liver, in treatment illustrates the
application of hepatoprotectors (Essentiale Forte (2 capsules) or
Kars(1 tablet 3 times daily for 1 month).Common side effects include
cracked lips, dry skin, nose bleeds, hair loss and muscle aches.
Local treatment is adequate for mild acne and is used with
systemic drugs for more severe cases.
The basic approach in treatment of acne should be directed to the
proper and gentle care for skin. The application of alcohol-containing
and other aggressive agents on the skin can further disrupt the skin
barrier function and lead to exacerbation of the process. Therefore,
cleansing or washing with gentle detergent can only promote a
positive result during the treatment.
In the presence of inflammatory cells on the skin treatment should
start with the prescription of external antibacterial agents. They are
mainly used against P. acnes.
Antibiotics, e.g. Clindamycin (Dalacin T), Erythromycin alone
(Stiemycin) or with zinc (Zineryt) or Benzoyl peroxide (Benzamycin)
can be used for mild or moderately severe acne. They may also have
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anti-inflammatory properties. Commonly prescribed topical antibiotics
include erythromycin and clindamycin alone or in combination with
benzoyl peroxide. Clindamycin and erythromycin are available in a
variety of topical agents. They may be applied once or twice a day. Gels
and solutions may be more irritating than creams or lotions. Topical
antibiotics are not comedolytic, and bacterial resistance may develop to
any of these agents. The development of resistance is lessened if topical
antibiotics are used in combination with benzoyl peroxide.
Benzoyl peroxide (Panoxyl, Acnecide, Brevoxyl, Baziron as)
cream or gel, applied twice a day, effects by reducing the number of
P.acnes. They may also have anti-inflammatory properties.
Topical retinoids are comedolytic and anti-inflammatory. They
cause epidermal differentiation and, thus, normalize follicular
hyperproliferation and hyperkeratinization. Topical retinoids reduce
the numbers of microcomedones, comedones, and inflammatory
lesions. They may be used alone or in combination with other acne
medications. The most commonly prescribed topical retinoids include
adapalene, tazarotene, and tretinoin. Tretinoin (Retin A cream or gel)
is good in reducing the number of comedones, but may be irritant.
Skin irritation with peeling and redness may be associated with the
use of topical retinoids. The use of mild, nondrying cleansers and non-
comedogenic moisturizers may help reduce this irritation.
With remission of acute inflammation certain medical remedies
are added, influencing the process of keratinization of epidermal cells,
thereby reducing the formation of comedones.
Azelaic acid (Skinoren) has this property, and the cream form of
this drug has depigmenting properties.
Adapalene (Differin) is available as a gel or cream. It has
tretinoin-like activity in the terminal differentiation process of the hair
follicle. Adapalene has anti- inflammatory activity. 0.1% adapalene
gel is as effective as 0.025% tretinoin gel for mild-to-moderate acne.
It is better tolerated than tretinoin gel. It does not cause sun sensitivity.
Other therapies
Acne cysts may require injection with triamcinolone acetonide (a
steroid), or sometimes excision or cryotherapy. Comedones can be
removed using an extractor.
The positive effect is provided by the combination of these drugs
(antibacterial skinoren and external means) with conducting 15-20
sessions of selective phototherapy, or treatment with a helium-neon laser.
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 Prognosis
In male patients, acne generally clears by early adulthood. Female
patients frequently have adult acne. The overall prognosis for people
with acne is good. However, acne can result in long-term psychosocial
impairment and physical scarring.

Unit 3
Rosacea
Rosacea is a chronic inflammatory facial dermatosis characterized by
erythema and pustules. The disease is very common. It is more common
in women older than 30 years. The peak of the disease 40-50 years.
Rosacea is Latin for “Rosacea” means “Like a rose”. Beautiful
name, but the manifestations are not so attractive. This is not a
contagious disease, not life-threatening, but is expressed cosmetic
defect, especially extreme manifestation of the disease is rhinophyma
(nose pineal), is more common in men. Histologically, dilated dermal
blood vessels, sebaceous gland hyperplasia and an inflammatory cell
infiltrate are seen. Sebum excretion is normal.
Causes of Rosacea
The cause of the disease is unknown. Significant increase in the
hair follicle mite, Demodex folliculorum, is found in rosacea.
Hot and spicy dishes, bath, sauna, Solarium, alcohol, hot tea and
coffee, face massage, emotional overload, i.e. everything that
stimulates circulation will enhance redness. Sunlight and topical
steroids exacerbate the condition.
Clinical Presentation
The earliest symptom is flushing. Erythema, small vessels shine
through the skin (called telangiectasias), papules and pustules and
occasionally lymphoedema involving the cheeks, nose, forehead and chin
are manifestations of the disease. One or all of these features may be
present.
The disease is chronic, lasting for years, with the episodes of
recurrence followed by remission periods of variable length.
Granuloma formation occurs in some patients (granulomatous
rosacea). It is characterized by hard papules or nodules that may be
severe and lead to scarring.
Complications of Rosacea
Chronic, deep inflammation of the nose leads to an irreversible

93
hypertrophy called rhinophyma (due to the growth of glandular and
connective tissue). The skin thickens on the forehead (cushion-like
thickening of the forehead is called metophyma) , and on the eyelids(
called blepharophyma), and on the earlobe (called otohime – the
expansion of the skin in the form of cauliflower), and on the chin
(called gnetophyta). Other signs of rosacea include eye symptoms, i.e.,
redness, which may be accompanied by small soreness, sensation of
grit in the eyes and watery eyes. Rhinophyma and eye involvement by
blepharitis and conjunctivitis are typical complications. Severe
complications are keratitis and corneal ulcer.
Diagnosis of Rosacea
The diagnosis is made by physical examination.
Primary features (the presence of one or more out of the
following is possible):
x Flushing (transient erythema).
x Non-transient erythema.
x Telangiectasia.
x Papules and pustules.
Secondary features (one or more out of the following may be
present):
x Plaques
x Dry appearance
x Edema.
x Ocular manifestations
x Peripheral location
x Phymatous changes
x Burning or stinging
General blood count and blood for hormones (if anything
changes, consult a gynecologist-endocrinologist, therapist). Analysis
on Demodex.
Treatment
Rosacea treatment may be general or local.
Oral treatment
Both the skin and eye manifestations of rosacea respond to
doxycycline (100 to 200 mg/day) or tetracycline or erythromycin (1
gm/day in divided doses). Resistant cases can be treated with 100 to
200 mg/day of minocycline or with 200 mg of metronidazole twice
daily. Azithromycin 500 mg on Monday, Wednesday, and Saturday
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within the first month; 250 mg on Monday, Wednesday, and Saturday
within the second month; and 250 mg on Tuesday and Saturday within
the third month are as effective as doxycycline. Medication is ceased
when the pustules have cleared.
Isotretinoin (0.5 mg/kg/day for 20 weeks or 10 mg/day, for 16
weeks) can be used but is less effective than in acne.
Local treatment
Topically, metronidazole gel (Metrogel, Rozex) twice daily or 1%
metronidazole applied once each day may be helpful.
The acne medications benzoyl peroxide 5%/erythromycin 3% gel,
benzoyl peroxide 5%/clindamycin 1% gel, and benzoyl peroxide alone
are effective.
Clindamycin as lotion is less effective.
Azelaic acid 20% cream or 15% gel applied once or twice each day
is effective and well tolerated in the treatment of papulopustular rosacea.
Pimecrolimus 1% cream is effective for steroid-induced rosacea.
Other therapies
Patients with rhinophyma may benefit from specialized procedures
performed by plastic or dermatologic surgeons. These include
electrosurgery, carbon dioxide laser, and surgery. Unsightly telangiectatic
vessels can be eliminated with careful electrocautery or laser.

Checkup Questions
1. What are the causes of rosacea?
2. What is the clinical picture of seborrheic dermatitis?
3. What diseases should be used for differential diagnosis of
seborrhea?
4. How can you prevent seborrheic dermatitis from recurrence?
5. How can seborrhea be treated?
6. What are the causes of acne?
7. What are the clinical manifestations of acne?
8. What types of acne do you know?
9. What forms of acne have the most severe clinical course?
10. What treatments for acne are applied?
11. When is retinoids prescribed for acne treatment?
12. What clinical manifestations are characteristic of rosacea?
13. What are the complications of rosacea?
14. What complication of rosacea is treated only surgically?
15. What medicines are used in the treatment of rosacea?
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CHAPTER X
CONNECTIVE TISSUE DISEASES
Autoimmune diseases are a group of disorders that are
characterized by abnormal reactions of the immune system against
one’s own body. These usually manifest during the middle year and
are, most of the time, chronic.
Autoimmune diseases are associated with circulating
autoantibodies, which bind self-protein. Pathogenesis may be then
mediated by autoimmune T lymphocytes and other immune
mechanisms. Autoantibodies either are responsible for the
manifestations of autoimmune disease or are markers of future
disease. Autoantibodies may be found in serum samples many years
before disease onset in several of these diseases. Autoimmunity is
common in the population, but systemic autoimmune diseases, such as
the connective tissue diseases, are relatively rare.
Connective tissue diseases (CTDs) are generally referred to as a
group of inflammatory, immune-mediated multisystem disorders of
unknown etiology with abnormalities in the tissues containing
collagen and elastin. Usually, CTDs (or collagen vascular diseases)
are characterized by overactivity of the immune system from
unknown causes resulting in production of autoantibodies. Many
serum antibodies directed at cellular components (autoantibodies)
have been found in each disease and are probably responsible for the
clinical manifestations.
In addition, antibodies form against normal tissues and cellular
components; these disorders are therefore classed as autoimmune.
1 in 10 people have a connective tissue disoder.

Unit 1
Lupus Erythematosus
Lupus Erythematosus (LE) is an autoimmune disease that
includes a broad spectrum of clinical forms, ranging from skin lesions
to systemic LE (SLE).
Systemic lupus erythematosus (SLE) is a multisystem disease of
unknown origin characterized by the production of numerous diverse
96
types of autoantibodies that, through immune mechanisms in various
tissues, cause several combinations of clinical signs, symptoms, and
laboratory abnormalities. The natural history of SLE is characterized
by episodes of relapses, flares, and remissions. The outcome is highly
variable, ranging from remission to death.
Types of Lupus Erythematosus:
1. Cutaneous lupus erythematosus:
xAcute.
xSubacute.
xChronic:
- Discoid lupus erythematosus.
- Lupus erythematosus panniculitis (Lupus erythematosus
profundus).
- Chilblain LE (Hutchinson).
- Tumid LE.
- Hypertrophic LE (Verrucous ).
- Lupus erythematosus-lichen planus overlap syndrome.
2. Systemic lupus erythematosus (SLE).
Discoid lupus erythematosus
Discoid lupus erythematosus (DLE) is the most common form of
chronic cutaneous lupus erythematosus (CCLE).
x Localized form associated with 5% with SLE.
x Generalized form associated with 20% with SLE.
Epidemiology
The prevalence is between 17 and 48 per 100,000 people.
Discoid lupus erythematosus (DLE) usually presents in people
aged between 20 and 40 years of age. Women are much more often
affected than men. (aged 20 to 50). Cutaneous LE can be provoked by
sunlight but it is actually more common in dark skinned than in fair
skinned people.
Patogenesis
Expression of skin involvement in patients with LE is very
common and showgs great variation. That is why it is difficut to create
a unifying concept. Photosensitivity's relationship to and influence on
the systemic manifestations of lupus remains to be defined.
Mechanisms for photosensitivity might include: modulation of
autoantibody location, cytotoxic effects, apoptosis induction with
autoantigens in apoptotic blebs, upregulation of adhesion molecules
and cytokines, induction of nitric oxide synthase expression and
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ultraviolet-generated antigenic DNA. Tumor necrosis factor alpha also
seems to play a role in the development of photosensitivity.
Clinical Presentation
Lesions predominate in sun-exposed areas, especially the face,
scalp, upper chest, upper back, and extensor arms.
Early lesions consist of sharply demarcated, discret, erythematous,
often hyperpigmented, hyperkeratotic papules and small plaques with
adherent scale involving the malar areas and the bridge of the nose while
sparing the nasolabial folds. The surface is smooth in the earliest lesions
but soon becomes covered with a thin adherent grey scale, this
manifestation of hyperkeratosis is best seen in the follicular orifices, so
that horny plug may be seen projecting from the undersurface of the
scale (nutmeg appearance) when it is forcibly removed.
The lesions enlarge slowly often coalescing, and the picture then
consists of an active, fairly well-demarcated edge and a sunken,
atrophic centre which may show teleangiectasis. The individual
lesions spread peripherally (similar lesions may occur in V-neck and
forehead), resulting in atrophy and central scarring which may be
associated with alopecia, telangiectasia, and depigmentation.
Acute LE is characterised by localized erythema known as «malar
rash» or «butterfly rash» in the central pertion of the face that is
frequent misdiagnosied with the sunburn. The scalp may be affected
and cause permanent scarring alopecia.
Generalised rash is known as «photosensitive lupus rash» is less
common. Superficial ulcerations of the oral cavity may occur. DLE
may affect the lips and inside the mouth, causing ulcers and scaling,
and predisposing to squamous cell carcinoma. Sometimes generalized
rash appear first.
Differential Diagnosis
x Systemic lupus erythematosus (SLE).
x Dermatomyositis.
x Plaque psoriasis.
x Actinic keratosis.
x Lichen planus.
x Warts.
x Sarcoidosis.
x Squamous cell carcinoma (SCC).
x Syphilis.
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 Investigations
x Biopsy for histology may be required. Histopathological
changes are characteristic but depend on the type and age of the
lesion. Most patients with discoid lupus erythematosus (DLE) show a
direct positive immunofluorescence in biopsies of lesions but this is
not very specific.
x Serology: approximately 20% of patients with DLE have a
positive antinuclear antibody (ANA).
x LE cells may be expected in about 5% of the cases.
x There may be a low white cell count and raised ESR.
x Rheumatoid factor may be positive.
x Complement levels may be low.
x Urinalysis may indicate renal involvement with albuminuria.
Blood tests should be repeated periodically, perhaps annually
when the condition appears stable, to check for the onset of systemic
disease.
Treatment
The mainstay of treatment includes sun protection, topical or
intralesional steroids, and antimalarial drugs.
Nondrug
x Sun exposure must be minimised by avoiding going out in
bright sun as much as possible, protective clothing and high factor
sunscreens. The lesions are unsightly and usually in visible places, so
cosmetic camouflage is required.
x Infections especially of the upper respiratory tract should be
promptly controlled.
x General nutrition should be improved.
x Indiscrimiate use of photosensiting drugs be strictly avoided.
Drugs
Corticosteroids may be used topically or injected intralesionally.
Local application of steroids is the treatment of first choice.
Very potent forms are necessary for hypertrophic lesions.
Systemic steroids do not seem to be effective.
When systemic treatment is required, hydroxychloroquine is the
first-line agent. Hydroxychloroquine (oral antimalarial) and acitretin
(an oral retinoid) appear to be of equal efficacy, although adverse
effects are more frequent and more severe with acitretin.
Other possible treatments include topical retinoids and
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immunosuppressive agents (e.g. azathioprine or methotrexate).
Surgical
x Burned-out scarred lesions may be excised.
x Laser therapy can be considered for lesions with prominent
telangiectasias.
Complications
x A minority of patients with discoid lupus erythematosus (DLE)
(less than 5%) progress to systemic lupus erythematosus (SLE).
x Malignant degeneration (basal cell carcinoma or squamous cell
carcinoma (SCC) may occur but is uncommon. Dark skin may lose its
inherent protection with depigmentation.
Prognosis
Spontaneous remission of the disease occurs in some patients. In
the rest, if untreated, the disease persists. Pain in lesions may continue
and disfiguration from scars and atrophy will be permanent. Early
treatment may reduce scarring or atrophy.
Systemic Lupus Erythematosus
Systemic Lupus Erythematosus (SLE) is a heterogeneous,
inflammatory, multisystem autoimmune disease in which antinuclear
antibodies occur (often years before clinical symptoms).
Lupus erythematosus describes the typical rash of SLE and the
term systemic emphasises the potential for multi-organ involvement.
The cause of SLE is unknown.
Epidemiology
Prevalence is 50-100 cases per 100,000. The peak age of onset is
in the twenties or early thirties, but cases do occur in children and the
elderly. Women are affected nine times more frequently than men. It
is more common in those of Chinese, Southeast Asian (1 in 1,000) and
Afro-Caribbean origin (1 in 500). Prevalence is least common in
women of Northern European origin (prevalence 1 in 2,800).
Risk factors
x Certain human leukocyte antigen DRB1 types are more
common in lupus patients, e.g. DR3 and DR2.
x Patients who have a defective C4 complement gene (C4A null
allele) also develop a lupus-like illness.
x Environmental factors include ultraviolet light, viruses, e.g.
the Epstein-Barr virus, and some drugs.
x Drugs known to cause drug-induced lupus include

100
chlorpromazine, methyldopa, hydralazine, isoniazid, d-penicillamine
and minocycline.
Clinical Presentation
x Systemic lupus erythematosus (SLE) is a remitting and
relapsing illness.
x Symptoms and signs are often nonspecific,4 e.g. fatigue (can
be severe and debilitating), malaise, fever, splenomegaly,
lymphadenopathy, weight loss, arthralgia and fatigue, oral ulcers,
photosensitive skin rashes, pleuritic chest pains, headache,
paraesthesiae, dry eyes and mouth. Raynaud's phenomenon, mild hair
loss and myalgia.
x The symptoms of lupus can range from minor aching pains
and rash to life-threatening disease.
x Any major organ involvement tends to develop within five
years of the disease onset.
x Arthralgia:
- Joint and muscle pains are common, often with early morning
stiffness.
- Joint swelling is unusual and the arthritis is usually non-
erosive.
- Some patients develop joint deformity and subluxation when
tendons and peri-articular soft tissues are affected (Jaccoud's
arthropathy).
- Peripheral, symmetrical, flitting polyarthritis is typical.
x Secondary fibromyalgia is common.
x Raynaud's phenomenon occurs in about one fifth of patients but
is often mild.
x Mucocutaneous:
- Photosensitivity rash.
- Classical feature is the malar (butterfly) rash: often
precipitated by sunlight. It is erythematous and may be raised and
pruritic. It spares the naso-labial folds.
- Discoid rash: can occur in the absence of any systemic
features. It tends to occur in sun-exposed areas. It is erythematous,
well demarcated and associated with scaling.
- Other manifestations include livedo reticularis, diffuse or
patchy non-scarring alopecia and vasculitic rashes. Mouth ulcers can
be large, multiple and painful.

101
 x Pulmonary: pleurisy, fibrosing alveolitis, obliterative
bronchiolitis. Patients with the secondary antiphospholipid syndrome
(APLS) are at increased risk of pulmonary embolus.
x Cardiovascular: pericarditis, hypertension, Libman-Sacks
endocarditis, an increased risk of coronary heart disease.
x Renal: nephritis is often asymptomatic and is detected by
proteinuria, haematuria, hypertension or a raised serum urea or
creatinine. Glomerulonephritis is common in lupus patients.
x Neuropsychiatric: anxiety and depression are common. Patients
may also develop psychosis, seizures, neuropathy, meningitis and
organic brain syndrome.
x Lupus can be associated with almost any neurological
manifestation. Strokes may be due to vasculitis or thrombosis
associated with APLS.
Diagnosis
The American College of Rheumatology Classification system for
systemic lupus erythematosus (SLE) suggests that a person may be
classified as having lupus if 4 or more of the following 11 criteria are
present (which do not have to occur at the same time but can be
cumulative over a number of years):
x Malar rash.
x Discoid lupus.
x Photosensitivity.
x Oral or nasopharyngeal ulcers.
x Non-erosive arthritis involving 2 or more peripheral joints.
x Pleuritis or pericarditis.
x Renal involvement with persistent proteinuria or cellular casts.
x Seizures or psychosis.
x Haematological disorder: haemolytic anaemia or leukopenia or
lymphopenia or thrombocytopenia.
x Immunological disorder: anti-DNA antibody or anti-Sm or
antiphospholipid antibodies.
x A positive antinuclear antibody.
Investigations
x When systemic lupus erythematosus (SLE) is suspected,
useful screening investigations are an FBC, ESR or plasma viscosity
and antinuclear factor.
x FBC and ESR:
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 - Mild normochromic normocytic anaemia is common.
Anaemia in patients with lupus may be drug-induced or due to chronic
disease, but it is sometimes due to haemolytic anaemia. In this case,
Coombs' antibody, reticulocyte count and haptoglobins may need to
be checked.
- Leukopenia and thrombocytopenia occur frequently but can
also be due to immunosuppressive therapy.
- ESR is raised but CRP may be normal unless there is
intercurrent infection or serositis.
x Autoantibodies:
- ANA: screening test with a sensitivity of 95% but not
diagnostic in the absence of clinical features. Is a nonspecific antibody
that is also present in many patients with systemic autoimmune
conditions, e.g. systemic sclerosis (scleroderma), polymyositis and
primary Sjögren's syndrome. The titre does not alter significantly with
disease activity.
- Anti-dsDNA: high specificity but sensitivity only 70%. The
level reflects disease activity. The value often varies with disease
activity and sometimes guides changes in therapy. A rise in antibody
titre may indicate that immunosuppression needs to be increased.
- Anti-Sm is the most specific antibody but sensitivity is only
30-40%.
- Anti-SSA (Ro) or Anti-SSB (La) are present in 15% of
patients with SLE and other connective-tissue diseases, e.g. Sjögren's
syndrome; also associated with neonatal lupus.
- Anti-ribosomal P are uncommon antibodies that may
correlate with lupus cerebritis.
- Anti-RNP may indicate mixed connective-tissue disease with
overlap SLE, scleroderma, and myositis.
- Anti-histone: drug-induced lupus ANA antibodies are often
this type.
x Antiphospholipid antibodies: anticardiolipin antibodies and
lupus anticoagulant should be checked in lupus patients, as they are
associated with antiphospholipid syndrome (APLS).
x Complement C3 and C4 levels are decreased and C3d (a
degradation product) increased with increased disease activity.
x Other investigations will depend on system involvement, e.g.
MRI brain scans, echocardiogram, renal biopsy.
x Women with SLE are at greatly increased risk of premature
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atherosclerosis and the risk is independent of established
cardiovascular risk factors. Monitoring for all cardiovascular risk
factors is therefore essential.
Associated Diseases
x Antiphospholipid syndrome (APLS).
x Overlap syndromes: some patients with 'lupus' do not have
pure systemic lupus erythematosus (SLE) as described, but have
overlapping features with other connective-tissue diseases, such as
scleroderma, polymyositis, rheumatoid arthritis and Sjögren's
syndrome.
x They are prone to other autoimmune conditions such as
thyroiditis. They also have a higher incidence of drug allergy and an
increased risk of infection.
x Patients with SLE are also at increased risk of certain other
comorbidities, including atherosclerosis, hypertension,
dyslipidaemias, diabetes, osteoporosis, avascular necrosis and
malignancies (especially non-Hodgkin's lymphoma).
Treatment
Patients often require considerable counselling about their
individual prognosis and symptoms. Avoid sun exposure as much as
possible and use sun screens.
Identify and treat any underlying cause (e.g. anaemia, depression)
and encourage regular aerobic exercise.
Joint and muscle pains, headaches, and musculoskeletal chest
pains respond to simple analgesics and non-steroidal anti-
inflammatory drugs (NSAIDs) (the latter should be used with caution
because of gastrointestinal, renal, and cardiovascular risks).
When simple analgesia and NSAIDs are insufficient to control
symptoms or disease, additional treatment is considered, depending on
the individual systems involved:
x Corticosteroids are very effective but also implicated in the
increased mortality in lupus, as a result of infection, cardiovascular
disease and complications of fractures. High-dose prednisolone is
reserved for life-threatening systemic lupus erythematosus (SLE).
x Hydroxychloroquine is useful for skin lesions, arthralgia,
myalgia and malaise. Cutaneous manifestations may respond within
days but, more often, clinical improvement takes 6-12 weeks of
treatment.

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 Hydroxychloroquine is generally very well tolerated but may
cause irreversible ocular toxicity.
Hydroxychloroquine remains first-line treatment for patients with
mild SLE, especially for those with arthralgia, skin rashes, alopecia,
and oral or genital ulceration.
x Cyclophosphamide is reserved for treatment of life-
threatening disease, particularly lupus nephritis, vasculitis and
cerebral disease.
The established treatment for lupus nephritis has been
cyclophosphamide combined with steroids8 or high-dose monthly or
quarterly intravenous pulse cyclophosphamide; however, recent
studies have shown that short courses of low-dose pulse
cyclophosphamide followed by azathioprine are as effective and less
toxic.
Cyclophosphamide appears to be more effective in the treatment
of neuropsychiatric involvement in SLE compared with
methylprednisolone.
x Azathioprine is used as a steroid-sparing agent. As an
alternative to cyclophosphamide, azathioprine is much safer but
probably less effective, particularly in active nephritis. Azathioprine
does predispose to infection but to a lesser extent than
cyclophosphamide or corticosteroid therapy.
x Other immunosuppressive agents used in severe SLE include
Methotrexate and Ciclosporin.
Intravenous high-dose pooled gammaglobulin and granulocyte-
colony stimulating factor have a role in autoimmune
thrombocytopenia and neutropenia. Intravenous immunoglobulins are
increasingly being used in the treatment of resistant lupus and also
have a role in patients who have concomitant infection and active
lupus, for whom immunosuppression treatment is often inappropriate.
Patients who are seriously ill with life-threatening disease may
undergo plasma exchange as a holding measure until the
immunosuppressive therapy takes effect.
Lupus patients should be offered the flu vaccination; they should
not receive live vaccinations.
Prognosis
The prognosis has improved with earlier recognition and
improved management. The five-year survival rate is over 90%.
Morbidity and mortality are usually higher in patients with
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extensive multisystem disease and multiple autoantibodies.2
Patients, who develop renal involvement, particularly focal and
diffuse proliferative glomerulonephritis, have a poorer prognosis.
Drug-induced lupus usually subsides when the responsible drug is
discontinued.

Unit 2
Scleroderma
The term scleroderma denotes sclerosis- a kind of tethering or
hardening of the skin; it is better appreciated by palpation rather than
visual inspection. Scleroderma is a chronic systemic autoimmune
disease (primarily of the skin) characterized by fibrosis (or hardening),
vascular alterations, and autoantibodies.
There are two major forms:
Limited systemic sclerosis/scleroderma involves cutaneous
manifestations that mainly affect the hands, arms and face. It was
previously called CREST syndrome in reference to the following
complications: Calcinosis, Raynaud's phenomenon, Esophageal
dysfunction, Sclerodactyly, and Telangiectasias. Additionally,
pulmonary arterial hypertension may occur in up to one-third of
patients, and is the most serious complication for this form of
scleroderma.
Diffuse systemic sclerosis/scleroderma is rapidly progressing
and affects a large area of the skin and one or more internal organs,
frequently the kidneys, esophagus, heart and lungs. This form of
scleroderma can be quite disabling. There are no treatments for
scleroderma itself, but individual organ system complications are
treated.
Other forms of scleroderma include systemic sine scleroderma,
which lacks skin changes, but has systemic manifestations, and two
localized forms which affect the skin, but not the internal organs:
morphea and linear scleroderma.
The prognosis is generally good for limited cutaneous
scleroderma patients who escape pulmonary complications, but is
worse for those with the diffuse cutaneous disease, particularly in
older age, and for males. Death occurs most often from pulmonary,
heart and kidney complications. In diffuse cutaneous disease, five-
year survival is 70%, and 10-year survival is 55%.

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 Etiopatogenesis
The cause is unknown. Scleroderma runs in families, but the
genes have not been identified. It affects the small blood vessels
(arterioles) in all organs. First, the endothelial cells of the arteriole die
off, along with smooth muscle cells, by a process of apoptosis. They
are replaced by collagen and other fibrous material. Inflammatory
cells, particularly CD4+ helper T cells, infiltrate the arteriole, and
cause further damage. Many of the inflammatory and destructive
protein signals have been identified, and they are potential targets for
drugs that could interrupt the process.
Classification
Scleroderma is characterized by the appearance of circumscribed
or diffuse, hard, smooth, ivory-colored areas that are immobile, and
which give the appearance of hidebound skin, a disease occurring in
both localized and systemic forms:
x Localized scleroderma:
- Localized morphea.
- Morphea-lichen sclerosus et atrophicus overlap.
- Generalized morphea.
- Atrophoderma of Pasini and Pierini.
- Pansclerotic morphea.
- Morphea profunda.
- Linear scleroderma.
x Systemic scleroderma:
- CREST syndrome.
- Progressive systemic sclerosis.
Epidemiology
This disease is found among all races worldwide, but women are
four times more likely to develop scleroderma than men. In the United
States, approximately one person in 1,000 is affected. Children rarely
suffer the systemic type, but localized scleroderma is common. Most
adults are diagnosed after their 30th birthday and before age 50. The
disease has high rates among the native American Choctaw tribe and
African American females.
Diagnosis
Typical morpheа begins as a rash in the form of erythema or
edema with a purple or pink border. Then the site of the lesion
progressively thickens and becomes with a white or yellow hue. As a
result, atrophy, hyperpigmentation or hypopigmentation may appear.
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Skin manifestations are characterized by three stages of the process:
inflammation, sclerosis and scarring.
Typical scleroderma is classically defined as symmetrical skin
thickening, with about 90% of cases also presenting with Raynaud's
phenomenon, nail-fold capillary changes, and antinuclear antibodies.
Patients may or may not experience systemic organ involvement.
Atypical scleroderma may show any variation of these changes
without skin changes or with finger swelling only. Additional
symptoms of scleroderma typically present themselves within two
years of Raynaud's phenomenon.
Laboratory testing can show antitopoisomerase antibodies
(causing a diffuse systemic form), or anticentromere antibodies
(causing a limited systemic form, and the CREST syndrome). Other
autoantibodies can be seen, such as anti-U3 or anti-RNA polymerase.
Severe complications from scleroderma include:
Heart: Untreated high blood pressure strains the heart; irregular
heart rhythm and enlargement of the heart lead to heart failure.
Kidney: Scleroderma renal crisis in which malignant
hypertension develops and causes acute renal failure was once a
common cause of death, but is now treatable with ACE inhibitors.
Lung: Two-thirds of all patients suffer from respiratory
problems, such as shortness of breath, coughing, difficulty breathing,
alveolitis (inflammation of lung air sacs), pneumonia, and cancer.
Digestive: Esophagus damage can make it difficult to swallow
food, and acid reflux is common. The stomach can develop gastric
antral vascular ectasia (GAVE), which occasionally may bleed
profusely. A sluggish intestine may cause pain and bloating;
undigested food can result in diarrhea, weight loss and anemia.
Skin and joints: Carpal tunnel syndrome is common, as are
muscle weakness, joint pain, and stiffness.
Mouth: Flat white patches, loss of attached gingival mucosa,
gingival recession, and diffuse widening of the periodontal ligament
(PDL) space are seen. Dysphagia may result from collagen deposition
in the lingual and esophageal submucosa. Resorption of posterior
ramus of the mandible, coronoid process, and condyle are seen due to
pressure from abnormal collagen production in adjacent areas.
Inelasticity of the mouth may make dentures or dental prostheses
difficult to insert and remove.

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 Treatment
There is no direct cure for scleroderma. Because the exact cause
is unknown, any treatment is patient-specific and aimed at
ameliorating symptoms of the disease. For example, patients who
experience Raynaud's phenomenon may be treated with agents to
increase blood flow to the fingers, including nifedipine, amlodipine,
diltiazem, felodipine, or nicardipine. Fibrosis of the skin has been
treated with varying degrees of success with agents such as D-
penicillamine, colchicine, PUVA, relaxin, and cyclosporine.
Because scleroderma is an autoimmune disease, one of the major
pillars of treatment involves the use of immunosuppressive agents.
These drugs include methotrexate, cyclophosphamide, azathioprine,
and mycophenolate.
Prognosis
Individuals with morphea or limited scleroderma have a relatively
positive outlook. They will usually die from natural causes or another
disease perhaps, but not from the scleroderma. Those with very
widespread skin and organ involvement (systemic) have a negative
prognosis. More women have scleroderma, but the disease kills more
men. Following diagnosis, two-thirds of patients live at least 11 years.
The higher the patients' age at diagnosis, the more likely they are to
die from the disease.
People with scleroderma have very different life expectancies.
Some – for example, those with limited or mild diffuse disease – can
expect to live 20 to 50 years after diagnosis, just like anyone else.
Others with severe, rapidly progressive disease – a group which
makes up less than 10% of the total number of patients with diffuse
scleroderma – might have a 50% chance of a five-year survival.

Checkup Questions
1. What is the main trigger factor in the etiology of lupus
erythematosus?
2. What are LE cells?
3. In which season are the most common manifestations of lupus
erythematosus?
4. What skin forms of lupus erythematosus do you know?
5. What laboratory methods are used for the diagnosis of lupus
erythematosus?
6. What medications are prescribed to treat lupus erythematosus?
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7. What form of scleroderma is the most common in patients?
8. What clinical picture is observed in localized morphea?
9. What is the difference between linear scleroderma and
localized morphea?
10. What methods of diagnosis of scleroderma are the most
relevant?
11. What is the treatment for scleroderma?

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CHAPTER XI
ALLERGIC SKIN DISEASES
Unit 1
Allergic Contact Dermatitis
Dermatitis precipitated by an exogenous agent, often a chemical,
is known as contact dermatitis. It is particularly common in the home,
amongst women with young children, and in industry where it is a
major cause of loss of time from work.
Cause
Allergic contact dermatitis is an example of type IV
hypersensitivity. It has the following features:
x Previous contact is needed to induce allergy.
x It is specific to one chemical and similar in composition
substances.
x After an allergy has been established, all areas of the skin will
react to the allergen.
x Sensitization exists indefinitely.
x Desensitization is seldom possible.
Allergens
In an ideal world, allergens would be replaced by less harmful
substances, and some attempts are already being made to achieve this.
A whole new industry has arisen around the need for predictive patch
testing before new substances or cosmetics are let out into the
community. Similarly, a chrome allergy is less of a problem now in
the enlightened countries that insists on adding ferrous sulphate to
cement to reduce its water-soluble chromate content. However,
contact allergens will never be abolished completely and family
doctors still need to know about the most common ones and where to
find them. In fact, most allergens are relatively simple chemicals that
have to bind to protein to become ‘complete’ antigens. Their ability to
sensitize varies-from substances that can do so after a single exposure
(e.g. poison ivy), to those that need prolonged exposure (e.g. chrome
bricklayers take on average 10 years to become allergic to it).

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 Clinical Presentation
The original site of the eruption gives a clue to the likely allergen
but secondary spread may later obscure this. Easily recognizable
patterns exist. Nickel allergy, for example, gives rise to eczema under
jewelry, bra clips and jean studs. The lax skin of the eyelids and
genitalia is especially likely to become oedematous. Possible allergens
are numerous and to spot the less common ones in the environment
specialist’s knowledge is required.
Allergic contact dermatitis should be suspected if:
x certain areas are involved, e.g. the eyelids, external auditory
meati, hands or feet, and around gravitational ulcers;
x there is known contact with the allergens;
x the individual’s work carries a high risk, e.g. hairdressing,
working in a flower shop, or dentistry.
Investigations
Questioning should cover both occupational and domestic
exposure to allergens.
Techniques are constantly improving and dermatologists will
have access to a battery of common allergens, suitably diluted in a
bland vehicle. These are applied in aluminum cups held in position on
the skin for 2 or 3 days by tape.
Patch testing helps identify any allergens involved and is
particularly useful in dermatitis of the face, hands and feet. The
exclusion of an offending allergen from the environment is desirable,
and if this can be achieved, the dermatitis may clear.
Differential Diagnosis
Contact dermatitis of the hands needs to be differentiated from
endogenous eczema, latex contact urticaria, psoriasis and a fungal
infection. Acute contact dermatitis of the face may resemble
angioedema or erysipelas.
Treatment
Topical corticosteroids give temporary relief, but far more
important is avoidance of a relevant allergen.
Reducing exposure is usually not enough: active steps have to be
taken to avoid the allergen completely. Job changes are sometimes
needed to achieve this. However, it is difficult to fully eliminate all
contacts with ubiquitous allergens such as nickel or colophony.
Similar irritants are often impossible to exclude. Some contact
with irritants may be inevitable due to the nature of certain jobs, but
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industrial hygiene often can be improved. Unnecessary contact with
irritants should be limited, protective clothing worn (notably PVC
gloves) and adequate washing and drying facilities provided.

Unit 2
Eczema
Eczema is a chronic recurrent skin disease characterized by
evolutionary polymorphism of skin lesions, weeping and itching.
Eczema is an inflammation of the epidermis (the outer layer of the
skin).
The term eczema is broadly applied. The disease is characterized
by the following symptoms: redness, skin edema (swelling), itching
and dryness, crusting, peeling, blistering, cracking, oozing or
bleeding.
The word eczema comes from Greek words that mean "to boil
over". In some languages, dermatitis and eczema are synonymous,
while in other languages dermatitis implies an acute condition and
"eczema" a chronic one.
Eczema makes up to 40% of all skin diseases according to some
authors.
In recent years, the number of people suffering from this disease
has increased significantly due to an increase in the number of various
environmental, domestic and industrial negative factors acting on the
human body.
Cause
The cause of eczema is unknown. It is a polyetiological disease
with a complex pathogenesis. Eczema develops as a result of the
combined effect of genetic predisposition, as well as neuroallergic,
endocrine, metabolic and exogenous factors. Dysfunction of the
immune system is of great importance in the pathogenesis of eczema.
All these factors cause sensitization of the body. Sensitization
develops to exogenous allergens (chemical and biological),
endogenous allergens (microbial antigens from chronic infection foci,
endotoxins and fungi) with an inadequate response of the immune
system.
Classification
There is currently no common classification for eczema. There
are four main types of eczema – true (which also includes pruriginous,

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dishydrotic, tilotic, intertriginous), microbial (including paratraumatic,
nummular, varicose and mycotic), seborrheic and professional.
Children's eczema (developing in infancy) is described separately.
Each type of eczema is divided into acute, subacute and chronic
depending on the course.
In accordance with the International Classification of Diseases X
Revision (ICD X), the terms "eczema" and "dermatitis" are used
interchangeably. True eczema corresponds to endogenous (allergic) –
L20.8 according to ICD X, dishydrotic – to dyshidrosis L30.1, tylotic
– to "hypertrophic eczema" L28.0, intertriginous is denoted L30.4.
Paratraumatic eczema corresponds to "infectious dermatitis" or
"pustular eczema" (L30.3), nummular is indicated by the code L30.0,
mycotic – "candidal and dermatophytotic skin autosensitization"
(L30.2), varicose or hypostatic eczema I83.1-I83.2 is considered in the
section "Vascular diseases" as a complication of a varicose disease.
Seborrheic eczema and seborrheic dermatitis according to ICD X are
the same disease with the code L21.9, the same applies to
occupational eczema and dermatitis (L25.9). Children's eczema is
coded L20.8, children's intertriginous or seborrheic – L21.1,
herpetiform – B00.0.
Clinical Presentation
Acute eczema develops suddenly. The skin of patients in this
stage is characterized by hypersensitivity to various factors. It
responds by increasing the inflammatory response and the appearance
of lesions on a variety of irritations. It is characterized by the intensity
of inflammation and the rapid change of the stages of an eczematous
process. The disease usually begins with the appearance of erythema
and a severe edema (edematous-erythematous stage), then small
papules (papular stage) appear, and after them, or at the same time,
papule-vesicles and vesicles (vesicular stage) develop. Pustules may
form as a result of the addition of a secondary infection. Vesicles and
pustules quickly open and turn into erosion of various sizes. Point
erosion, separated by small droplets of transparent exudate (exudation
stage). As a rule, in acute eczema, weeping and severe itching,
burning, pain, feeling of tightness of the skin are noted. Multiple
excoriations are the result of itching. There is a sleep disorder right up
to insomnia. The vesicles, pustules, and discharge of erosion can form
serous or purulent crusts and microcrusts (crustal stage). The crustal
stage enters the stage of desquamation and the formation of secondary
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dyschromia, without leaving behind scars and atrophy.
The evolution of skin rash with eczema is graphically represented
as a "Kreibich triangle" (Fig.4).

Fig. 4. – Kreibich triangle

Clinical manifestations of eczema are characterized by

polymorphism (often evolutionary) and many eruptions. Edema,
erythema, papules, vesicles, erosion, exudation, crusts and
desquamation are present simultaneously in one place.
The disease may initially acquire a subacute or chronic course.
The gradual transition of acute eczema to chronic through the
subacute stage is possible. The subacute course of dermatosis
manifests itself as a wet or dry process with increase in infiltration of
the affected skin areas and increase of lichenification in the skin
pattern. On the surface of moderately infiltrated, non-brightly
hyperemic skin, there is a small amount of small erosions, crusts and
microcrust. The process is accompanied by peeling, which can
suddenly turn into exudation.
Severe skin infiltration prevails in the clinic of chronic eczema.
In addition, signs of chronic eczema are moderate hyperemia,
lichenification, desquamation, and severe itching. Edema, erosion and
exudation are absent. Polymorphism is not pronounced. The stages of
the process do not change quickly. With a prolonged course of eczema
on the palms and soles, hyperkeratosis with fissures sometimes
appears. Nails are deformed. Chronic eczema takes a cyclical course
usually, lasting for years and decades. Periods of remission (when the
patient's skin becomes clear) or improvement may be replaced by
exacerbations at irregular intervals. Subacute or chronic eczema can

115
worsen at any time, acquiring a clinical picture of acute eczema. In
this case, edema, bright redness, vesicles and exudation appear on the
infiltrated skin. Increased itching and new rashes develop on healthy
skin.
This staged course is typical of all forms of eczema, but there are
also specific features for each.
True eczema
The clinical symptoms of true eczema manifest polymorphism
(true and evolutionary) and a clear change in the stages of the
eczematous process. The rash is symmetrical, more often localized on
the skin of the upper extremities, less often on the face, lower
extremities and body. The shape of lesions is usually irregular, their
boundary is fuzzy. The alternation of the affected skin with the
unaffected is characteristic. Development of eczematous erythroderma
is possible. Patients suffer from itching of various intensity. There
may be foci of dryness, peeling of the skin, fissures in the stratum
corneum. Frequently, the course of eczema is complicated by the
addition of a pyogenic infection: pustules and purulent crusts appear.
Pruryginous, dyshydrotic, tylottic and intertriginous eczemas
are varieties of true eczema. The clinical manifestations of these
varieties are associated with the predominant localization of the
process and the possible cause of the disease.
x Pruriginous eczema is characteristic of childhood, manifested
by rashes of small papules with a vesicle on top, forming on a
compacted base, not opened and not forming erosion. Lesions are
located on the skin of the face, around the large joints, in the groin, on
the extensor surfaces of the limbs. The disease is chronic, often recurs.
It is characterized by paroxysmal itching, severe neurotic reactions,
accompanied by sleep disturbance. Due to itching, excoriations appear
on the site of papules.
x Dyshidrotic eczema is localized on the palms, soles and lateral
surfaces of the fingers, characterized by the formation of small, dense-
to-touch vesicles against the background of edema and hyperemia.
Lesions of various sizes and shapes are formed. Vesicles shine
through the thick stratum corneum, resembling grains of cooked rice.
Patients often complain of severe itching. The formation of pustules is
possible at the accession of a secondary infection. Vesicles and
pustules can be opened, turning into erosion with a border of detached
epidermis on the periphery, or dry up, forming flat yellowish crusts. It
116
is characterized by a long course and resistance to treatment.
x Tilotic (hyperkeratotic) eczema can also develop on the palms
and soles. This form of the disease occurs with the greatest infiltration
and the appearance of powerful hyperkeratosis. It is characterized by
deep painful fissures and itching. Vesicles may not form. The clinical
picture is very similar to mycosis and psoriasis.
x Intertriginous eczema is characterized by localization in the
folds of the skin (axillary pits, inguinal region, under the mammary
glands, between the fingers, etc.). The lesions have clear boundaries,
bright red color, and a shiny, moist surface without scales and crusts.
It is characterized by exudation and the formation of deep painful
cracks. Itching is mild. The process can suddenly spread with the
development of the clinical picture of acute eczema.
x Microbial eczema is an allergic reaction, as a result of
monovalent sensitization to microorganisms, pathogenic fungi or their
metabolic products in the places of an acute or a chronic infection of
the skin, upper respiratory tract, dental area, internal organs
(pyoderma, infected wounds, pharyngitis and tonsillitis,
pyelonephritis, pharyngritis and etc.).
x Paratraumatic eczema is the most common form. It begins as
an asymmetrical process on the skin of the legs, the back of the hands,
the scalp - around the wound surface, the place of pyoderma, fistulous
passage, trophic ulcer, burn and etc. At first, small vesicles appear in
the area of the infectious focus. Then, one or several typical lesions
with clear boundaries and flaking horny layer of the epidermis along
the periphery are formed. The focus is characterized by a tendency to
slow peripheral growth. The focus of microbial eczema is a
moderately itchy area of acute inflammatory erythema with exudative
papules, microvesicles, pustules, weeping erosions, massive greenish-
yellow serous purulent and bloody crusts on the surface.
x Numular eczema (discoid eczema) is usually associated with
foci of infection on the skin (without the formation of a wound defect)
or in the internal organs. It is characterized by the appearance of
multiple or single slightly elevated above the skin sharply limited
edematous infiltrated plaques of a rounded shape, with a diameter of
1-5 cm or more. Foci are usually localized on the extremities, at least -
on the trunk and face. On their surface it is characterized by the
typical presence of erythema, papules and pronounced exudation,
serous-purulent crusts and scales. The disease also tends to
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disseminate the process, tends to relapse and is resistant to therapy.
With subacute and chronic course, when peeling is expressed, the
clinical course resembles psoriasis.
x Varicose eczema occurs in violation of hemodynamics and
microcirculation in the lower extremities. Lesions are localized on the
legs and feet in the area of varicose nodes, around the circumference
of varicose ulcers, against the background of hemosiderin deposits and
skin sclerosing sites. Polymorphism of the lesions, sharp, clear
boundaries of the foci, moderate itching, which makes varicose
eczema clinically similar to nummular and paratraumatic, are
characteristic.
x If the rash, characteristic of microbial eczema is the result of
sensitization to pathogenic fungi, the patient is diagnosed with
mycotic eczema. Lesions are localized mainly in the limbs, with
frequent lesions of the hands and feet.
x Seborrheic eczema develops in the individuals with a
seborrheic status. It is localized in the places with a large number of
sebaceous glands – on the skin of the scalp, face, chest, in the
interscapular region, behind the ears. Lesions in the form of rounded
yellowish-pink erythematous maculae with clear boundaries and
covered with fatty yellowish-gray scales and crusts. Dry skin is
characteristic; moderate infiltration, vesiculation and exudation are
present only in rare cases with irritation, irrational treatment, the
accession of a secondary infection. On the scalp, yellowish crusts and
scales are formed; the hair on the affected areas is shiny, sometimes
glued together. Patients complain of intense itching, which may
precede clinical manifestations. Rash can exist without changing for a
long time. The accession of a secondary infection is possible. There
may be a rapid dissemination process.
x Occupational eczema develops as a result of monovalent
sensitization to any irritant with which a person contacts in the process
of performing professional duties. The diagnosis is established only
when a professional allergen is found. Dermatosis begins with
manifestations of contact allergic dermatitis in the zone of influence of
a professional factor. At this stage, the rash is limited. For treatment, it
is enough to eliminate the irritant and prevent repeated contact with it.
Immune imbalance with the development of polyvalent sensitization
occurs in the case of prolonged exposure to a professional allergen. At
the same time, the clinical picture of the disease is similar to that in
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true or microbial eczema with a chronic recurrent course and a less
pronounced polymorphism of rash.
x Children's eczema is included in the concept of atopic
dermatitis.
x Herpetiform eczema Kaposi was first described in 1887 by
dermatologist Kaposi as a severe complication of eczema or
neurodermatitis mainly in young children. The main cause of the
disease is infection with the herpes simplex virus of a child suffering
from eczema or neurodermatitis, which usually occurs between the
ages of 6 months and 2 years. The disease develops acutely, with a
sudden rise in temperature to 39-40ºC. The onset of herpetiform
eczema is accompanied by increased edema and exudation in the area
of primary eczematous foci. Typical rashes in the form of groups of
vesicles and pustules with characteristic umbilical depression in the
center appear on the skin. Preferential localization: on the face, scalp,
neck, less often – on the limbs and torso. Rounded hemorrhagic crusts
appear during the evolution of vesicles and pustules in the majority of
patients. Bleeding easily occurs when removing such crusts. Aphthous
stomatitis, conjunctivitis, keratitis, damage to the mucous membranes
of the genitals can develop in children. Increased regional lymph
nodes. Herpes damage to the internal organs and the central nervous
system is possible. A secondary infection often develops with the
development of pyoderma, purulent otitis, bronchitis and pneumonia,
sepsis, in patients the ESR increases and the number of eosinophils in
the blood decreases. Small scars can remain in place of the vesicular-
pustular elements. Mortality in this disease ranges from 1 to 20%.
Herpatiform eczema Kaposi can also occur in adults, complicating the
course of chronic skin diseases – atopic dermatitis, ichthyosis,
eczema, pemphigus vulgaris.
Diagnosis
Diagnosis of eczema is based mostly on history and physical
examination. However, in uncertain cases skin biopsy may be useful.
Histopathology
Spongiosis in the germ layer of the epidermis is most
characteristic for the acute period of eczema. Parakeratosis is detected
in the stratum corneum. Edema of the papillary layer, swelling of
collagen fibers, dilation of blood vessels and the formation of
lymphocytic histiocytic infiltrate around them develops in the dermis.
Acanthosis, parakeratosis, more pronounced cellular infiltration
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of the dermis are characteristic of chronic eczema.
Moderate thickening the epidermis, parakeratosis, significant
acanthosis, the absence of a granular layer, mild vacuolar
degeneration is noted in seborrheic eczema. Spongiosis is not
pronounced. Minor perivascular lymphocyte and neutrophil infiltrate
is formed in the dermis.
Treatment
There is no known cure for eczema; therefore, treatments are
aimed at controlling the symptoms by reducing inflammation and
relieving itching.
Medications
Corticosteroids are highly effective in controlling or suppressing
symptoms in most cases. For mild-moderate eczema a weak steroid
may be used (e.g. hydrocortisone), while in more severe cases a
higher-potency steroid (e.g. clobetasol propionate) may be used. In
severe cases, oral or injectable corticosteroids may be used. While
these usually bring about rapid improvement, they have greater side
effects.
Side effects
Prolonged use of topical corticosteroids is thought to increase the
risk of side effects, the most common of which is the skin becoming
thin and atrophic. Because of this, if applied on the face or other
delicate skin, a low-strength steroid should be only used. Additionally,
high-strength steroids applied over large areas, or under occlusion,
may be significantly absorbed into the body, causing hypothalamic-
pituitary-adrenal axis suppression. Finally by their
immunosuppressive action they can, if used without antibiotics or
antifungal drugs, lead to some skin infections (fungal or bacterial).
Care must be taken to avoid the eyes, as topical corticosteroids applied
to the eye can cause glaucoma or cataracts.
Because of the risks associated with this type of drugs, steroids of
an appropriate strength should be sparingly applied only to control an
episode of eczema. Once the desired response has been achieved, it
should be discontinued and replaced with emollients as maintenance
therapy. Corticosteroids are generally considered safe to use in the
short- to medium-term for controlling eczema, without significant side
effects differing from the treatment with non-steroidal ointment.
Topical immunosuppressants
Topical immunosuppressants like pimecrolimus (Elidel and
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Douglan) and tacrolimus (Protopic) were developed after topical
corticosteroids had come into widespread use. These newer agents
effectively suppress the immune system in the affected area, and
appear to yield better results in some populations.
Oral and parenteral immunosuppressants
When eczema is severe and does not respond to other forms of
treatment, immunosuppressant drugs are sometimes prescribed. These
dampen the immune system and can result in dramatic improvement
to the patient's eczema. However, immunosuppressants can cause side
effects on the body. The most commonly used immunosuppressants
for eczema are ciclosporin, azathioprine and methotrexate. These
drugs were generally designed for other medical conditions but have
been found to be effective for eczema.
Itch relief
Anti-itch drugs, often antihistamines, may reduce the itch during
a flare up of eczema, and the reduced scratching in turn reduces
damage and irritation to the skin (the "itch cycle"). However, in some
cases, significant benefit may be due to the sedative side effects of
these drugs, rather than their specific antihistamine effect. Thus
sedating antihistamines such as promethazine or diphenhydramine
may be more effective at preventing night time scratching than the
newer, non-sedating antihistamines.
Capsaicin applied to the skin acts as a counter irritant.
Hydrocortisone applied to the skin aids in temporary itch relief.
Moisturizers
Eczema can be exacerbated by dryness of the skin. Moisturizing
is one of the most important self-care treatments for eczema. Keeping
the affected area moistened can promote skin healing and relief of
symptoms. Soaps and detergents should not be used on affected skin
because they can strip natural skin oils and lead to excessive
dryness.
Moistening agents are called emollients. In general, it is best to
match thicker ointments to the driest, flakiest skin. Moisturizing
gloves (gloves which keep emollients in contact with skin on the
hands) can be worn while sleeping. Generally, twice-daily
applications of emollients work best. Ointments, with less water
content, stay on the skin longer and need fewer applications, but they
can be greasy and inconvenient. Steroids may also be mixed in with
ointments.
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 Recently, ceramides, which are the major lipid constituent of the
stratum corneum, have been used in the treatment of eczema. They are
often one of the ingredients of modern moisturizers. These lipids were
also successfully produced synthetically in the laboratory.
Light therapy
Light therapy (or deep penetrating light therapy) using ultraviolet
light can help control eczema. UVA is mostly used, but UVB and
Narrow Band UVB are used as well.
When light therapy alone is found to be ineffective, the treatment
is performed with the application (or ingestion) of a substance called
psoralen. This PUVA (Psoralen + UVA) combined therapy is termed
photo-chemotherapy. Psoralens make the skin more sensitive to UV
light, thus allowing lower doses of UVA to be used. However, the
increased sensitivity to UV light also puts the patient at greater risk for
skin cancer.

Unit 3
Toxicoderma
Toxicoderma is an acute inflammation of the skin and rarely
mucous membranes that develops under the influence of an allergic,
toxic or toxic-allergic factor that enters the body through the
respiratory tract, digestive tract, by intravenous, subcutaneous,
intramuscular injection. Thus, the etiological factor does not act
directly on the skin, as with dermatitis, but penetrates it in a
hematogenous manner.
Recently, the problem of toxicoderma has intensified, which is
associated with a large use of household chemicals, environmental
degradation, and the emergence of new drugs.
Etiology
In the etiology of toxicoderma the main role is played by
exogenous causes, less often – endogenous. Exogenous causes include
drugs, food, industrial and household chemicals that enter the body
through the digestive and respiratory tract. In addition, drugs can
cause toxicoderma with any method of their administration:
intravenous, intramuscular, subcutaneous.
Endogenous causes are auto-intoxications by unusual metabolic
products that appear in the body due to dysfunction of the
gastrointestinal tract, liver, kidneys, thyroid gland; neoplasms,

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metabolic diseases, helminthic invasions.
The basis of the pathogenesis of toxicoderma is an allergic
reaction. In most cases we face drug toxicoderma. Drug toxicoderma
is a manifestation of the sensitizing effect of the drug. In its
pathogenesis, toxic and allergic components are often combined. This
leads to the development of multiple lesions of the skin, mucous
membranes, nervous and vascular systems, internal organs
characteristic of drug disease.
Drug toxicoderma may occur as a result of prolonged
administration of the drug and is a variant of a drug disease. The cause
of the development of toxicoderma can be a variety of drugs:
antibiotics, sulfonamides, barbiturates, amidopyrine, halides,
tranquilizers, vaccines and serums, vitamins, iodine, aminazin, ACTH
and many others. There are even cases of the development of
toxicoderma to antihistamines and corticosteroids.
Drug toxicoderma occurs in 2 to 3% of hospitalized patients and
accounts for 19% of all complications of medical treatment. To
predict the appearance of toxic-allergic reactions, as a rule, is
impossible. The risk of toxicoderma is considered high (3–5%) when
treated with penicillins, carbamazepine, allopurinol, and gold
medications. The average risk of developing toxicoderma is in
treatment with sulfonamides, oral hypoglycemic agents, diuretics,
nonsteroidal anti-inflammatory (NSAIDs), isoniazid,
chloramphenicol, erythromycin, streptomycin. There is a low risk
when treated with barbiturates, benzodiazepines, phenothiazines,
tetracyclines.
Toxic reaction can be caused by the use of poor-quality food, as
well as by ingestion of arsenic or mercury. The cause of toxicoderma
can be idiosyncrasy to any substance. Toxicoderma can be caused by
some allergenic foods. These include: eggs, honey, nuts, strawberries,
citrus fruits, chocolate, coffee, many spices, smoked meats, pickles,
seafood, etc. Among the factors of household chemicals you need to
select washing powders, detergents, paints, varnishes, solvents,
gasoline, kerosene, insecticides, dyes for furs and clothing (especially
those containing ursol), synthetic polymeric compounds, epoxy
resins, etc.
Pathogenesis
Allergen, penetrating into the cells of the skin and other tissues,
enters into connection with the functional structures of the cytoplasm
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(nucleoproteins, mitochondria). Skin lesions can occur as a result of
the suppression of enzyme systems by a drug, toxic damage to tissues,
blood vessels and changes in the body's reactivity. Antibodies appear
in the blood serum during allergic toxicoderma. Sensitization, i.e.
hypersensitivity to any substance is determined by the amount of
allergen entering the body, the frequency of its exposure and antigenic
activity; the body's immune reactivity. Other allergic diseases,
hereditary predisposition to allergic processes contribute to
sensitization.
Immune mechanisms of drug toxicoderma
x Allergic reactions of immediate type are mediated by IgE. An
antigen is a drug. The interaction of the drug with IgE leads to the
release of histamine, prostaglandins and other substances from the
mast cells. Manifestations: urticaria, angioedema, anaphylactic shock.
x Cytotoxic allergic reactions. The drug (antigen) is fixed on the
cell membrane. The binding of the drug (penicillins; cephalosporins;
sulfonamides; rifampicin) with a cytotoxic antibody leads to activation
of complement and lysis of platelets and leukocytes. When the
antibody-dependent cellular cytotoxicity of the antibody with the drug
(quinine, quinidine, salicylamide, isoniazid, chlorpromazine,
sulfonamides), activates cell lysis or phagocytosis.
x Immune complex allergic reactions. The drug (antigen) in the
blood forms immune complexes with antibodies that are deposited in
the walls of small vessels; activate the complement and migration of
neutrophils. This is the pathogenesis of serum sickness. The latent
period of the reaction is 5-7 days. Manifestations: vasculitis, urticaria,
arthritis, nephritis, alveolitis.
x Allergic reactions of a delayed type are mediated by T-
lymphocytes. An antigen is a drug. Sensitized lymphocytes, after
binding to the antigen, release cytokines that trigger the inflammatory
response. This mechanism can develop a drug rash.
Non-immune mechanisms of drug toxicoderma
x Hereditary enzyme deficiency.
x Cumulation (for example, melanosis in the treatment of drugs
with gold or amiodarone).
x Local irritant effect of the drug.
xIndividual intolerance to the drug.
xThe combined effect of the drug and ultraviolet radiation
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(phototoxic reactions). It is also possible the development of immune
photoallergic reactions.
Clinical Presentation
Toxicoderma in most cases occurs acutely. It is characterized by
widespread, disseminated, symmetrical and monomorphic rash
consisting of macules, papular, nodular, vesicular, bullous, pustular
and papulopustular itchy rashes.
The mucous membranes may be involved into the process.
Among macular toxicoderma can be distinguished: hyperemic,
hemorrhagic (purpura) and pigment (toxic melasma from arsenic,
metacycline, petroleum hydrocarbons or coal). Macular hyperemia
may be located in isolation from each other (roseola) or form
extensive areas of hyperemia, sometimes reaching universal skin
lesions (erythroderma). Rash may be ring-shaped.
When resolving, peeling is often observed, in case of the damage
to the palms and soles, the complete rejection of the stratum corneum
is possible. Severe itching, connection with taking a drug or a poor-
quality product, multiple rash on the extremities, presence of rashes on
the face, relapses of the disease – all these symptoms are characteristic
of toxicoderma.
For papular toxicoderma is characterized by disseminated lesion.
A rash of flat polygonal papules resembling lichen planus appears, its
appearance can be caused by prolonged administration of hingamin,
quinine, phenothiazines, PAS, streptomycin, tetracycline, drugs
containing iodine, mercury, etc.
Nodus of toxicoderma is characterized by the formation of
painful, inflammatory nodus slightly elevated above the skin level.
Vesicular toxicoderma is characterized by the appearance of large
vesicles bordered with hyperemia. The process is disseminated.
Pustular toxicoderma is usually associated with exposure to
bromine, iodine, chlorine, fluorine (halogen) preparations.
Staphylococci located in the hair follicles and sebaceous glands play a
certain role in their development.
They are activated under the influence of these drugs. These
substances are excreted from the skin with sebum, so the
manifestations of toxicoderma are more pronounced in the areas more
rich in sebaceous glands (chest, face, upper back). The rash consists of
pustules or blackheads (for example, iodine acne). Vitamins B6, B12,
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isoniazid, barbiturates, steroids, and lithium can be the cause of the
development of acne toxicoderma.
Localized and disseminated forms are isolated from bullous
toxodermia. The localized form appears in a limited area and is called
fixed. Fixed toxicoderma is characterized by the appearance of one or
several rounded macules, their diameter reaches 2-3 cm. After a few
days they become bluish and then brown. The bulla is formed in the
center of some maculae. The favorite localization of fixed
toxicoderma is the genitals and oral mucosa. Also, the rash can be
localized in other areas of the skin. When rash appears on the mucous
membrane of the mouth, the blisters quickly open forming erosion.
Fixed toxicoderma develops as a result of intaking sulfonamides,
barbiturates, salicylates, antibiotics, chloral hydrate, arsenic, and other
drugs. With each repeated intake of the corresponding drug, the
process recurs in the same sites, increasing pigmentation, and
gradually spreads to other areas of the skin. If the drug is
discontinued, then within 7-10 days the process is allowed. The
process can take longer time in case of relapses.
The clinical picture of generalized bullous toxicoderma may be
similar to the manifestations of exudative erythema multiforme. In
favor of the latter, there are: a predominant lesion of the dorsum of the
hands and feet, unexpressed pruritus, seasonality of relapses (spring
and autumn), general catarrhal phenomena and lack of communication
with the use of medicines.
The most severe form of exudative erythema multiforme –
Stevens-Johnson syndrome – usually begins suddenly and acutely
with a high fever. A yellow or white-yellow patina forms on the
conjunctiva of the eyelids. It can occupy the conjunctiva of the eyeball
and the cornea. It disappears within 3-6 weeks. In complicated cases,
conjunctival scars remain. Almost simultaneously with changes in the
conjunctiva, erythematous maculae, blisters or tuberculums, edema
and bloody-serous exudate appear on the lips and mucous membrane
of the mouth with a fetid purulent discharge from the mouth and
external genital organs.
In case of severe toxicoderma, general disturbances in the nervous
system (irritability, alternating with depressive state, insomnia,
emotional lability, etc.), fever accompanied by general malaise,
weakness, transient arthralgia, the symptoms of cardiovascular
lesions, including small vessels (which leads to the development of
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the hemorrhagic component) as well as the liver and kidneys (drug
disease). Subjective symptoms are itching and burning.
Diagnostics
To establish the cause of toxicoderma is not easy, and often
impossible. In the diagnosis of drug toxicoderma all other causes of the
rash are excluded, in particular, infectious ones. Various diagnostic tests
are used including skin tests to confirm the causal role of the suspected
factor. There are diagnostic tests carried out outside the human body,
such as: Fleck leukocyte agglomeration reaction, Shelley basophil
degranulation test, lymphocyte blast transformation, platelet reactions,
hemolytic tests, etc. These samples are based on the reaction of the
patient's blood cells to the chemical that caused sensitization. Both false-
positive and false-negative reactions are possible.
Differential Diagnosis
Its aim is to differentiate bullous toxicoderma on the genitals (in
the erosive stage) from chancre, genital herpes and erosive
balanoposthitis.
Other forms differentiated from are syphilides of the secondary
period of syphilis, rubella, measles, chicken pox and pyoderma.
Treatment
The most important condition for the treatment of toxicoderma is
interruption of the etiological factor effect. It is recommended to
prescribe a hypoallergenic diet. For removal of toxic substances from
the body diuretics, laxatives are prescribed. Gastrointestinal, liver, and
kidney functions are restored. As desensitizing drugs solutions of
calcium gluconate, sodium thiosulfate intravenously or calcium
gluconate intramuscularly are administered. Antihistamines and
sorbents are prescribed as well. To improve the gastrointestinal tract,
enzymes and eubiotics (bifidumbacterin, colibacterin, lactobacterin)
are effective. In severe toxicoderma, corticosteroids (prednisone,
dexamethasone) are prescribed for systemic therapy. Topical
treatment is usually carried out with corticosteroid ointments
(betamethasone, flumethasone, budesonide, etc.), creams and aerosols.

Unit 4
Toxic epidermal necrolysis (Lyell's syndrome)
It is a severe form of drug toxicoderma, described by Lyell in
1956. Lyell's syndrome develops as a reaction to the combined effects

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of toxic, medicinal and infectious agents, occurring on the background
of a high degree of hypersensitivity of the body.
Etiology and Pathogenesis
The most common causes of Lyell's syndrome are such drugs as
sulfonamides and antibiotics (erythromycin, penicillins, tetracyclines,
streptomycin, etc.), barbiturates, analgesics (phenylbutazone,
salicylates, paracetamol, piroxicam, diclofenac, cephalosporins,
fluoroquinolones and others). The disease can develop as a result of
the combined administration of several drugs. Other causes of Lyell's
syndrome can be chemical intoxication or spoiled food.
The basis of the pathogenesis of Lyell's syndrome is an allergic
reaction. Immune mechanisms include a cytotoxic effect of
lymphocytes on the epidermal cells.
Clinical Presentation
The disease develops within a few hours or days after the first
dose of the drug (from 1 day to 3 weeks). Sometimes there is a
prodromal period with such symptoms as fever, weakness, and
headache, muscle pain, burning or itching of the conjunctiva.
Suddenly, the temperature rises to 39-40°C, macular and/or
petechial rash appears, urticaria or blisters can occur, the rash
resembling frequently a multiforme exudative erythema. Often, the
first rash appears on the mucous membranes of the mouth, nose,
genitals and eyes. Painful erythroderma develops over several days,
due to this the epidermis begins to detach.
There is a symptom of “wet clothes”: when you touch the skin it
begins to wrinkle, is easily pulled off and then rejected with the
formation of painful erosions. Sometimes there are blisters with flabby
tires. When pressing slightly on them, their area increases. Nikolsky's
symptom is positive, when rubbing outwardly healthy skin in the areas
adjacent to the rash, erosion appears.
The patients complain of sharp skin soreness, burning, increased
sensitivity and paresthesia. Then there is a sharp deterioration in the
general condition. There is high fever, severe headaches, drowsiness
or anxiety, prostration is possible as well. The symptoms of
dehydration are observed. They are severe thirst and dryness of the
oral mucosa. Swallowing is difficult due to pain; therefore the patients
refuse to eat. Kidney function is impaired (acute tubular necrosis);
urination is painful. Ulceration of the trachea mucous membrane,
bronchi, and gastrointestinal tract is possible. The disease progresses
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within the first 3 days. Further, the course is in many ways similar to
that of a burn disease. The prognosis depends on the prevalence of
necrosis. Frequent complications are renal failure, bacterial infections
and sepsis. Cachexia (due to increased catabolism) and diffuse
interstitial pneumonia may develop. Mortality in Lyell's syndrome
reaches 30%.
Diagnostics
At the onset of the disease, differential diagnosis is carried out
with multiform exudative erythema, scarlet fever, phototoxic
reactions, maculopapular toxicodermas, and graft versus host disease.
Late manifestations of Lyell's syndrome must be differentiated
from thermal burns, exfoliative erythroderma, Stevens-Johnson
syndrome, and acute febrile pemphigus. Before the development of
necrolysis of the epidermis, it is difficult to make a correct diagnosis.
An important diagnostic sign is the appearance of a severe pain at the
site of rash and intact skin.
Blood tests show anemia, lymphopenia, and sometimes
eosinophilia. The occurrence of neutropenia is a poor prognostic sign.
Pathological examination reveals vacuolization and necrosis of
keratinocytes of the basal layer. Acantolysis leads to detachment of
the upper layers of the epidermis. Edema, polymorphic perivascular
infiltrates are observed in the dermis. To exclude other diseases
involving the formation of blisters immunofluorescent study is
performed.
Treatment
Treatment is carried out in the intensive care or burn department.
Glucocorticoids and antibiotics are prescribed, as well as symptomatic
treatment. It is imperative to identify quickly and cancel the drug that
caused the disease. The patient must be injected intravenously to 2 or
more liters of fluid (dextrans, polyvidone, plasma and saline) per day,
to correct electrolyte disorders parenteral nutrition should be
conducted. Anabolic steroids are prescribed.
Glucocorticosteroids are administered parenterally. The initial
dose corresponds to 120-150 mg of prednisolone. An antibiotic with a
broad spectrum of action is chosen that does not have a nephrotoxic
action and a prolonged effect. You cannot assign penicillins and
tetracyclines. It is necessary to check the sensitivity to the selected
antibiotic, using the data of anamnesis and the results of in vitro
allergy tests. Topically used aqueous solutions of aniline dyes
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(fukortsin, methylene blue), corticosteroid sprays, on the moist areas –
antibacterial lotions. Solcoseryl ointment or cream will be prescribed
in the future.
Patient care is very important! The patient should be in a warm
room equipped with germicidal lamps. It is necessary to change the
underwear and bed linen (sterile) 2-3 times a day. It is necessary to
administer analgesics before dressing. Necrotic skin is removed.

Checkup Questions
1. What substances is the most common cause of allergic
dermatitis?
2. What test is used to identify the allergen?
3. What factors are involved in the development of eczema?
4. How is eczema classified?
5. What are the clinical manifestations of true eczema? What are
the varieties of true eczema?
6. How does microbial eczema manifest? What are the varieties
of microbial eczema?
7. What methods are used in the diagnosis of eczema?
8. What are the causes of toxicoderma?
9. What methods of diagnosis are used to define toxicoderma?
10. What kind of etiology and pathogenesis does Lyell's syndrome
have?
11. How does Lyell's syndrome manifest?

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CHAPTER XII
NEURODERMATITIS
Unit 1
Atopic Dermatitis
Atopic dermatitis (AD, a type of eczema) is an inflammatory,
chronically relapsing, non-contagious and pruritic (that is, itchy) skin
disorder. It has been given names like "prurigo Besnier,"
"neurodermitis," "endogenous eczema," "flexural eczema," "infantile
eczema," and "prurigo diathésique".
Atopic dermatitis is one of the most frequent chronic
inflammatory skin diseases, affecting up to 25% of children and 1–3%
of adults worldwide. The condition is characterized by intense pruritus
and a course marked by exacerbations and remissions.
Etiology and pathogenesis
The precise cause of atopic dermatitis is not known. A complex
interaction of genetic and environmental factors are believed to induce
immunological and biochemical changes that produce the pruritic,
inflammatory dermatosis.
Predisposal factors:
x Genetic Factors
Atopy is a genetic predisposition to form excessive IgE
antibodies.
Atopic dermatitis runs in families. The prevalence of AD in
children is about 50% when on parent has AD, while it may be as high
as about 80% when both parents have the disease The precise mode
of inheritance in not known, it is probably polygenic. Genetic factors
may produce disease through abnormality in IgE synthesis, expression
of IgE receptors on cells, or through cytokine production by
leukocytes.
x Immunologic abnormalities
Functionally, there are two subsets of helper T lymphocytes: (a)
TH1 cells which mainly produce interferon gamma, interleukin-2 and
mediate cell-mediated immune response and (b) TH2 cells, that
produce IL-4, IL-5, IL-6, and Il-10 and promote antibody-mediated

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immune response. IL-4 induces IgE production and inhibits gamma
interferon production and prevents differentiation of TH1 cells. In
atopic dermatitis, there is a TH2 cell predominance which leads to
increased IgE production by B lymphocytes and by its suppressive
action of TH1 cells, diminishes cellular immune response.
In response to various allergens, AD patients are genetically
prone to produce high levels of IgE. IgE-mediated allergic reaction
causes mediator release from mast cells, this reaction is biphasic, the
immediate reaction producing redness and itching and the delayed
reaction may cause chronic inflammation.
Langerhans cells of AD patients express high levels of IgE
receptors; they capture specific allergens more avidly and present
them to TH2 cells more efficiently.
Tissue specificity of the TH2 cell response is explained by high
CLA (cutaneous lymphocyte antigen) expression on circulating T cells
that specifically home to the skin.
Increased prostaglandin E2 (PGE2) secretion by monocytes of
atopic dermatitis patients inhibits interferon gamma production, this
inhibits TH1 cells.
Monocytes of AD patients have increased Cyclic AMP-
phosphodiesterase enzyme activity – this leads to increased IgE
synthesis by B lymphocytes and release of histamine from basophils.
Keratinocytes, injured by scratching may also secrete cytokines
that helps migration of TH2 cells to the skin, thus modulation the
immunological phenomenon.
x Allergens
- Food (A subset of patients, particularly infants and children,
may have hypersensitivity to foods, particularly to milk, peanuts,
fruits, fish and soybeans.);
- Aeroallergens (House dust mites, pollens, and animal danders
may exacerbate or perpetuate disease in a number of patients.)
x Microbial products
Staphylococcal toxins may act as superantigens and stimulates the
allergic reaction. Other infections like dermatophytes of pityrosporum
may also act as allergens.
x Dryness of skin
Dry skin is a prominent feature in many atopic dermatitis patients.
Abnormalities in lipid metabolism with reduced synthesis of ceramide
may lead to decreased water-binding capacity of skin. Dryness causes
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microfissures on the skin surface that promotes entry of irritants,
allergens and microbes).
x Climatic factors
A dry and cool environment increases xerosis of skin. Sweating in
hot, humid climates may cause irritation, while sunlight tends to
improve the symptoms.
x Psychological factors
The psychological impact of the disease on the patients leading to
depression, anxiety, and frustration may cause reduced itch
threshold and increase the inherent irritability of the skin, thus
contributing to the pathogenesis of the disease.
Clinical presentation
Atopic dermatitis principally affects infants and children, about
eighty per cent of the cases are said to occur in children below the age
of five.
AD is more prevalent in temperate climate, and the incidence is
increasing in recent years.
The dominant symptom of AD is itching. The pruritus of AD
persists throughout the day but increases during evening and night.
The itching of AD is characteristically paroxysmal and often
uncontrollable. It causes varying degrees of sleep disturbance in
affected individuals. There is a reduced threshold for itching to
irritants and the itch exacerbates with sweating, and low humidity.
Chronic itching leads to scratching, often violent, and scratching
leads to secondary changes in the skin like excoriation, infections and
thickening, that leads to more itching. Thus, a vicious cycle (itch-
scratch-itch cycle) is established which perpetuates the condition.
The lesions of atopic dermatitis take the form of erythematous
papules, vesicles, and oozing with crusting in the acute stage. In the
subacute stage the lesions are reddish scaly papules.
Chronicity leads to thickened plaques with accentuated skin
markings (lichenification). Excoriations due to scratching are the
commonest secondary lesions. In all phases of AD, dryness of the
skin, exaggerated during conditions of low temperature and humidity,
may be prominent findings.
The morphology and distribution of the lesions evolve in the
following phases:
x Infantile AD (from two months to two years)
Atopic dermatitis usually starts in the first year of life. During this
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phase, the there is facial erythema, vesicles, oozing and crusting
located mainly on the face, scalp, forehead and extensor surface of the
extremities. Buttocks and diaper area are frequently spared.
x Childhood AD
The lesions tend to be drier and scaly. Flexor surfaces and skin
creases are predominantly involved. Facial lesions with eyelid
involvement and lesions around the neck also occur. Lichenification
from chronic itching and scratching occur over flexor surfaces.
Psychological effects often are very prominent.
x Adolescent and adult AD
Flexural predilection of lesions persists. Localized, eczematous or
lichenified plaques often predominates the clinical picture. Prurigo
papules and nodules tend to occur. Resolved cases show dryness and
irritability of the skin with a tendency to itch with sweating and other
triggers. Recurrent and persistent hand dermatitis is a frequent feature.
Diagnosis
Diagnosis of atopic dermatitis is done clinically. Since there is no
single diagnostic clinical finding or laboratory abnormality in AD,
diagnosis of the disease is based on a combination of clinical features.
The following diagnostic guideline (the UK working group
criteria) is simple and useful:
x Patients must have an itchy skin condition (or parental report of
scratching or rubbing in children).
x Patients must also have 3 or more of the following:
 History of involvement of the skin creases, such as folds of
elbows, behind the knees, fronts of ankles, or neck.
 Personal history of asthma or hay fever (or a history of atopic
disease in a first-degree relative in patients younger than 4 years).
 History of a generally dry skin last year.
 Visible flexural dermatitis (or dermatitis involving cheeks or
forehead and outer limbs in children younger than 4 years)
 Onset younger than age 2 years (not used if child is <4 y).
Elevated serum IgE level is a frequent finding, but this is non-
specific.
Histopathology shows features of an eczematous dermatitis.
There is no role of allergy tests in the diagnosis of AD.

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 Differential diagnosis
x Scabies.
x Seborrheic dermatitis .
x Contact dermatitis.
x Drug eruption.
x Pityriasis rosea.
x Candidiasis.
Treatment
Prevention is the mainstay of treatment for atopic dermatitis.
General measures
x Provide psychological support.
x Avoidance of factors that promotes dryness, itching or
inflammation.
x Avoidance of contact with local irritants like woolen
garments, use soft cotton garments.
x Clothing and linens should be washed in mild detergents and
rinsed well.
x Fingernails should be kept short.
x Avoidance of contact with animals, dust, sprays and perfumes.
x Avoidance of excessive bathing.
x Soaps should be bland and non-irritant
x Foods that are suspected to aggravate symptoms in individual
patients should be avoided.
x Avoidance of extremes of temperature and humidity.
x In severe cases, hospitalization for a short period may promote
rapid reduction of symptoms mainly by providing a changed
environment.
Specific treatments:
Specific measures are aimed at modifying the following
pathogenetic factors: dryness, inflammation, infection and itching.
Corticosteroids:
- Systemic steroids
A short course of systemic steroids (prednisolone, triamcinolone)
may occasionally be needed to suppress acute flare-ups.
Intralesional steroids
Triamcinolone acetonide may help resolve thickened plaques of
eczema not responding to topical agents.
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 - Topical steroids
These are the cornerstones of therapy of atopic dermatitis. The
following principles should be adhered to while instituting topical
steroid therapy:
x High potency steroids are used for a short period to rapidly
reduce inflammation.
x Maintenance therapy, if needed is best done with mild steroids
like hydrocortisone.
x On face and intertriginous areas, mild steroids should be used,
mid-potency formulations are used for trunk and limbs.
x Topical steroids are applied initially twice or thrice a day After
the symptoms are lessened, frequency of application should be
reduced. Intermittent use if topical steroid may be alternated with
application of emollients.
x Ointments are superior to creams or lotions.
x The potential side-effects of topical steroids should always be
kept in mind.
Emollients
Atopic dermatitis patients frequently have dry skin which
aggravates during winter months. Xerosis breaks the barrier function
of the skin and promotes infection and inflammation. Ointments are
preferred over lotions or creams. Emollients should be applied
immediately after a soaking bath to retain the moisture. Emollients
containing urea or alpha-hydroxy acids often cause stinging or
burning sensations. Adding emulsifying oils to bath water is also
helpful.
Antihistamines
Antihistamines give variable results in controlling pruritus of
atopic dermatitis since histamine is not the only mediator of itching in
atopic patients. Any of the non-sedating antihistamines like cetirizine,
loratadine or fexofenadine may be used. The conventional
antihistamines like diphenhydramine or hydroxyzine may give better
results for their additional actions as sedative or anxiolytic. Topical
antihistamines should be avoided for their sensitizing potential.
Antimicrobials
Atopic eczema frequently secondarily colonized with a bacterium
(up to 30%). Infections and colonization with Staphylococcus aureus
may aggravate or complicate AD. Antibiotics like erythromycin,
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cephalosporins, or cloxacillin are usually prescribed. Dermatophytosis
or Pityrosporum infections are treated with antifungals. Acyclovir or
other appropriate antiviral agents should be promptly advised for
treatment of herpes simplex infections.
Tar compounds
Liquor carbonis detergens in ointment or other vehicles are useful
adjuncts to topical steroids in pats with chronic dermatitis by their
antipruritic and antiinflammatory actions. They may be used
alternately with topical steroids.
Phototherapy
Ultraviolet B (UVB) alone, or in combinations with UVA may be
beneficial in selected patients. Narrow-band UVB (311nm) is also
used. In adult patients, psoralens in association with UVA (PUVA) are
often beneficial.
Cyclosporine
By virtue of its immunomodulating action, cyclosporine has a
limited role in controlling atopic dermatitis in recalcitrant adult cases.
The potential side effects should always be kept in mind.
Azathioprine
This immunosuppressive agent has also been used in severe adult
cases. Again, potential side effects limit its role in selected cases.
Topical Immunosuppressants
A new class of the drugs that can be used in AD is local
immunosuppressors (creams, ointments) – Pimecrolimus (cream 1%
(trade name Elidel)), Tacrolimus (0.03%, 0.1% cream (trade name
Protopic)).They have no side effects as corticosteroids and may be
used continuously.
Topical ascomycin and phosphodiesterase inhibitors
Topical application of these agents has given beneficial results in AD.
Course and prognosis
Most infantile and childhood cases improve over time and the
prevalence of atopic dermatitis diminishes significantly in older ages.
Children tend to outgrow the condition. The length of remission may vary
from months to years and the condition may reappear during puberty.
Some patients’ disease may persist through adulthood. In others, a
tendency for dry and irritable skin which easily develops eczematous
changes may persist after AD has resolved. A propensity for recurrent
hand dermatitis may remain in adults who had AD in their childhood.
Many children later on develop allergic rhinitis or bronchial
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asthma. There is no reliable marker for predicting the course of the
disease, but early age of onset, severe affection, personal history of
other atopic diseases or family history of AD are associated with poor
prognosis.

Unit 2
Skin Itch (Pruritus)
The relevance of the phenomenon of itching is determined by its
high prevalence. The prevalence of itching in the general population
ranges from 8.8 to 13.9%.
Itching is a subjective sensation that causes the desire to scratch a
piece of skin or mucous membranes.
The itch receptors have not been detected yet. According to some
researchers, itch receptors are free nerve endings that perceive pain,
and itching is a modified sense of a pain.
Pruritus can be an independent disease, and a symptom of
diseases of the blood, liver, kidney, pancreas, metabolic disorders.
Itching is often caused by plants, insect bites, mechanical irritations,
and chemicals.
Classification
Pruritus can be localized and generalized, acute and chronic.
It is divided into primary (when there is a single manifestation of
skin pathology) and secondary (if there are various dermatoses, such
as urticaria, lichen planus, atopic dermatitis).
Acute skin itching lasts a short period of time and quickly
disappears. It is more frequently localized. Chronic itching occurs
much more frequently. It can persist for many months and varies in
intensity. It can be short-term, paroxysmal or permanent. Itching for 6
weeks and more, according to the conclusion of the International
Forum on Studies of Itch (IFSI), refers to chronic.
The diagnosis of pruritus as an independent disease is made when
other diseases, in which itchy skin is a symptom are excluded.
The following forms of itchy skin are distinguished.
Senile itching of the skin occurs in people over 60 years. It
intensifies at night. It may be paroxysmal. The development of senile
pruritus contributes to dehydration and dry skin, sclerosis of vessels
and other disorders of the nervous system, internal organs and skin
associated with aging.

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 Winter itching occurs on the skin of the legs in places of contact
with wool underwear. The cause may be dry skin.
High-altitude skin itch appears when rising up to the height of
more than 8 thousand meters, and also due to immersion in water. It is
associated with a change in a barometric pressure.
Localized pruritus occurs in the anus and genitals, scalp and palms.
Itching of the anus may be caused by constipation, rectal fissures,
worms, hemorrhoids, paraproctitis, proctitis, vesiculitis, cooperite,
prostatitis and chronic inflammation of the genitals, especially when
hygiene is not followed. It might be associated with an impaired
function of apocrine sweat glands, an allergic reaction to food as well as
localization in the perianal areas of syphilides, mycosis, genital warts,
and manifestations of recurrent herpes simplex.
Genital pruritus is more common in the vulva or vagina in
women, and in the scrotum and glans penis in men. The itch of this
localization can be caused by gonorrhea, trichomoniasis,
gardnerellesis, urea-and mycoplasmosis, chlamydiosis, an irritating
effect of urine in diabetes and gout, dysmenorrhea, endocrine
disorders, worms, sexual neurosis, urethritis, prostatitis, and
gonorrhea, recurrent herpes simplex, genital warts, manifestations of
syphilis, Bowen's disease, cancer of the genital organs, toxicosis of
pregnant women.
Itching of the vulva may precede kraurosis.
Scalp itching associated with dryness of the skin in this area
often develops because of impaired blood supply to the aponeurosis
(cerebral arteriosclerosis, Gorton's temporal arteritis). It can occur in
psychiatric patients. But it can accompany chronic pyoderma scalp,
fungal infection, seborrhea, psoriasis and syphilis as well.
Itching of the palms is often caused by mental or neurological
impairments; it may be a manifestation of peripheral vascular lesions
or an allergic reaction to domestic and industrial allergens.
Pruritus as a symptom occurs in the following diseases:
x Internal diseases: jaundice, uremia, chronic diseases of the
digestive tract, hypovitaminosis and gout.
x Hematological diseases: leukemia.
x Oncological diseases: cancer of the urogenital tract, cancer with
bone metastases and paraneoplastic itching.
x Endocrinological diseases: diabetes, myxedema, thyrotoxicosis,
ovarian failure.
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 x Obstetric and gynecological diseases: pregnancy, menopause,
inflammatory diseases of the genitals, cancer of the genitals.
x Peripheral circulatory disorders: arterial blood supply
(obliterating endarteritis, stenotic atherosclerosis, angiopathies in
metabolic diseases); venous blood supply (thrombophlebitis,
phlebothrombosis, postthrombotic syndrome).
x Infectious diseases: chickenpox, measles, erysipelas.
x Allergic diseases: drug disease, food allergies, allergic reactions
to external irritants (nettle, insect bites, plant pollen, plant contact etc.).
x Mental and neurological diseases: psychosis, vascular dystonia,
neurosis and neuritis.
x Parasitic diseases: scabies, lice, helminthes.
x Dermatoses: allergic and contact dermatitis; eczema; mycoses
and candidiasis; lichen planus; herpes; dermatitis herpetiformis;
pyoderma; pruritic dermatosis (atopic dermatitis, urticaria, prurigo);
psoriasis.
x Intoxication: drug addiction, substance abuse; alcoholism at
work as well as at home.
Treatment
Treatment of pruritus is very difficult. The success of therapy
depends on the cause of itching. If you manage to eliminate the cause,
it often leads to recovery. The following medications are used to
reduce the intensity of itching: antihistamines, mast cell inhibitors,
systemic corticosteroids, opioid receptor agonists, antidepressants,
serotonin antagonists, cyclosporin A. Topical treatment includes
administration of corticosteroid ointments, antipruritic suspensions,
creams and pastes. Tacrolimus and Pimecrolimus for local treatment
are recommended as well. Topical treatment depends on patient's skin
type. Alcohol base is used for oily skin, cooling ointment – for dry
skin. Some other antipruritic drugs such as menthol (1-2%), carbolic
acid (1-2%), anestezin (10–15%), citric acid (2–5%), thymol (1-2%),
diphenhydramine (0.5-2%), tar (2-10%) are used. Emollients are
applied after each bath or shower if the skin is dry.

Unit 3
Urticaria
Urticaria is one of the most common skin diseases characterized
by the appearance of skin rash represented by weals.
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 Epidemiology
Urticaria occurs at least once in life in 15-25% of the population.
49% of patients have a combination of urticaria and angioedema, 40%
– only urticaria, 11% – isolated angioedema. In 70-75% of patients,
the disease has an acute course, in 25-30% – chronic. Acute urticaria
affects children and adolescents more often. Chronic urticaria is more
typical for people from 20 to 40 years.
Classification
There are acute and chronic forms of urticaria.
The diagnosis of acute urticaria suggests disease duration of less
than six weeks. Chronic urticaria is characterized by the occurrence of
itchy weals daily (or almost daily) for more than six weeks.
According to the new nomenclature of allergic diseases proposed
by the European Academy of Allergology and Clinical Immunology,
the urticaria caused by immunological mechanisms is designated by
the term “allergic urticaria”, and if the disease is caused by IgE
antibodies, the term “IgE-mediated urticaria” is used. Chronic
urticaria should be considered non-allergic until immunological
involvement has been proven.
Acute urticaria develops as a result of an allergic reaction to foods
(nuts, eggs, fish and seafood) or medicines (penicillin, aspirin and
other nonsteroidal anti-inflammatory drugs). In children, acute
urticaria may be associated with a viral infection. Insect bites (bees,
wasps, etc.) can cause urticarial as well.
In most patients with chronic urticaria, the cause of the disease
remains unknown, that is, urticaria is idiopathic.
Forms of chronic urticaria
x Chronic idiopathic urticaria – 75-80%.
x Urticaria caused by physical factors – 15-20%.
x Other forms of urticaria, including allergic – 5%.
The causes of physical urticaria are: exposure to high and low
temperatures, sunlight, pressure, vibration and contact with water.
According to a new concept, chronic urticaria has an autoimmune
nature. It was established that in 30–52% of the patients with chronic
urticaria functional autoantibodies to the IgE receptor and to IgE were
determined. At the same time, antibodies to the IgE receptor are a
causal factor of chronic urticaria in approximately 25-40% of patients,
and anti-IgE antibodies in approximately 5-10% of patients. IgE
receptor autoantibodies activate basophils or mast cells by binding to
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the receptor that leads to histaminoliberation and causes certain
clinical manifestations of urticaria.
Urticaria can be an independent disease, and can also be a
symptom of a number of diseases.
Diseases in which the development of chronic urticaria is
possible as a symptom are as follows:
x Infections (bacterial, viral, fungal)
x Parasitic invasions
x Endocrine pathology (diabetes, hypothyroidism, thyrotoxicosis,
ovarian dysfunction)
x Autoimmune diseases (collagenosis)
x Dysparaprothemia
x Tumors (Hodgkin's lymphoma, leukemia, colon, rectum, lung,
liver, lung and ovarian carcinoma)
x Other diseases (sarcoidosis, amyloidosis)
Allergic reactions play a major role in the pathogenesis of patients
with acute urticaria and are an extremely rarely cause of the
occurrence of daily symptoms in a chronic course of the disease. It is
known that mast cells have an increased ability to degranulate in
patients with chronic urticaria.
Hyperactivity of mast cells of the skin may return to normal with
remission of the disease. Immunological and non-immunological
factors can cause the activation of mast cells in the skin in urticaria. In
acute urticaria, as a rule, immunological IgE-mediated mechanisms
for the activation of mast cells prevail.
In chronic urticaria immunological mechanisms of mast cell
activation are also possible (in the autoimmune form of the disease).
However, the action of well-known non-specific triggers of chronic
urticaria (emotional stress, premenstrual period, alcohol, physical factors,
etc.) is realized through the non-immunological activation of mast cells.
Non-immunological factors of mast cell activation:
x Neuropeptides (substance P, vasoactive intestinal polypeptide,
neurokinins).
x Hormones (estrogens, ACTH, gastrin).
x Medicines (aspirin, NSAIDs, codeine, polymyxin B).
x Physical effects (high and low temperatures, pressure, etc.).
x Poisons of animal origin.
x Radiocontrast agents.
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 Clinical presentation
In this condition itching red weals develop; they resemble the
effects of stinging nettle (Urtica dioica) on the skin. A feature of the
urticaria is a rapid onset and rapid disappearance of wheals (within 24
hours) without the formation of secondary skin lesions.
Rash in urticaria can have any localization, including the scalp,
palms and soles. The number of mast cells in the skin is greater in the
head and neck area as compared to other skin areas. Therefore,
urticaria and itching of this localization are characterized by greater
intensity. The duration of acute urticaria is several days, while chronic
urticaria is characterized by a long relapsing course with occasional
exacerbations. The duration of the disease may be different.
Histopathology
The histological changes may be very slight but usually there is
some oedema, vasodilatation, and a cellular infiltrate of lymphocytes,
polymorphs, and histiocytes.
Angioedema is due to oedema of the subcutaneous tissues; it can
occur rapidly. In addition, when angioedema is possible damage to the
mucous membranes of various organs and systems (respiratory,
digestive, urinary, nervous, etc.) occur. Quincke oedema can cause
disfigurement of the face (swelling of the lips, eyelids, and auricles)
and cause a dangerous laryngeal damage.
Diagnostics
x Detailed history
x Physical examination
x Screening laboratory tests
When making your training case report, you need to pay attention
to the features and localization of an urticarial rash, to clarify the
triggers and the time period within which wheals are present on the
skin.
Diagnosis of urticaria during physical examination is not difficult
for a clinician. Attention should be paid to the visual characteristics of
urticarial eruptions, the presence of common symptoms, such as fever,
lymphadenopathy, hepato-and splenomegaly, and swelling in the
joints.
Screening laboratory tests:
x Blood tests
x Urinalysis

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 x Screening for Hepatitis B and C (HbsAg and HCV antibodies)
x RPR
x Bacteriological studies (feces, material from the mucous
membranes of the oropharynx, etc.)
x Coproscopy
x Detection of antibodies to parasite antigens
Instrumental studies:
x Ultrasound of internal organs
x Esophagogastroduodenoscop
x Electrocardiogram
x X-ray examination of the organs of the thoracic cavity and
paranasal sinuses (if indicated)
Additional examinations according to indications:
x • Allergological examination (skin tests with allergens)
x • Virological examination
x • Detection of pathogens
Differential Diagnosis:
x Urticarial vasculitis
x Erythema multiforme
x Bullous pemphigoid
x Herpetiform dermatitis
The main disease in the differential diagnosis is urticarial
vasculitis.
Signs of urticarial vasculitis:
Clinical
• Rashes persisting for more than 24 hours
• Wheals more frequently accompanied by painful sensations than
itching
• Hemosiderin staining remains after resolving the rash
• Rash accompanied by common symptoms (arthralgia, low-grade
fever, abdominal pain, etc.)
• Low clinical efficacy of antihistamine drugs
Laboratory
• Increased ESR and elevated concentrations of acute phase
proteins
Histological
• Edema and detachment of the postcapillary venues endothelium
• Leukocyte infiltration of the dermis around postcapillary venues
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 • Leukocytosis (neutrophilic nuclear detritus)
• Fibrin deposits
• Extravasation of red blood cells.
Treatment
Treatment of patients with chronic urticaria and angioedema
includes educational programs for patients, non-pharmacological
interventions (elimination, etc.) and pharmacological treatment.
All patients with urticaria and angioedema should avoid taking
acetylsalicylic acid and other non-steroidal anti-inflammatory drugs,
since these drugs cause exacerbation of urticaria in 50% of cases.
In such patients it is also necessary to exclude the use of
angiotensin-converting enzyme inhibitors, since the development of
angioedema may be a side effect of these drugs.
Patients should avoid foods that contain histamine and histamine
liberators: citrus, papaya, strawberries, pineapple, nuts, tomatoes,
spinach, chocolate, egg protein, eggplants, tomato ketchup, white and
red wine, beer, sardines, herring, cheeses (Gouda, Camembert,
Emmental, Swiss, Parmesan, salami sausages, ham, food additives and
spices. They are not causative factors, but may worsen the course of
the disease when used excessively.
Basic therapy of chronic urticaria is carried out with antihistamines.
To treat urticaria is quite difficult. Antihistamines are not effective in all
patients because of the participation of not only histamine, but also other
mediators in the pathogenesis of chronic urticaria.
The use of classic antihistamines is limited by the side effects of
these drugs. Classic sedative antihistamines can not only cause
drowsiness, but also change the time of the central nervous system
reflex reaction.
Other side effects of classic antihistamines include dizziness,
incoordination, blurred vision, diplopia, and symptoms of paradoxical
CNS stimulation. Epileptic activity can occur in patients prone to
epilepsy, since antihistamines easily penetrate the blood-brain barrier
and bind to the H1-histamine receptors in the brain. Side effects, such
as dry mucous membranes, urinary retention, palpitations, anxiety and
increased intraocular pressure are also identified.
Currently, new non-sedative antihistamines are still considered
the first choice in treatment of urticaria. These drugs (loratadine,
cetirizine, ebastine, fexofenadine, desloratadine) have significant
advantages over the classical ones, since they do not have undesirable
145
effects on the central nervous system.
The use of systemic corticosteroids for urticaria is shown:
• In a severe disease
• In complete ineffectiveness of antihistamine drugs
Adrenaline can be used for acute attacks, particularly if there is
angioedema of the respiratory tract.

Unit 4
Prurigo
Prurigo is a chronic disease from the group of
neuroallergodermatosis, characterized by papular, papulovesicular,
nodular eruptions, accompanied by severe itching.
Classification
x children prurigo (strophulus);
x adults prurigo (prurigo vulgaris);
x Prurigo nodular (urticaria papular resistant, neurodermitis
nodular).
There are symptomatic forms of prurigo vulgaris: pregnant
prurigo, summer prurigo, winter prurigo, lymphatic (leukemic) and
lymphogranulomatous prurigo.
Prurigo of children (strophulus, children's urticaria) develops in
children aged from 6 months to 3 years (sometimes up to 5 years).
Pathogenesis is associated with some foods (cow's milk,
chocolate, honey, citrus fruits, strawberries, etc.) sensitization. Less
commonly, the disease is caused by drug sensitization or helminthic
invasion.
In the development of strophulus, some anatomical and
physiological features of the structure of the skin in children play role.
In younger children, the dermis is thinner and differs in structure from
the dermis of adults. Cellular elements prevail in it, and fibrous
structures are not sufficiently differentiated. A significant number of
mast cells that actively produce biologically active substances
contribute to the fact that the skin of children becomes a target organ
involved in allergic and pseudo-allergic reactions. The leading role in
the formation of allergic dermatosis and strophulus is played by the
state of the child’s nervous system. It was revealed that the
parasympathetic nervous system prevails most often in infants with
allergic diseases.
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 Clinical Presentation
Prurigo of children is manifested by pink swollen papules of 3-5
mm in diameter, in the center of which a small vial (papulo-vesicle) is
formed, at the base of which a blister is often found. As a result of
scratching a nodule is formed, covered with a bloody crust in the
center. The rash is localized on the trunk, extensor surfaces of the
limbs, buttocks and face.
In place of excoriation, a pyogenic infection usually develops,
most often in the form of vulgar impetigo. The disease has a chronic
course with slight remissions and usually ends independently at 3–5
years of age.
Prurigo in adults is a disease that is more common in women of
middle and old age, often due to dysfunction of the gastrointestinal
tract, endocrine (diabetes, etc.), neuropsychiatric or oncological
diseases.
The development of prurigo in adults can contribute to the
alimentary factor (excessive consumption of honey, chocolate, coffee,
alcohol and other allergenic products).
On the skin of the extensor surfaces of the limbs, and then
hemispherical papules of red-brown color, dense texture, covered with
a bloody crust, in the size of lentils appear on the trunk. Usually their
diameter does not exceed 3 mm.
The nodules are accompanied by severe itching. The course is
chronic, recurrent, from several weeks to several months and years.
Differential Diagnosis
Differential diagnosis is carried out with scabies, dermatitis
herpetiformis.
Prurigo nodular (de Hyde) is a rare polyetiological disease, in
the pathogenesis of which metabolic disorders, autointoxication,
endocrine pathology, atopy, helminthic invasions are present. Among
the causal factors, some authors have noted the influence of nervous
stress and mosquito bites.
Recent studies indicate the role of immune changes in the
development of dermatosis, since patients often have rise in serum IgE
levels, change in the ratio of T- and B-lymphocytes.
Prurigo nodular (de Hyde) is more common in women after 40
years. The disease begins with the strongest itch. It is clinically
characterized by the presence of solid hemispherical papules of
brownish-red color, in size from pea to hazelnut, which are usually
147
localized in the region of the extremities. Due to scratching because of
intense paroxysmal itching, the surface of the papules becomes
covered with bloody crusts or verrucous growths. Rashes in some
cases are single, in others – multiple, sometimes with a tendency to
group, but not to merge. Rashes persist for a long time, and then
resolve with the formation of scars, pigmented along the periphery.
The differential diagnosis is carried out with a warty form of
lichen planus, tuberculosis verrucosa cutis, and small-nodular
sarcoidosis.
Diagnostics and Treatment
Examination of patients to exclude foci of chronic infection,
cancer, endocrine disorders is performed.
The beginning of the treatment for prurigo in adults and children
is following a hypoallergenic diet, namely, elimination (exclusion) of
obligatory food allergens, products with dyes, acute irritating (spicy)
foods, alcohol, and salt restriction.
The basis of the therapy for the disease is antihistamines
administration, the duration of which depends on the severity of
dermatitis. Recommended drugs for oral administration are
chloropyramine, mebhydrolin, hifenadine, clemastine, dimetinden,
loratadine, desloratadine and cetirizine.
In addition to antihistamines, it is recommended to prescribe such
medical remedies as hyposensitizing agents (calcium gluconate,
calcium pantothenate, calcium glycerophosphate, sodium thiosulfate)
and enterosorbents (enterosgel, lactofiltrum). If it is necessary,
enzyme preparations for a course of three weeks (Pancreatin, Enzistal)
and sedative herbal remedies (tinctures of valerian or peony) are
included. Corticosteroid ointments are prescribed topically.
In severe cases of prurigo or without tendency to regress of
lesions detoxification therapy should be performed with
glucocorticosteroids administered systemically (prednisone 15–20 mg
for 14–25 days, with a further decrease) and tranquilizers. An
alternative approach may be surgical methods such as dying off rash
elements with dexamethasone, hydrocortisone, celeston; irrigation
with chloroethyl, liquid nitrogen; cryodestruction and
diathermocoagulation.
Physiotherapy
Ultrasound or phonophoresis of hydrocortisone into the spine can
be used from 6-7 years old child. Among other physical methods
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diadynamic therapy on the region of the cervical sympathetic nodes
may be applied. Selective phototherapy with 20-30 sessions 4-5 times
a week may be also used.

Checkup Questions
1. At what age do the first symptoms of atopic dermatitis occur?
2. What stages of atopic dermatitis do you know, depending on
the age of the patients?
3. What primary skin lesions appear on the skin during
exacerbation of atopic dermatitis?
4. What recommendations on nutrition and care should the
mother of a child with atopic dermatitis follow?
5. Is full recovery possible with atopic dermatitis?
6. How is pruritus classified? What forms can skin itch have?
7. What diseases of the internal organs may be accompanied by
pruritus?
8. What principles are used for treatment of pruritus?
9. What forms of urticaria are distinguished?
10. Under what conditions can chronic urticaria be a symptom?
11. What methods are used to diagnose urticaria?
12. What forms of prurigo are distinguished according to its
classification?

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CHAPTER XIII
PAPULOSQUAMOUS DISEASES
Unit 1
Psoriasis
Psoriasis is a chronic, multifactorial, non-infectious inflammatory
dermatosis characterized by hyperproliferation of epidermal cells,
impaired keratinization, and inflammation in the dermis and
pathological changes in the joints.
Psoriasis is a skin condition that tends to flare-up from time to
time. Treatment with various creams or ointments can often clear or
reduce patches of psoriasis. Special light therapy and/or powerful
medication are treatment options for severe cases where creams and
ointments appeared to be not effective.
Psoriasis is not a contagious disease.
The severity of psoriasis varies greatly. In some people it is mild
with a few small patches that develop and are barely noticeable. In
others, there are many patches of various sizes. In many people the
disease severity is between these two extremes.
Epidemiology
Psoriasis is one of the most frequent skin diseases. It affects
1.5-3% of the population in Europe and North America, but is less
common in Africa and Japan. This disease is more common in
representatives of the white race than those of other races. The
population of Asian, African and Latin American countries suffers
from psoriasis least frequently (from 0.3 to 0.9%).
The gender incidence is equal. The condition may start at any age,
but it most commonly starts between the ages of 15 and 30 years or
after the age of 40 years. About 1 among 50 people develops psoriasis
at some stage of life.
A person with psoriasis may have other family members with the
same problem. Also, one large study found that smokers (and ex-
smokers for up to 20 years after giving up) have an increased risk of
developing psoriasis as compared with non-smokers. One hypothesis
for this is that toxins (poisons) in cigarette smoke may affect parts of
the immune system suffered from psoriasis.
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 Etiopathogenesis
Theories of psoriasis etiopathogenesis:
• genetic;
• parasitic and infectious;
• viral;
• neurogenic;
• endocrine changes;
• metabolic disorders;
• allergic.
Aggravating factors
In most people who have psoriasis, there is no apparent reason
why a flare-up develops at any time. However, in some people,
psoriasis is more likely to flare up in certain situations. They include
the following:
Stress
It is difficult to measure stress and to prove some relationship
between stress and psoriasis. However, it is thought that stress can
contribute to a flare-up of psoriasis in some people. There is some
evidence to suggest that treatment of stress in some people with
psoriasis may be of benefit.
Infections
Certain types of infections may cause a flare-up of psoriasis. In
particular, a sore throat caused by a certain type of bacteria called
Streptococcus spp. can cause a flare-up of guttate psoriasis or chronic
plaque psoriasis.
Medication
Some medicines may possibly trigger or worsen psoriasis in some
cases. Medicines that have been supposed of doing this include: beta-
blockers (propranolol, atenolol, etc.), antimalarial medication, lithium,
anti-inflammatory painkillers (ibuprofen, naproxen, diclofenac, etc.),
angiotensin-converting enzyme (ACE) inhibitor drugs, and some
antibiotics. In some cases psoriasis may not flare up until the
medication has been taken for weeks or months.
Smoking
As mentioned before, smoking may help to trigger psoriasis in
some cases. The toxins from cigarette smoke may also aggravate
existing psoriasis.
Trauma
An injury to the skin, including excessive scratching, may trigger
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a patch of psoriasis. The development of psoriatic plaques at the site
of an injury is known as Köbner's reaction.
Sunlight
Most people with psoriasis say that sunlight seems to relieve their
psoriasis. Many people find that their psoriasis is less troublesome
within summer months. However, some people notice an opposite
effect, i.e. a strong sunlight seems to make their psoriasis worse.
Severe sunburn (which is in fact, a skin injury) can also lead to a flare-
up of psoriasis.
Hormonal changes
Psoriasis in females tends to be worst during puberty and during a
menopause. These are periods when there are some major changes in
females’ hormone levels. Some pregnant women with psoriasis find
that their symptoms improve when they are pregnant, but it may flare
up within the month just after having a baby. This is thought to be
related to changes in hormone levels.
Alcohol
Consumption of much alcohol may also cause a flare-up in some
people.
Current hypothesis
Psoriasis is a T-cell mediated autoimmune disease. Current
hypothesis is that unknown skin antigens stimulate the immune
response. Antigen-specific T-cells are primary mediators. They lead to
impaired differentiation and hyperproliferation of keratinocytes.
Clinical presentation
x well-defined and sharply demarcated;
x round/oval-shaped lesions;
x usually symmetrical lesions;
x erythematous, raised plaques;
x lesions covered with silvery scales.
Common sites affected by psoriasis
Psoriasis can affect any part of the body – usually scalp, elbow,
knees and sacrum. The disease severity varies.
Types of psoriasis
There are different types of psoriasis:
x Chronic plaque;
x Guttate (drop);
x Flexural;

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 x Erythrodermic;
x Pustular;
- Localized (palmoplantar);
- Generalized;
x Psoriatic arthritis.
However, chronic plaque psoriasis is the most common and
typical type.
Local forms:
x Scalp psoriasis,
x Nail psoriasis
Chronic plaque psoriasis
8 or 9 out of 10 people with psoriasis have chronic plaque
psoriasis. The rash is made up of patches on the skin, called plaques.
These plaques appear on the background of the normal skin.
Each plaque usually looks pink or red with overlying flaky,
silvery-white rough scales. There is a sharp border between a plaque
and normal skin.
The most common areas affected are over elbows and knees, the
scalp, and the lower back. However, plaques may appear anywhere on
the skin. But they do not usually occur on the face.
The extent of the rash varies in different people, and can also vary
from time to time in the same person. Many people have just a few
small plaques (about 1cm) when their psoriasis flares up. Others have
a more widespread rash with large plaques of several centimeters
across. Sometimes, small plaques that are near to each other merge to
form large plaques. Chronic plaque psoriasis can be itchy, but it does
not usually cause too much discomfort.
Guttate (drop) psoriasis
This type typically occurs following a sore throat which is caused
by a bacterium (germ). Round/oval plaques of psoriasis are small (less
than 1 cm - drop size) but occur over many areas of the body. Guttate
psoriasis normally lasts a few weeks, and then fades away. However,
it may last for three to four months in some people. In many people,
once it goes it never returns.
Flexural psoriasis
This is also a type of chronic plaque psoriasis. It occurs in the
creases of the skin (flexures) such as in the armpit, groin, under
breasts, and in the skin folds. The affected skin looks slightly different
from typical plaque psoriasis. It is red and inflamed but the skin is
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smooth and does not have any rough scaling.
Erythrodermic psoriasis
This type of psoriasis causes a widespread erythema (redness) of
plenty of the skin surface, which is painful. Individual plaques of
psoriasis cannot be seen because they have merged together. There is
still redness and scaling of the skin and the skin is warm with
touching. A person with erythrodermic psoriasis may also have fever.
This type of psoriasis is rare, but it is severe and needs urgent
treatment and admission to hospital. This is because it can interfere
with the body's ability to control temperature and it can cause
excessive protein and fluid loss, leading to dehydration, heart failure
and severe illness.
Pustular psoriasis
This type of psoriasis usually affects the palms and soles. That is
why it is sometimes called palmoplantar pustulosis. The affected skin
develops crops of pustules, which are small fluid-filled spots. The
pustules do not contain germs (bacteria) and are not infectious. The
skin under and around the pustules is usually red and tender. Pustular
psoriasis that affects only the palms and soles is the second most
common type of psoriasis.
Rarely, this form of pustular psoriasis can affect the skin apart
from the palms and soles. This more widespread form is a more severe
form of psoriasis and needs urgent treatment under the care of a
dermatologist.
Scalp psoriasis
About a half of people with chronic plaque psoriasis affecting the
skin of their bodies will also have psoriasis affecting their scalps.
However, scalp psoriasis may occur alone in some people. Scalp
psoriasis is usually a form of chronic plaque psoriasis. It looks like
severe dandruff. The whole scalp may be affected, or there may just
be a few patches. If severe, it can lead to hair loss in some people.
Nail psoriasis
About a half of people with any type of psoriasis may have
fingernail psoriasis. Nail psoriasis may also occur alone without the
skin rash.
Nail psoriasis can take several forms:
x Pitting – discrete, well-circumscribed depressions on nail surface;
x subungual hyperkeratosis – silvery white crusting under free
edge of nail with some thickening of nail plate;
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 x onycholysis – nail separates from the nail bed at a free edge;
x «oil-drop sign» – pink/red сolor changes on the nail surface.
Psoriatic arthritis
About 1 or 2 from 10 people with chronic plaque psoriasis also
develop inflammation and pains in some joints. This is called psoriatic
arthritis. Any joint can be affected but it most commonly affects the
joints of fingers and toes (distal interphalangeal joints). This is often a
symmetrical polyarthritis. Psoriatic spondylarthropathy and arthritis
mutilans may develop. The cause of this is not clear.
Diagnostics
Psoriasis is usually diagnosed by a typical appearance of the rash
and Koebner phenomenon (trauma to the epidermis and dermis, such
as a scratch or surgical scar, can precipitate psoriasis in the damaged
skin). Occasionally, a biopsy of skin is taken to be seen under
microscope if there is a doubt about the diagnosis. The main changes
are the following:
• Parakeratosis (nuclei retained in the horny layer).
• Irregular thickening the epidermis but thinning over dermal
papillae is apparent clinically when bleeding is caused by scratching
and removal of scales (Auspitz’s sign).
• Polymorphonuclear leucocyte microabscesses (described
initially by Munro).
• Dilated and tortuous capillary loops in the dermal papillae.
• T-lymphocyte infiltrate in the upper dermis.
Differential Diagnosis
• Eczema
• Seborrhoeic dermatitis
• Pityriasis rosea
• Secondary syphilis
• Cutaneous T-cell lymphoma
• Lichen simplex
• Leprosy
• Lichen planus
• Candidiasis
• Discoid lupus erythematosus
• Parapsoriasis.
Treatment
Treatment aims at clearing rash as much as possible. There are
various treatment options. The treatment may depend on the severity,
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site and type of psoriasis. Three main modalities of therapy are used:
topical, phototherapy and systemic agents. These are used either alone
or in combinations.
Unless psoriasis is very severe, treatment tends to start with
topical treatments. This means treatments that can be applied directly
to the skin, as creams or ointments.
Moisturizers (emollients)
They help to soften hard skin and plaques as well as to prevent
itching, reduce cracking of the skin and to remove scales. Using a
moisturizer may also mean that other treatments can be more
effective. Moisturisers can also be used instead of soap.
Vitamin D-based treatments using calcipotriol, calcitriol and
tacalcitol
They are creams, ointments or lotions that are easy to use, are less
messy, and have less of a smell than coal tar or dithranol creams and
ointments. These remedies are used to slow the rate at which skin cells
divide. They can cause skin irritation in some people. There is also a
scalp preparation of calcipotriol that can be used to treat scalp
psoriasis.
A vitamin D-based treatment is sometimes used in combination
with other treatments for psoriasis if the treatment is not sufficient.
For example, an ointment that contains calcipotriol and a steroid is
sometimes used.
Steroid creams or ointments
These are other commonly used remedies. They effect by
reducing inflammation. They are easy to use and may be a good
treatment for difficult areas such as the scalp and face. However, one
problem with steroids is that in some cases, once you stop using the
cream or ointment, psoriasis may rebound back even worse than it was
initially. Side-effects may also occur in long-term use, especially with
more potent preparations.
A steroid cream or ointment should not be used regularly for
more than four weeks. Steroid lotions are useful for flare-ups of scalp
psoriasis.
Coal tar
Creams, ointments, lotions, pastes, bath additives and shampoos
that contain coal tar may reduce the turnover of the skin cells as well
as inflammation and may have anti-scaling properties. Traditional tar
preparations are messy to use but modern formulas are more pleasant.
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 Coal tar preparations can have an unpleasant smell and can stain
clothes. They may cause skin irritation in some people and skin can
become sensitive to sunlight. Coal tar preparations should not be used
during the first three months of pregnancy. However, they can be used
later in pregnancy and during breast-feeding.
Dithranol
It has been used for many years for psoriasis. In most cases a daily
application of dithranol to a psoriasis plaque will eventually cause the
plaque to resolve. However, dithranol irritates healthy skin. Therefore,
you need to apply it carefully to the psoriasis plaques only. To reduce
the chance of skin irritation it is usual to start with a weekly acting
remedies and pass on to drastic ones gradually over a few weeks.
Short contact dithranol therapy is popular. It involves putting a
high-strength dithranol preparation on the plaques of psoriasis for 5-
60 minutes dayly and then washing it off.
Salicylic acid
It is often combined with other remedies such as coal tar or steroid
creams. This acid tends to loosen and lift the scales of psoriasis on the
body or the scalp. Other remedies tend to effect better if the scale is
treated first with a salicylic acid. A salicylic acid can be used as a long-
term remedy. However, it can cause skin irritation in some people.
Tazarotene
It is a vitamin A-based preparation. Irritation of the normal
surrounding skin is a common side-effect. This can be minimized by
applying tazarotene sparingly to the plaques and avoiding the
normal skin.
For scalp psoriasis
A coal tar-based shampoo is often tried first and often effects
well. Some preparations combine a tar shampoo with either a salicylic
acid preparation, a coconut oil and salicylic acid combination
ointment, a steroid preparation, calcipotriol scalp application or more
than one of these.
Combined preparations for psoriasis
Some preparations use a combination of ingredients. For example,
calcipotriol combined with a steroid may be used when calcipotriol
alone has failed to cure. As mentioned before, it is not usually wise to
use a long-term steroid. Therefore, one treatment strategy is
sometimes to use calcipotriol combined with a steroid for four weeks
alternating calcipotriol alone for four weeks.
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 Other combinations such as a coal tar preparation and a steroid
are sometimes used. Using both a vitamin D preparation and a steroid
preparation at the same time can also be more effective than using one
medical preparation in some people. Other rotating treatment
strategies are sometimes used. For example, a steroid can be used for a
few weeks followed by a course of dithranol treatment.
Scalp treatments often contain a combination of ingredients such
as a steroid, coal tar, and a salicylic acid.
Other treatments
Phototherapy (light therapy) is one of treatments that can be
used. This may involve treatment with ultraviolet B (UVB) light.
Another type of phototherapy is called PUVA – psoralen and
ultraviolet light in the A band. Psoralen can be taken as a tablet or
added to a bath prior to treatment.
Systemic treatments
Systemic treatments are prescribed when both topical treatments
and phototherapy have failed. They are also used for patients with
very active psoriatic arthritis, erythrodermic psoriasis and generalized
pustular psoriasis.
• Methotrexate is the most popular agent. A weekly oral or
intramuscular dose of 15 to 25 mg is used.
• Acitretin – a synthetic vitamin A derivative is used in a dose of
10 to 20 mg/day gradually increased to the maximum dose of
50mg/day.
• Cyclosporine – a selective inhibitor of T-helper cell production
of IL-2 which produces an immunosuppressive effect. Its usual dosage
is 3 to 6mg/kg per day.
• Mycophenolate mofetil – a newly introduced drug inhibits
synthesis of nucleotide guanosine. The recommended dosage is 500
mg four times a day with a maximum dose of 4 g.
• Sulphasalazine may be used to treat psoriasis either alone or
combined with methotrexate, particularly in psoriatic arthropathy.
Injectable medicaments for psoriasis include etanercept,
adalimumab, infliximab, ustekinumab, secukinumab and
ixekizumab.

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 Unit 2
Lichen Planus
Lichen planus is an acute or chronic inflammatory dermatosis
involving the skin and/or mucous membranes, characterized by flat-
topped (Latin: planus, “flat”), violaceous, shiny, pruritic papules on
the skin and milky white papules in the mouth.
Cause
The precise cause of lichen planus is unknown, but the disease
seems to be mediated immunologically. A chronic graft-vs.-host
disease can cause an eruption rather like lichen planus in which
histoincompatibility causes lymphocytes to attack the epidermis.
Lichen planus is also associated with auto-immune disorders, such as
alopecia areata, vitiligo and ulcerative colitis. Drugs can cause lichen
planus too. Some patients with lichen planus also have hepatitis B or
C. Lichen planus itself is not contaginous.
Clinical Presentation
Typical lesions are violaceous or lilac-coloured, intensely itchy, flat-
topped papules, 1.0 to 10.0 mm, sharply defined, shiny, that usually arise
on the extremities, particularly on the volar aspects of the wrists and legs.
The shape of papules is polygonal or oval. A close look is needed to see a
white streaky pattern on the surface of these papules (Wickham’s striae).
Wickham’s striae are seen best through hand lens after application of
mineral oil. White asymptomatic lacy lines, dots, and occasionally small
white plaques are also found in the mouth, particularly inside the cheeks,
in about 50% of patients, and oral lesions may be a sole manifestation of
the disease. Reticular lichen planus is the most common pattern of oral
lichen planus, it presents reticulate (netlike) pattern of lacy white
hyperkeratosis on the buccal mucosa, lips, tongue, and gingiva.
In plaque lichen planus leukoplakia with Wickham’s striae arises on
the buccal mucosa. In atrophic lichen planus shiny red plaques, often with
Wickham’s striae in the surrounding mucosa develop. Erosive or
ulcerative lichen planus presents superficial erosion with overlying fibrin
clot; it occurs on the tongue and buccal mucosa; shiny red painful erosion
appears on the gingiva (desquamative gingivitis). Bullous lichen planus is
intact blisters up to several centimeters in diameter; their rupture results in
erosive lichen planus. Milky-white papules, with white lacework on the
buccal mucosa can develop; they may become erosive and painful.
The genital skin may be similarly affected. The variants of a
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classical pattern are rare and often difficult to diagnose. It is curiously,
although the skin plaques are usually itchy, patients rub rather than
scratch, so that excoriations are uncommon. Like psoriasis, Koebner’s
phenomenon may occur. This isomorphic phenomenon (Koebne’s
reaction) typically develops 7-14 days after the skin has been injured.
The nails are usually normal, but in about 10% of the patients
show changes ranging from fine longitudinal grooves to destruction of
the entire nail fold and bed.
Scalp lesions can cause a patchy scarring alopecia.
Course
Individual lesions may last for many months and the eruption as a
whole tends to last about 1 year. However, a hypertrophic variant of
the disease with thick warty lesions usually around the ankles often
lasts for many years. As lesions resolve, they become darker, flatter
and leave discrete brown or grey macules. About one in six patients
will have a recurrence.
Complications
Nail and hair loss can be permanent. The ulcerative form of lichen
planus in the mouth may lead to squamous cell carcinoma. Ulceration,
usually over bony prominences, may be disabling, especially if it is on
the soles. Any association with liver disease is probably caused by the
coexisting hepatitis infections mentioned above.
Differential Diagnosis
Lichen planus should be differentiated from the other
papulosquamous diseases.
Lichenoid drug reactions can mimic lichen planus closely. Gold
and other heavy metals have often been implicated. Other drug causes
include antimalarials, β-blockers, non-steroidal anti-inflammatory
drugs, para-aminobenzoic acid, thiazide diuretics and peni cillamine.
Contact with chemicals used to develop colour film can also produce
similar lesions. It may be hard to differ lichen planus from generalized
discoid lupus erythematosus if only a few large lesions are present, or
if the eruption is on the palms, soles or scalp. Wickham’s striae or oral
lesions favour the diagnosis of lichen planus. Oral candidiasis can also
cause confusion.
Investigations
The diagnosis is usually obvious clinically. The histology is
characteristic, so a biopsy wills confirm the diagnosis if necessary.
The inflammation manifests with hyperkeratosis, an increased
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granular layer, irregular acanthosis, and bandlike mononuclear
infiltrate that hugs the epidermis. Lymphocytes are predominantly
CD4+ helper inducer cells. Degenerate keratinocytes (colloid, Civatte
bodies) are found at the dermal-epidermal junction.
Treatment
Treatment can be difficult. If drugs are suspected as the cause,
they should be stopped and unrelated ones substituted. Potent topical
steroids will sometimes relieve symptoms and flatten the plaques.
Systemic steroid courses work too, but are recommended only in
special situations. Oral prednisone is effective for individuals with
symptomatic pruritus, painful erosions, dysphagia, or cosmetic
disfigurement. A short, tapered course is preferred: 70 mg initially,
tapered by 5 mg daily.
Systemic retinoids (acitretin or etretinate) 1 mg/kg per day is
helpful as adjunctive measure in severe cases but usually requires an
additional topical treatment.
Cyclosporine in very resistant and generalized cases, 5 mg/kg per
day will induce rapid remission, quite often not followed by
recurrence. (E.g. unusually extensive involvement, nail destruction or
painful and erosive oral lichen planus).
Antihistamines may blunt the itch.
Mucous membrane lesions are usually asymptomatic and do not
require treatment; if they do, then applications of a corticosteroid or
tacrolimus in a gel base (medium) may be helpful.
Treatment by photochemotherapy with psoralen and ultraviolet A
(PUVA) or with narrow-band UVB may reduce pruritus and help to
clear up the skin lesions.

Unit 3
Pityriasis Rosea
Cause
The cause of pityriasis rosea is unknown. Several features of the
disease suggest a viral etiology. A seasonal variation, a generalized
rash following a primary patch, a limited course and rarity of the
second attack and familial clustering the cases resemble the features of
viral exanthem. The disorder does not seem to be contagious.
Pityriasis rosea-like eruption may be caused by a number of drugs
like bismuth, gold, metronidazole, captopril, penicillamine,

161
barbiturates, isotretinoin, levamisole, omeprazole, ketotifen and
clonidine.
Clinical Presentation
Pityriasis rosea is common, particularly in winter. It can occur in
any age but it is commoner in the age group 10 to 35, and second
attacks are rare. Relatively it is more common in females. There is no
racial preference.
Most patients develop one plaque (the ‘herald’ or ‘mother’
plaque) before the others. It is larger (2-5 cm in diameter) than later
lesions, and is rounder, redder and more scaly.
After several days many smaller plaques appear, mainly on the
trunk, but some on the neck and extremities as well. About half of the
patients complain of itching. An individual plaque is oval, salmon
pink and shows a delicate scaling, adherent peripherally as a
collarette. The configuration of such plaques is often specific. On the
trunks they occur parallel to the ribs giving rise to specific like
‘Christmas tree’ appearance. Purpuric lesions are rare.
Course
A herald plaque precedes the generalized eruption by several
days. Subsequent lesions enlarge over the first week or two. A
minority of patients have systemic symptoms such as aching and
tiredness. The eruption lasts between 2 and 10 weeks and then
resolves spontaneously, sometimes leaving hyperpigmented patches
that fade more slowly.
Diagnostics
Pityriasis rosea is diagnosed mostly on clinical grounds.
There is no pathognomonic histologic change in pityriasis rosea,
but a biopsy may be helpful in the differential diagnosis, especially in
atypical cases. The epidermis shows mild acanthosis with focal
parakeratosis in mounds and spongiosis with exocytosis of
lymphocytes. In the dermis, a perivascular infiltrate of lymphocytes,
histiocytes and eosinophils are found. Extravasation of erythrocytes is
a helpful finding.
There is no significant alteration of routine laboratory values.
Since the lesions of PR closely resemble the rash of secondary
syphilis, a VDRL test is frequently necessary.
Differential Diagnosis
Although herald plaques are often mistaken for ringworm, the two
disorders most likely to be misdiagnosed early in the general eruption,
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they are guttate psoriasis and secondary syphilis. Tinea corporis and
pityriasis versicolor can be distinguished by a microscopical
examination of scales, and secondary syphilis by its other features
(mouth lesions, palmar lesions, condyloma lata, lymphadenopathy,
alopecia) and by serology. Gold and captopril are the drugs most
likely to cause a pityriasis rosea-like drug reaction, but barbiturates,
penicillamine, some antibiotics and other drugs can also act so.
Treatment
No treatment is curative, and active treatment is seldom needed.
A moderately potent topical steroid or calamine lotion will relieve
itching. One per cent salicylic acid in soft white paraffin or
emulsifying ointment reduces scaling. For relief of pruritus,
antihistamines may be prescribed. Topical steroids are often
prescribed for relatively severe cases. A short course of systemic
steroids may rarely be necessary. Phototherapy with UVB may also be
used.

Checkup Questions
1. What factors contribute to the development of psoriasis?
2. How is psoriasis classified?
3. In what forms is there a severe course of psoriasis?
4. What clinical picture is characteristic of psoriasis?
5. How is psoriasis diagnosed?
6. What medications are used for topical therapy?
7. What methods of physiotherapy are applied to treat psoriasis?
8. What current medicines are used for systemic therapy of
psoriasis?
9. What clinical manifestations are typical of lichen planus?
10. What are Wickham’s striae?
11. What atypical forms of lichen planus do you know?
12. What methods are used in the diagnosis of lichen planus?
13. What are the causes of pityriasis rosea progression?
14. What clinical manifestations are characteristic of pityriasis
rosea?
15. What does the term "herald" plaque mean?
16. What is the localization of rashes in pityriasis rosea?

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CHAPTER XIV
VIRAL INFECTIONS OF THE SKIN
Unit 1
Herpes simplex
Herpes simplex is a viral disease caused by both Herpes simplex
virus type 1 (HSV-1) and type 2 (HSV-2), belonging to the family
Herpesviridae and to the subfamily Alphaherpesvirinae. Herpes
simplex viruses contain a core of double-stranded DNA surrounded by
a protein coat with symmetrically arranged sub-units in an outer
envelope which encloses the inner structures (nucleocapsid). HSV-1
causes mostly oral lesions and HSV-2 - genital lesions. Infection with
the herpes virus is categorized into one of several distinct disorders
based on the site of this infection.
Pathogenesis
Herpes viruses cycle between periods of active disease as blisters
containing infectious virus particles and these periods last from 2to 21
days, followed by a remission. Genital herpes, however, is often
asymptomatic, though viral shedding may still occur. Herpes viruses
cause cytolytic infections; therefore, pathologic changes are due to
cell necrosis as well as inflammatory changes. Fluid accumulates
between the dermis and the epidermal skin layers and causes vesicle
formation.
The fluid then is absorbed, crusts are formed, and healing is
completed without evidence of scarring.
HSV is characterized by the following unique biological
properties:
x Neurovirulence – a capacity to invade and replicate in the
nervous system.
x Latency – the establishment and maintenance of latent infection
in the nerve cell ganglia. After initial infection, the viruses are
transported along sensory nerves to the sensory nerve cell bodies,
where they become latent and reside life-long.
x Reactivation and replication of latent HSV can be induced by a
variety of stimuli (e.g., fever, trauma, emotional stress, sunlight,

164
menstruation), resulting in overt or covert recurrent infection and
peripheral shedding of HSV. Reactivation is more frequent and severe
in immunocompromised patients.
The previously latent virus then multiplies new virus particles in
the nerve cell and these are transported along the axon of each neuron
to the nerve terminals in the skin, where they are released. Over time,
episodes of active disease reduce in frequency and severity.
Distribution of HSV is worldwide. The mode of transmission is
by close direct contact, and infection occurs via inoculation of virus
into susceptible mucosal surfaces (e.g., oropharynx, cervix,
conjunctiva) or through small cracks in the skin. Barrier protection
methods are the most reliable methods of preventing transmission of
herpes, but they merely reduce rather than eliminate risk. The virus is
readily inactivated at room temperature and by drying.
Once infected, the virus remains in the body for life. After the
patient begins to produce antibodies, the infection becomes latent in
the sensory ganglia. HSV-1 infection remains latent in the trigeminal
ganglia, and HSV-2 in the sacral ganglia.
Classification and Symptoms
Herpes simplex is divided into two types: HSV type 1 and HSV
type 2. HSV-1 causes primarily mouth, throat, face, eye, and central
nervous system infections (orofacial herpes), whereas HSV-2 causes
primarily anogenital infections of genitalia (genital herpes).
However, each may cause infections in all areas.
More serious disorders occur when the virus infects and damages
the eye (herpes keratitis), or invades the central nervous system,
damaging the brain (herpes encephalitis).
Herpetic gingivostomatitis is a combination of gingivitis and
stomatitis, or an inflammation of the oral mucosa and gingiva.
Herpetic gingivostomatitis is often an initial presentation during the
first ("primary") herpes simplex infection. It is of greater severity than
herpes labialis (cold sores) which is often the subsequent
presentations.
Primary herpetic gingivostomatitis is caused predominantly by
HSV-1 and generally affects children under the age of three and
young adults. There are prodromal symptoms (fever, malaise,
irritability, headache, vomiting, lymphadenopathy) 1–2 days prior to
local lesions. Then small, yellowish vesicles form, which rupture
quickly, resulting in shallow, round, discrete ulcers with erythematous
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halo. It affects both the free and attached mucosa. Sub-mandibular
lymphadenitis, halitosis and refusal to drink are usual concomitant
findings.
The symptoms can be mild or severe and may include:
x Sores on the inside of the cheeks or gums;
x Fever;
x General discomfort, uneasiness, or ill feeling;
x Very sore mouth with no desire to eat;
x Bad breath.
Treatment includes fluid intake, good oral hygiene and gentle
debridement of the mouth. In healthy individuals the lesions heal
spontaneously in 7-14 days without any scar.
Herpes labialis or "orolabial herpes" is an infection of the lip
by herpes simplex virus (HSV-1). An outbreak typically causes small
vesicles or erosions on or around the mouth. The sores typically heal
within 2-3 weeks, but the herpes virus remains dormant in the facial
nerves, following orofacial infection, periodically reactivating (in
symptomatic people) to create sores in the same area of the mouth or
face at the site of the original infection.
People with the condition typically experience one to three
attacks annually. The frequency and severity of outbreaks generally
decreases over time. Cold sore outbreaks may be influenced by stress,
menstruation, sunlight, sunburn, fever, dehydration, or local skin
trauma. Surgical procedures such as dental or neural surgery, lip
tattooing, or dermabrasion are also common triggers.
Symptoms typically progress in a series of eight stages:
1. Latent (weeks to months incident-free), i.e., remission period.
After initial infection, the viruses move to sensory nerve ganglia
(Trigeminal ganglion), where they reside as life-long latent viruses.
Asymptomatic shedding of contagious virus cells can occur during
this stage.
2. Prodromal (day 0–1): Symptoms often precede a recurrence.
Symptoms typically begin with tingling (itching) and reddening of the
skin around the infected site. This stage can last from a few days to a
few hours preceding the physical manifestation of an infection and is
the best time to start treatment.
3. Inflammation (day 1): Virus begins reproducing and infecting
cells at the end of the nerve. The intact cells react to the invasion with
swelling and redness displayed as symptoms of infection.
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 4. Pre-sore (day 2-3): This stage is defined by the appearance of
tiny, hard, inflamed papules and vesicles that may itch and are
painfully sensitive to touch. In time, these fluid-filled blisters form a
cluster on the lip (labial) tissue, the area between the lip and skin
(vermilion border), and can occur on the nose, chin, and cheeks.
5. Open lesion (day 4): This is the most painful and contagious of
the stages. All the tiny vesicles break open and merge to create one
big, open, weeping erosion. Fluids are slowly discharged from blood
vessels and inflamed tissue. This watery discharge is teeming with
active viral particles and is highly contagious. Depending on the
severity, one may develop a fever and swollen lymph glands under the
jaw.
6. Crusting (day 5-8): A honey/golden crust starts to form from
the syrupy exudate. This yellowish or brown crust or scab is not made
of active virus but from blood serum containing useful proteins such
as albumin and globulins. This appears as the healing process begins.
The sore is still painful at this stage, but, more painful, however, is the
constant cracking of the scab as someone moves or stretches their lips,
as in smiling or eating. Virus-filled fluid will still ooze out of the sore
through any cracks.
7. Healing (day 9-14): New skin begins to form underneath the
crust as the virus retreats into latency. A series of scabs will form over
the sore (called Meier Complex), each one smaller than the last.
During this phase irritation, itching, and some pain are common.
8. Post-crust (12-14 days): A reddish area may linger at the site
of viral infection as the destroyed cells are regenerated. Virus
shedding can still occur during this stage.
The recurrent infection is thus often called herpes simplex
labialis. Rare reinfections occur inside the mouth (intraoral HSV
stomatitis) affecting the gums, alveolar ridge, hard palate, and the
back of the tongue, possibly accompanied by herpes labialis.
Treatment
The duration of symptoms can be reduced by a small amount if an
antiviral, anaesthetic or non-treatment cream (such as zinc oxide or
zinc sulfate) is applied promptly.
Effective antiviral medications include acyclovir and penciclovir,
which can speed healing by as much as 10%.
Famciclovir or valaciclovir, taken in pill form, can be effective
using a single day, high-dose application and is more cost effective
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and convenient than the traditional treatment of lower doses for
5–7 days.
Herpes genitalis (or genital herpes) refers to a genital infection
by Herpes simplex virus.
HSV is believed to be asymptomatic in the majority of cases, thus
aiding contagion and hindering containment. The typical
manifestation of a primary HSV-1 or HSV-2 genital infection are
inflamed papules and vesicles on the outer surface of the genitals,
resembling cold sores. These usually appear 4–7 days after sexual
exposure to HSV for the first time.
In males, the lesions occur on the glans penis, shaft of the penis or
other parts of the genital region, on the inner thigh, buttocks, or anus.
In females, lesions appear on or near the pubis, labia, clitoris, vulva,
buttocks or anus. Other common symptoms include pain, itching, and
burning. Less frequent, yet still common, symptoms include discharge
from the penis or vagina, fever, headache, muscle pain (myalgia),
swollen and enlarged lymph nodes and malaise. Women often
experience additional symptoms that include painful urination
(dysuria) and cervicitis. After 2–3 weeks, existing lesions progress
into erosions and then crust and heal, although lesions on mucosal
surfaces may never form crusts.
Treatment
Presently, genital herpes cannot be cured. There are however
some drugs that can shorten outbreaks and make them less severe or
even stop them from happening. Among these drugs are: acyclovir,
valacyclovir and famciclovir.
Acyclovir is an antiviral drug used against herpes viruses,
varicella-zoster, and Epstein-Barr Viruses. This drug reduces the pain
and the number of lesions in the initial case of genital herpes.
Furthermore, it decreases the frequency and severity of recurrent
infections. It comes in capsules, tablets, suspension, injection, powder
for injection, and ointment. The ointment is used topically and it
decreases pain, reduces healing time, and limits the spread of the
infection.
Valacyclovir is also used to treat herpes virus infections. Once in
the body, it becomes the anti-herpes medicine, acyclovir. It helps
relieve the pain and discomfort and the sores heal faster. It only comes
in caplets and its advantage is that it has a longer duration of action
than acyclovir.
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 Famciclovir is another antiviral drug that belongs to the same
class of acyclovir and valacyclovir. Famciclovir is a prodrug that is
converted to penciclovir in the body. The latter is the one active
against the viruses. This drug has a longer duration of action than
acyclovir and it only comes in tablets.
Herpetic whitlow and Herpes gladiatorum
Herpes whitlow is a painful infection that typically affects the
fingers or thumbs. On occasion, infection occurs on the toes or on the
nail cuticle. Individuals that participate in contact sports such as
wrestling, rugby, and soccer sometimes acquire a condition caused by
HSV-1 known as herpes gladiatorum, scrumpox, wrestler’s herpes, or
mat herpes, which presents as skin ulceration on the face, ears, and
neck. Symptoms include fever, headache, sore throat and swollen
glands. It occasionally affects the eyes or eyelids.
Herpesviral encephalitis and herpesviral meningitis
It is a herpetic infection of the brain that is thought to be caused
by the retrograde transmission of virus from a peripheral site on the
face following HSV-1 reactivation, along the trigeminal nerve axon,
to the brain. HSV is the most common cause of viral encephalitis.
When infecting the brain, the virus shows a preference for the
temporal lobe. HSV-2 is the most common cause of Mollaret's
meningitis, a type of recurrent viral meningitis.
Herpes esophagitis
Symptoms may include painful swallowing (odynophagia) and
difficulty swallowing (dysphagia). It is often associated with impaired
immune function (e.g. HIV/AIDS, immunosuppression in solid organ
transplants).
Other herpeses
Neonatal herpes simplex is a HSV infection in an infant. It is a
rare but serious condition, usually caused by vertical transmission of
HSV (type 1 or 2) from mother to newborn. During
immunodeficiency herpes simplex can cause unusual lesions in the
skin. One of the most striking is the appearance of clean linear
erosions in skin creases, with the appearance of a knife cut.
Herpetic sycosis is a recurrent or initial herpes simplex infection
affecting primarily the hair follicle. Eczema herpeticum is an infection
with herpes virus in patients with chronic atopic dermatitis may result
in spread of herpes simplex throughout the eczematous areas.
Herpetic keratoconjunctivitis is a primary infection typically
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presents as swelling of the conjunctiva and eyelids
(blepharoconjunctivitis), accompanied by small white itchy lesions on
the surface of the cornea.

Unit 2
Herpes Zoster
Herpes zoster (or simply zoster), commonly known as shingles
and also known as zona, is a viral disease characterized by a painful
skin rash with blisters in a limited area on one side of the body, often
in a stripe.
The initial infection with varicella zoster virus (VZV) causes the
acute (short-lived) illness chickenpox which generally occurs in
children and young people. Once an episode of chickenpox has
resolved, the virus is not eliminated from the body but can go on to
cause shingles – an illness with very different symptoms – often many
years after the initial infection. Herpes zoster is not the same disease
as herpes simplex despite the name similarity (both the varicella zoster
virus and herpes simplex virus belong to the same viral subfamily
Alphaherpesvirinae).
Varicella zoster virus can become latent in the nerve cell bodies
and less frequently in non-neuronal satellite cells of dorsal root,
cranial nerve or autonomic ganglion, without causing any symptoms.
Years or decades after a chickenpox infection, the virus may break out
of nerve cell bodies and travel down nerve axons to cause viral
infection of the skin in the region of the nerve. The virus may spread
from one or more ganglia along nerves of an affected segment and
infect the corresponding dermatome (an area of the skin supplied by
one spinal nerve) causing a painful rash. Although the rash usually
heals within two to four weeks, some sufferers experience residual
nerve pain for months or years, a condition called postherpetic
neuralgia.
Clinical Presentation
The earliest symptoms of herpes zoster, which include headache,
fever, and malaise, are nonspecific, and may result in an incorrect
diagnosis. These symptoms are commonly followed by sensations of
burning pain, itching, hyperesthesia (oversensitivity), or paresthesia
("pins and needles": tingling, pricking, or numbness). The pain may be
mild to extreme in the affected dermatome, with sensations that are

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often described as stinging, tingling, aching, numbing or throbbing,
and can be interspersed with quick stabs of agonizing pain.
Herpes zoster in children is often painless, but older people are
more likely to get zoster as they age, and the disease tends to be more
severe.
In most cases after 1-2 days, but sometimes as long as 3 weeks,
the initial phase is followed by the appearance of a characteristic skin
rash. The pain and rash most commonly occurs on the torso, but can
appear on the face, eyes or other parts of the body. At first the rash
appears similar to the first appearance of hives; however, unlike hives,
herpes zoster causes skin changes limited to a dermatome, normally
resulting in a stripe or belt-like pattern that is limited to one side of the
body and does not cross the midline. "Zoster without herpes"
describes a patient who has all of the symptoms of herpes zoster
except this characteristic rash.
Later the rash becomes vesicular, forming small blisters filled
with a serous exudate, as the fever and general malaise continue. The
painful vesicles eventually become cloudy or darkened as they fill
with blood, crust over within seven to ten days; usually the crusts fall
off and the skin heals, but sometimes, after severe blistering, scarring
and discolored skin remain.
Herpes zoster may have additional symptoms, depending on the
dermatome involved. Herpes zoster ophthalmicus involves the orbit of
the eye and occurs in approximately 10-25% of cases. It is caused by
the virus reactivating in the ophthalmic division of the trigeminal
nerve. In a few patients, symptoms may include conjunctivitis,
keratitis, uveitis, and optic nerve palsies that can sometimes cause
chronic ocular inflammation, loss of vision, and debilitating pain.
Herpes zoster oticus, also known as Ramsay Hunt syndrome type II,
involves the ear. It is thought to result from the virus spreading from
the facial nerve to the vestibulocochlear nerve. Symptoms include
hearing loss and vertigo (rotational dizziness).
Pathophysiology
The causative agent for herpes zoster is varicella zoster virus
(VZV), a double-stranded DNA virus related to the Herpes simplex
virus group. Most people are infected with this virus as children, and
suffer from an episode of chickenpox. The immune system eventually
eliminates the virus from most locations, but it remains dormant (or
latent) in the ganglia adjacent to the spinal cord (called the dorsal root
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ganglion) or the ganglion semilunar (ganglion Gasseri) in the base of
the skull. Repeated attacks of herpes zoster are rare, and it is
extremely rare for patients to suffer more than three recurrences.
Herpes zoster occurs only in people who have been previously
infected with VZV; although it can occur at any age, approximately
half of the cases in the USA occur in those aged 50 years or older. The
disease results from the virus reactivating in a single sensory ganglion.
In contrast to Herpes simplex virus, the latency of VZV is poorly
understood. The virus has not been recovered from human nerve cells
by cell culture and the location and structure of the viral DNA is not
known. Virus-specific proteins continue to be made by the infected
cells during the latent period, so true latency, as opposed to a chronic
low-level infection, has not been proven. Although VZV has been
detected in autopsies of nervous tissue, there are no methods to find
dormant virus in the ganglia in living people.
Unless the immune system is compromised, it suppresses
reactivation of the virus and prevents herpes zoster. Why this
suppression sometimes fails is poorly understood, but herpes zoster is
more likely to occur in people whose immune system is impaired due
to aging, immunosuppressive therapy, psychological stress, or other
factors. Upon reactivation, the virus replicates in the nerve cells, and
virions are shed from the cells and carried down the axons to the area
of skin served by that ganglion. In the skin, the virus causes local
inflammation and blisters. The short- and long-term pain caused by
herpes zoster comes from the widespread growth of the virus in the
infected nerves, which causes inflammation.
As with chickenpox and/or other forms of herpes, direct contact
with an active rash can spread VZV to a person who has no immunity
to the virus. This newly infected individual may then develop
chickenpox, but will not immediately develop shingles. Until the rash
has developed crusts, a person is extremely contagious. A person is
also not infectious before blisters appear, or during postherpetic
neuralgia (pain after the rash relieves).
Diagnosis
If the rash has appeared, identifying this disease (making a
differential diagnosis) requires only a visual examination, since very few
diseases produce a rash in a dermatomal pattern (see map). However,
herpes simplex virus (HSV) can occasionally produce a rash in such a
pattern. The Tsanck smear is helpful for diagnosing acute infection with
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a herpes virus, but does not distinguish between HSV and VZV.
When the rash is absent (early or late in the disease, or in the case
of zoster sine herpete), herpes zoster can be difficult to diagnose.
Apart from the rash, most symptoms can occur also in other
conditions.
Laboratory tests are available to diagnose herpes zoster. The most
popular test detects VZV-specific IgM antibody in blood; this appears
only during chickenpox or herpes zoster and not while the virus is
dormant. In larger laboratories, lymph collected from a blister is tested
by polymerase chain reaction for VZV DNA, or examined with an
electron microscope for virus particles.
In a recent study, samples of lesions on the skin, eyes, and lung
from 182 patients with presumed herpes simplex or herpes zoster were
tested with real-time PCR or with viral culture. In this comparison,
viral culture detected VZV with only 14.3% sensitivity, although the
test was highly specific (specificity=100%). By comparison, real-time
PCR resulted in 100% sensitivity and specificity. Overall testing for
herpes simplex and herpes zoster using PCR showed 60.4%
improvement over viral culture.
Treatment
The aims of treatment are to limit the severity and duration of
pain, shorten the duration of a shingles episode, and reduce
complications. Symptomatic treatment is often needed for the
complication of postherpetic neuralgia. However, a study on untreated
herpes zoster shows that, once the rash has cleared, postherpetic
neuralgia is very rare in people under 50 and wears off in time; in
older people the pain wore off more slowly, but even in people over
70, 85% were pain free one year after their shingles outbreak.
Analgesics
People with mild to moderate pain can be treated with over-the-
counter analgesics. Topical lotions containing calamine can be used
on the rash or blisters and may be soothing. Occasionally, severe pain
may require an opioid medication, such as morphine. Once the lesions
have crusted over, capsaicin cream (Zostrix) can be used. Topical
lidocaine and nerve blocks may also reduce pain. Administering
gabapentin along with antivirals may offer relief of postherpetic
neuralgia.
Antivirals
Antiviral drugs inhibit VZV replication and reduce the severity
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and duration of herpes zoster with minimal side effects, but do not
reliably prevent postherpetic neuralgia. Of these drugs, acyclovir has
been the standard treatment, but the new drugs valaciclovir and
famciclovir demonstrate similar or superior efficacy and good safety
and tolerability. The drugs are used both as prophylaxis (for example
in AIDS patients) and as therapy during the acute phase. Antiviral
treatment is recommended for all immunocompetent individuals with
herpes zoster over 50 years old, preferably given within 72 hours of
the appearance of the rash. Complications in immunocompromised
individuals with herpes zoster may be reduced with intravenous
acyclovir. In people who are at a high risk for repeated attacks of
shingles, five daily oral doses of acyclovir are usually effective.
Steroids
Orally administered corticosteroids are frequently used in
treatment of the infection, despite clinical trials of this treatment being
unconvincing. Nevertheless, one trial studying immunocompetent
patients older than 50 years of age with localized herpes zoster,
suggested that administration of prednisone with aciclovir improved
healing time and quality of life. Upon one-month evaluation, aciclovir
with prednisone increased the likelihood of crusting and healing of
lesions by about twofold, when compared to placebo. This trial also
evaluated the effects of this drug combination on quality of life at one
month, showing that patients had less pain, and were more likely to
stop the use of analgesic agents, return to usual activities and have
uninterrupted sleep. However, when comparing cessation of herpes
zoster-associated pain or post herpetic neuralgia, there was no
difference between aciclovir plus prednisone and aciclovir alone.
Because of the risks of corticosteroid treatment, it is recommended
that this combination of drugs only be used in people more than 50
years of age, due to their greater risk of postherpetic neuralgia.

Unit 3
Warts
A wart is generally a small, rough growth, typically on human’s
hands or feet but often on the other locations that can resemble a
cauliflower or a solid blister. They are caused by a viral infection,
specifically by one of the many types of human papilloma virus. There
are as many as 10 varieties of warts; the most common considered being

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mostly harmless. It is possible to get warts from others; they are
contagious and usually enter the body in an area of broken skin. They
typically disappear after a few months but can last for years and can recur.
Types
A range of types of wart have been identified, varying in shape
and site affected, as well as the type of human papillomavirus
involved.
These include:
x Common wart (Verruca vulgaris), a raised wart with
roughened surface, most common on hands, but can grow anywhere
on the body;
x Flat wart (Verruca plana), a small, smooth flattened wart,
flesh-coloured, which can occur in large numbers; most common on
the face, neck, hands, wrists and knees;
x Filiform or digitate wart, a thread- or finger-like wart, most
common on the face, especially near the eyelids and lips;
x Genital wart (venereal wart, Condyloma acuminatum,
Verruca acuminata), a wart that occurs on the genitalia.
x Mosaic wart, a group of tightly clustered plantar-type warts,
commonly on the hands or soles of the feet;
x Periungual wart, a cauliflower-like cluster of warts that occurs
around the nails;
x Plantar wart (verruca, Verruca plantaris), a hard sometimes
painful lump, often with multiple black specks in the center; usually
only found on pressure points on the soles of the feet.
Cause
Warts are caused by the human papilloma virus (HPV). There are
about 130 known types of human papilloma viruses. HPV infects the
squamous epithelium, usually of the skin or genitals, but each HPV
type is typically only able to infect a few specific areas on the body.
Many HPV types can produce a benign growth, often called a "wart"
or "papilloma", in the area they infect. Many of the more common
HPV and wart types are as follows:
x Common warts – HPV types 2 and 4 (most common); also
types 1, 3, 26, 29, and 57 and others.
x Cancers and Genital dysplasia – "high-risk" HPV types are
associated with cancers, (cervical cancer and can also cause some
vulvar, vaginal, penile, anal and some oropharyngeal cancers. "low-
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risk" types are associated with warts or other conditions.)
x High-risk: 16, 18 (cause the most cervical cancer); also 58, 33,
45, 31, 52, 35, 39, 59, and others.
x Plantar warts (myrmecia) – HPV type 1 (most common); also
types 2, 3, 4, 27, 28, and 58 and others.
x Anogenital warts (condylomata acuminata or venereal warts) –
HPV types 6 and 11 (most common); also types 42, 44 and others.
x Low-risk: 6, 11 (most common); also 13, 44, 40, 43, 42, 54, 61,
72, 81, 89, and others.
x Flat warts – HPV types 3, 10, and 28.
x Butcher's warts – HPV type 7.
x Heck's disease (Focal epithelial hyperplasia) – HPV types 13
and 32.
Pathophysiology
Common warts have a characteristic appearance under the
microscope. They have thickening of the stratum corneum
(hyperkeratosis), thickening of the stratum spinosum (acanthosis),
thickening of the stratum granulosum, rete ridge elongation, and large
blood vessels at the dermoepidermal junction.
Treatment
There are many treatments and procedures associated with wart
removal. One review of 52 clinical trials of various cutaneous wart
treatments concluded that topical treatments containing salicylic acid
were the best supported, with an average cure rate of 75%, compared
with 48% for the placebo in six placebo-controlled trials including a
total of 376 participants. The reviewers also concluded that there was
little evidence of a significant benefit of cryotherapy over salicylic
acid or duct tape.
One complicating factor in the treatment of warts is that the wart
may regrow after it has been removed.
Medication
x Application of podophyllum resin paint [podophyllum resin
I.P.'66 (20% w/v), benzoin I.P. (10% w/v), aloes I.P. (2% w/v),
isopropyl alcohol I.P. to make (100% v/v)].
x Imiquimod, a topical cream that helps the body's immune
system fight the wart virus by encouraging interferon production.
Approved by the U.S. Food and Drug Administration (FDA) for
genital warts. The drug is very expensive.
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 x Cantharidin, a chemical found naturally in many members of
the beetle family Meloidae which causes dermal blistering, either used
by itself or compounded with podophyllin. Not FDA approved, but
available through Canada or select US compounding pharmacies.
x Bleomycin, not US FDA approved. One or two injections are
used. It can cause necrosis of digits and Raynaud syndrome.
x Dinitrochlorobenzene (DNCB), like salicylic acid, is applied
directly to the wart. Some studies showed this method was effective
with a cure rate of 80%. But DNCB must be used much more
cautiously than salicylic acid; the chemical is a known mutagen, able
to cause genetic mutations. So a physician must administer DNCB.
This drug induces an allergic immune response resulting in
inflammation that wards off the wart-causing virus.
x Fluorouracil, which inhibits DNA synthesis, is being used as an
experimental treatment. It is applied directly to the wart (especially
plantar warts) and covered, for example, with tape). This treatment is
combined with the use of a pumice stone, but tends to work very slowly.
x Salicylic acid can be prescribed by a dermatologist in a higher
concentration than that found in over-the-counter products. Examples
include a topical solution marketed by Elorac, Inc. under the trade
name Durasal.
There are several over-the-counter options. The most common
ones involve salicylic acid. These products are readily available at
drugstores and supermarkets. There are typically two types of
products: adhesive pads treated with salicylic acid or a bottle of
concentrated salicylic acid solution. Removing a wart with salicylic
acid can be done by cleaning the area, applying the acid, and
removing the dead skin with a pumice stone or emery board. It may
take up to a year to remove a wart.
Another product available over-the-counter that can aid in wart
removal is silver nitrate in the form of a caustic pencil, which is also
available at drug stores. In a placebo-controlled study of 70 patients,
silver nitrate given over nine days resulted in clearance of all warts in
43% and improvement in warts in 26% one month after treatment
compared to 11% and 14%, respectively, in the placebo group. The
instructions must be followed to minimize staining of skin and
clothing. Occasionally pigmented scars may develop.
Cryosurgery or cryotherapy devices using dimethyl ether –
propane mixture are inexpensive. A disadvantage is that the sponge
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applicator is too large for small warts, and the temperature achieved is
not nearly as low as with liquid nitrogen. Complications include
blistering of normal skin if excess freezing is not controlled.
Several randomized, controlled trials have found that zinc sulfate,
consumed orally often reduces or eliminates warts. The zinc sulfate
dosage used in medical trials for treatment of warts was about 5 to 10
mg/kg/a day. For elemental zinc, a lower dosage of 2.5 mg/kg/day
may be appropriate as large amounts of zinc may cause a copper
deficiency. Other trials have found that topical zinc sulfate solution or
zinc oxide is also effective.
Procedures
x Keratolysis of dead surface skin cells usually uses salicylic
acid, blistering agents, immune system modifiers
("immunomodulators"), or formaldehyde, often with mechanical
paring of the wart with a pumice stone, blade and etc.
x Electrodesiccation
x Cryosurgery, which involves freezing the wart (generally
with liquid nitrogen), creating a blister between the wart and
epidermal layer, after which the wart and surrounding dead skin falls
off by itself. On average 3-4 treatments are required for warts of the
thin skin. Warts on the calloused skin like plantar warts might take
dozens or more treatments.
x Surgical curettage of warts;
x Laser treatment – often with a pulse dye laser or carbon
dioxide (CO2) laser. Pulse dye lasers (wavelength – 582 nm) work by
selective absorption blood cells (specifically haemoglobin). CO2
lasers work by selective absorption by water molecules. Pulse dye
lasers are less destructive and more likely to heal without scarring.
CO2 laser works by vaporizing and destroying tissue and skin. Laser
treatments can be painful, expensive (though covered by many
insurances), and can cause little scarring when used appropriately.
CO2 lasers will require a local anaesthetic. Pulse dye laser treatment
needs neither conscious sedation nor local anesthetic. It takes 2 to 4
treatments but can be many more for extreme cases. Typically, 10-14
days are required between treatments. Preventative measures are
important. They are:
x Infrared coagulator – an intense source of infrared light in a
small beam like a laser. This works essentially on the same principle

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as laser treatment. It is less expensive. Like the laser, it can cause
blistering pain and scarring.
x Duct tape occlusion therapy involves placing a piece of duct
tape over the wart. The evidence as to whether or not it is effective is
poor. Thus it is not recommended as routine treatment.

Unit 4
Molluscum Contagiosum
Molluscum contagiosum (MC) is a viral infection of the skin or
occasionally of the mucous membranes. It is caused by a DNA
poxvirus called a molluscum contagiosum virus (MCV). MCV has no
animal reservoir, infecting only humans. There are four types of
MCV, MCV-1 to - 4; MCV-1 is the most prevalent and MCV-2 is
seen usually in adults and often sexually transmitted. This common
viral disease has a higher incidence in children, sexually active adults,
and those who are immunodeficient, and the infection is most
common in children aged one to ten years old. MC can affect any area
of the skin but is most common on the trunk of the body, arms, and
legs. It is spread through direct contact or shared items such as
clothing or towels.
The virus commonly spreads through skin-to-skin contact. This
includes sexual contact or touching or scratching the bumps and then
touching the skin. Handling objects that have the virus on them
(fomites), such as a towel, can also result in infection. The virus can
spread from one part of the body to another or to other people. The
virus can be spread among children at day care or at school.
Molluscum contagiosum is contagious until the bumps are gone
(which, if untreated, may last up to 6 months or longer).
The time from infection to the appearance of lesions can range up to
6 months, with an average incubation period between 2 and 7 weeks.
Clinical Presentation
Molluscum contagiosum papules are flesh-colored, firm, smooth,
dome-shaped, and pearly in appearance. They are often 1-5
millimeters in diameter, with a dimpled center. They are generally not
painful, but they may itch or become irritated.
Picking or scratching the papules may lead to further infection or
scarring. The average duration of an untreated lesion is 6-9 months but
may be as long as 5 years.

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 They may occasionally be complicated by secondary bacterial
infections. In some cases the dimpled section may bleed once or
twice. The viral infection is limited to a localized area on the topmost
layer of the epidermis. Once the virus containing head of the lesion
has been destroyed, the infection is gone. The central waxy core
contains the virus. In a process called autoinoculation, the virus may
spread to neighboring skin areas. Children are particularly susceptible
to autoinoculation, and may have widespread clusters of lesions.
In children, lesions are situated mainly on the trunk and
extremities. In adults, lesions often are located on the lower abdominal
wall, inner thighs, pubic area, and genitalia.
Diagnosis
Diagnosis is made on the clinical appearance; the virus cannot
routinely be cultured. The diagnosis can be confirmed by excisional
biopsy.
Histologically, molluscum contagiosum is characterized by
molluscum bodies in the epidermis above the stratum basale, which
consist of large cells with: abundant granular eosinophilic cytoplasm
(accumulated virons), and a small peripheral nucleus.
Treatments
Individual molluscum lesions may go away on their own and are
reported as lasting generally from 6 to 8 weeks, to 2 or 3 months.
However via autoinoculation, the disease may propagate and so an
outbreak generally lasts longer with mean durations variously reported
as 8 months, to about 18 months, and with a range of durations from 6
months to 5 years.
Treatment is often unnecessary depending on the location and
number of lesions, and no single approach has been convincingly
shown to be effective. It should also be noted that treatments causing
the skin on or near the lesions to rupture may spread the infection
further, much the same as scratching does. Nevertheless, treatment
may be sought for the following reasons:
Medical issues include:
x Bleeding;
x Secondary infections;
x Itching and discomfort;
x Potential scarring;
x Chronic keratoconjunctivitis;

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 Social reasons:
x Cosmetics;
x Embarrassment;
x Fear of transmission to others.
Many health professionals recommend treating bumps located in
the genital area to prevent them from spreading. The virus lives only
in the skin and once the growths are gone, the virus is gone and cannot
be spread to others. When treatment has resulted in elimination of all
bumps, the infection has been effectively cured and will not reappear
unless the patient is infected again. In practice, it may not be easy to
see all of the molluscum contagiosum bumps. Even though they
appear to be gone, there may be some that were overlooked. If this is
the case, one may develop new bumps by autoinoculation, despite
their apparent absence.
Cryotherapy
Cryotherapy involves killing infected cells by "freezing" them
with a pressurized liquid spray, usually liquid nitrogen or nitrous
oxide. The procedure can be mildly uncomfortable to painful
depending on quantity and location of infected cells. The procedure
can be performed by any medical professional.
Astringents
Astringent chemicals applied to the surface of molluscum lesions
to destroy successive layers of the skin include potassium
hydrochloride, and cantharidin.
Benzoyl peroxide
Application cream benzoyl peroxide 10% twice daily for 4 weeks
is effective.
Over-the-counter substances
Daily topical application of tretinoin cream (0.025% Retin-A)
may also trigger resolution. These treatments require several months
for the infection to clear, and are often associated with intense
inflammation and possibly discomfort.
Imiquimod
Imiquimod is a form of immunotherapy. Immunotherapy triggers
the immune system to fight the virus causing the skin growth.
Imiquimod is applied 3 times per week, left on the skin for 6 to 10
hours, and washed off. A cure may take from 4 to 16 weeks. Another
dose regimen: application of imiquimod three times daily for 5
consecutive days each week. This treatment regimen is reserved for
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1% Imiquimod cream. If a higher concentration is used in a similar
method, chemical burns or plausible nerve damage are possible.
Surgical treatment
Surgical treatments include cryosurgery, in which liquid nitrogen
is used to freeze and destroy lesions, as well as scraping them off with
a curette. Application of liquid nitrogen may cause burning or stinging
at the treated site, which may persist for a few minutes after the
treatment. Scarring or loss of color can complicate both these
treatments. With liquid nitrogen, a blister may form at the treatment
site, but it will slough off in two to four weeks. Cryosurgery and
curette scraping are not painless procedures. They may also leave
scars and/or permanent white (depigmented) marks.
Laser
Pulsed dye laser therapy for molluscum contagiosum may be the
treatment of choice for multiple lesions in a cooperative patient.
Prognosis
Most cases of molluscum will clear up naturally within two years
(usually within nine months). So long as the skin growths are present,
there is a possibility of transmitting the infection to another person.
When the growths are gone, the possibility for spreading the infection
is ended.
Unlike herpes viruses, which can remain inactive in the body for
months or years before reappearing, molluscum contagiosum does not
remain in the body when the growths are gone from the skin and will
not reappear on their own. However, there is no permanent immunity
to the virus, and it is possible to become infected again upon exposure
to an infected person.
Advantage of treatment is to hasten the resolution of the virus.
This limits the size of the "pox" scar. If left untreated, molluscum
growth can reach sizes as large as a pea or a marble. Spontaneous
resolution of large lesions can occur, but will leave larger crater like
growth. As many treatment options are available, prognosis for
minimal scarring is best if treatment is initiated while lesions are
small.

Checkup Questions
1. What types of herpes virus exist?
2. What is the pathogenesis of herpes simplex?
3. What forms does herpes simplex have?
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 4. What stages are typical of herpes labialis clinical picture?
5. How is genital herpes treated?
6. What is the cause of herpes zoster?
7. What clinical manifestations are characteristic of herpes
zoster?
8. What is the localization of the lesions characteristic of herpes
infection?
9. What types of warts do you know?
10. What is the etiology of warts?
11. What is the cause of molluscum contagiosum?
12. What primary skin lesions are characteristic of molluscum
contagiosum?

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CHAPTER XV
MYCOBACTERIAL INFECTIONS
Unit 1
Leprosy
Leprosy (Hansen's disease) is a chronic infectious disease from
the group of mycobacterioses, characterized by a long incubation
period and recurrent course. This disease affects the ectoderm
derivatives – the skin, mucous membranes and the peripheral nervous
system.
Leprosy has affected humanity for over 4,000 years, and was
well-recognized in the civilizations of ancient China, Egypt, and India.
The prevalence of leprosy in the world decreases from year to year.
According to the World Health Organization (WHO), the number of
new cases detected every year throughout the world decreased from
763,000 in 2001 to 249,000 in 2008. 215,656 new cases were detected
in 2013, 213,899 – in 2014 and 211,973 – in 2015.
World statistics show that 96% (203,600 people) of new cases of
leprosy were detected in 22 countries (such as India, Brazil, Angola,
Congo, Sudan, Ethiopia, etc.). Other countries account for 4%.
Brazil is one of the six countries with the highest prevalence of
leprosy. More than 30,000 new cases are diagnosed in this country
every year. In 2014, the prevalence of leprosy in Brazil was 1.27 cases
per 10,000 people. A significant role in the spread of the disease is
migration of the population
Etiology
The etiology of leprosy: Mycobacterium leprae (M. leprae) and
Mycobacterium lepromatosis (M. lepromatosis). M. leprae was first
discovered by the Norwegian physician Gerhard Hansen in 1873. This
microorganism belongs to the family of Mycobacteriaceae. It is an
acid- and alcohol-resistant bacterium, which is a gram-positive
bacillus. Its length is 1–7 μm and its diameter is 0.2–0.5 μm. M.
leprae can maintain viability at low temperatures and drying for a long
time. This microorganism is characterized by extremely slow growth
(one division lasts about 12 days). M. leprae is an obligate
intracellular parasite. M. leprae is able to persist in human
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macrophages for a long time.
M. lepromatosis (the second causative agent of leprosy) was
discovered in 2008. It is a non-acid-resistant bacterium and causes a
predominantly severe diffuse lepromatous type of leprosy.
The incubation period of leprosy is long. It varies from 2–3
months to 50 years (on average 4–6 years).
The main way of transmission is airborne. However, the other
ways of transmission of this infection such as through the bites of
blood-sucking insects and damaged skin are not excluded. Leprosy is
a little contagious disease. The causes of leprosy infection may be a
prolonged close contact with a patient who does not receive treatment;
increase of body resistance (as a result of malnutrition, heavy physical
exertion, frequent acute respiratory viral infections, alcoholism and
other intoxications) and immunogenetic susceptibility.
Resistance to M. lepra is provided by its low virulence and
individual features of the immune system. The integrity of the
epithelium, secretion of the glands and surface immunoglobulin A
(IgA) play an important role in maintaining immunity.
Classification
According to Madrid Classification (1953 г), two polar types of
leprosy are distinguished – tuberculous and lepromatous and two
intermediate types – undifferentiated and borderline (dimorphic).
In Ridley-Jopling Classification, three types of leprosy are
distinguished – undifferentiated (Indeterminate – I), tuberculoid
(Tuberculoid type – TT) and lepromatous (Lepromatous type – LL).
Ridley-Jopling Classification is not applied widely. In practice,
lepromatous and tuberculoid types of leprosy are distinguished, as
well as a borderline type, which can be transformed into one of the
first two forms in future.
Lepromatous leprosy is a more severe form of the disease, in
which there is a lesion of the skin, nervous system, mucous
membranes and internal organs. A characteristic sign of the skin
lesions is appearance of numerous symmetrically arranged small
reddish spots. Then their color changes to brownish. Local sensitivity
in the area of rash does not change in the early stages of the disease.
Gradually, massive infiltration is formed on the extensor surface
of the limbs and face. The infiltrates localized on the face, namely, on
the forehead, superciliary arches, nose and cheeks lead to changes in
facial expression and disfigurement of the face (the so-called "lion's
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muzzle", facies leonina). The lesions may be accompanied by hair
loss, hypo-or anhidrosis.
A subcutaneous fatty tissue is involved in the process when some
nodules (lepromas), tubercles in the size from 2 mm to 2 cm, of dense
consistency, brownish in color are formed. The tubercles tend to
ulceration. They are localized on the face, ears, skin of the limbs,
buttocks and more frequently on the back.
The peripheral and central nervous system are affected by a
lepromatous type of leprosy. In most cases, nerves thicken and
become available for palpation. In future motor and trophic disorders,
as well as sensitivity disorders, such as neuralgia, hyperesthesia,
paresthesia, an inadequate or delayed response to irritation, analgesia
can develop in such patients.
The process of mutation of hands and feet occurs due to trophic
disorders. Nonspecific changes are observed in the internal organs (the
liver, lungs, spleen, etc.).
Llepromatous leprosy is characterized by depressed cellular
immunity that manifests as a negative lepromin skin test (Mitsuda’s test).
Lepromatous leprosy has two clinical forms:
x Nodular
x Diffuse
A nodular form is characterized by nodules, erythematous
infiltrating plaques and hypopigmentation. In the mucosa there is a
lepromatous rhinitis that is associated with perforation of the
cartilaginous nasal septum causing the so-called “saddle” nose.
There is partial alopecia localized in the nodules involving
eyebrows, eyelashes and body. A neural leprosy is bilateral. In the eye
it can cause episcleritis, diffuse infiltrative or focal keratitis, iritis and
iridocyclitis. It affects all organs of the reticuloendothelium system.
A diffuse lepromatous leprosy (Lucio 1852 and Latapi 1946) is
characterized by a diffuse, generalized infiltration of the skin, that
never becomes nodular, and may present a special type of lepromatus
reaction known as “Lucio’s phenomenon” or necrotizing erythema.
A diffuse infiltration is almost imperceptible. It gives the skin
edematous, shiny, and tense and erythemato-violaceous appearance. In
its atrophic phase, the skin becomes thin, wrinkled, dry and scaly.
Rhinitis and total eye-brow, eyelashes and body hair alopecia is found.
There is a panneuritis without an ocular involvement. A visceral
involvement is more severe than in a nodular form.
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 Tuberculoid leprosy affects only the skin and the peripheral
nerves. Internal organs are rarely involved. It occurs as one or just a
few erythematous, infiltrative and asymmetric plaques in the skin. The
lesions are red or brown, oval or rounded. The central part of the
plaque becomes depigmented and atrophic as it grows. The damage of
the skin appendages is characterized by hair loss and impaired
sweating in the affected areas. A tuberculoid type of leprosy is
characterized by an early damage to the peripheral nervous system
with the formation of sensitivity disorders (pain, temperature and
tactile). A neural involvement is usually asymmetric.
There are no specific lesions in the undifferentiated form of
leprosy. This form is characterized by appearance of a small number
of macules of various sizes with fuzzy borders, and damage to the
peripheral nervous system (polyneuritis). Identification of the
pathogen in this category of persons is extremely rare.
Borderline cases are unstable. Most of them become
lepromatous.
Diagnostics
Data from the epidemiological history (visit to an endemic region,
contact with patients suffering from leprosy), an objective
examination (type of rash, signs of peripheral innervation disorders)
are taken into account in the diagnosis of leprosy.
Laboratory data
Bacterioscopic examination is generally accepted as a laboratory
diagnostic method for leprosy. Scrapes for research are taken from
lesions on the skin and nasal mucosa by lightly scraping. The smear is
placed on a glass slide and stained with Ziehl-Nielsen. Punctate from
femoral or inguinal lymph nodes is also examined. However,
bacterioscopic research has a very low sensitivity, especially in
patients with an intermediate or tuberculoid lesion.
The lepromin skin test (Mitsuda's test) is an indicator of a
host’s ability to maintain cellular immunity in M. leprae in its body.
Mitsuda's test is not always reliable. A negative reaction can be
observed in 10% of healthy people.
The lepromin skin test is useful for a better classification of cases.
It is positive in TT cases, negative in LL cases and variable in
borderline cases.
Serologic tests are not practical. The reaction of complement
fixation and the reaction of indirect hemagglutination are sometimes
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used for early serological diagnosis of leprosy.
The most sensitive method for the diagnosis of leprosy is a
polymerase chain reaction (PCR). PCR is currently considered the
most promising diagnostic technique. It is used to diagnose any type
of leprosy. The advantages of PCR are as follows: non-invasive and
easy to obtain clinical material.
Treatment
Treatment of the disease was standardized by the World Health
Organization (WHO) in 1981. Combination therapy involves the use
of three main drugs: dapsone, rifampicin and clofazimine.
In 1997, WHO established the duration of treatment: 6 months for
multibacillary forms of leprosy and 12 months for paucibacillary.
Dapsone is prescribed in the dosage of 100 mg for adults once a day,
rifampicin in the dosage of 600 mg once a month, clofasimine in the
dosage of 300 mg once a month. For treatment of children lower doses
of drugs are used.

Unit 2
Cutaneous Tuberculosis
Cutaneous tuberculosis is a clinically and morphologically
heterogeneous group of skin diseases. The cause of the disease is a
direct or indirect effect of Mycobacterium tuberculosis. Cutaneous
tuberculosis ranks fifth among all localizations of extrapulmonary
tuberculosis.
Etiology
Cutaneous tuberculosis has, as its main etiologic agent,
Mycobacterium tuberculosis that belongs to the class of
Actinobacteriaceae; order Actinomycetales, family Mycobacteriaceae and
genus Mycobacterium. Occasionally it is also caused by Mycobacterium
bovis or BCG vaccine (an attenuated strain of M. bovis).
Mycobacterium tuberculosis is a straight or slightly bent (rod-
shaped), non-motile, non sporulated, unencapsulated bacillus,
measuring from 1 to 10μm long by 0.2 to 0.6μm wide; its most
important feature is that it becomes stained red by fuchsin and does
not discolor under the actions of alcohol and acid (acid-fast bacillus).
Its cellular wall has a high lipid content which grants resistance
against the action of chemical agents, though, it is susceptible to the
action of physical agents (heat and ultraviolet radiation).

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 This bacillus is a strict aerobic pathogen that requires certain
conditions to grow and multiply: oxygen, nutrients and an adequate
pH in the medium. It has approximately 4,000 genes with most of
them involved in the mechanisms of immune system evasion. For
example, 200 of the genes are involved in lipid metabolism. So much
emphasis occurs because lipids are a main energy source of
Mycobacterium tuberculosis and therefore are directly responsible for
its ability to multiply in host tissue and form cellular walls. It can also
be considered a facultative intracellular parasite, since it is able to
survive and multiply both outside and inside phagocytic cells.
The clinical appearance of cutaneous tuberculosis is various.
Inflammatory papules, verrucous plaques, suppurative nodules, chronic
ulcers and other lesions can be identified. Clinical manifestations depend
on the interaction of several factors including the host's immunity and
the ways of mycobacteria penetration into the skin.
Ways of penetration of mycobacteria into the skin:
x exogenous inoculation;
x «per continuitatem» ( spread from the nearby foci of infection);
x hematogenous inoculation (spread from other sites of
infection).
Cutaneous tuberculosis is secondary, as a rule, in patients who
have previously recovered or are ill with tuberculosis of other organs.
A primary skin lesion due to an exogenous infection is extremely rare,
due to the fact that a barrier function is characteristic of the skin. An
exogenous infection is possible only with a massive infection through
the damaged skin, when the skin resistance to Mycobacterium
tuberculosis is impaired.
Mycobacterium tuberculosis enters the skin by a hematogenous or
lymphohematogenous way from the lungs, lymph nodes and other
affected organs.
There is no generally accepted classification of cutaneous
tuberculosis. According to the National Phthisiology Guidelines 2015,
cutaneous tuberculosis is divided into:
x True cutaneous tuberculosis (localized, granulomatous or
bacterial);
x Skin lesions as a result of allergic immune (paraspecific)
inflammation, manifested in the form of allergic vasculitis. It is called
disseminated, hyperergic cutaneous tuberculosis. G. Darrieus
classified these manifestations as “tuberculids”.
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 Classification by S.T. Pavlov (Russia, 1969): cutaneous
tuberculosis is divided into localized and disseminated forms.
Classification by J. Lai-Cheong et al. (2007) depending on the
way of infection: exogenous, endogenous and hematogenous.
Tuberculosis variants can also be classified according to bacterial
load on the skin: multibacillary forms are those in which bacilli are
easily detected in the cutaneous tissue or isolated in exudate; whereas
in paucibacillary forms it is difficult to isolate the organisms, with
bacilli being sparse or even not visualized in histology.
Classification of cutaneous tuberculosis depending on the
bacterial contamination may is as follows:
x Paucibacillary forms (lupus vulgaris, tuberculosis verrucosa
cutis);
x Multibacillary forms (scrofuloderma, tuberculous chancre,
acute miliary tuberculosis, orificial tuberculosis, and metastatic
abscess (tuberculous gumma)).
There are also tuberculids, a category of skin disorders associated
with tuberculosis that represents most likely immune hypersensitivity
reactions to Mycobacterium tuberculosis antigens. This category
includes three variants: papulonecrotic tuberculid, lichen
scrofulosorum and erythema induratum of Bazin.
Cutaneous Tuberculosis Classification:
x Exogenous cutaneous tuberculosis (Tuberculous chancre and
Tuberculosis verrucosa cutis):
x Endogenous cutaneous tuberculosis (By continuity («per
continuitatem») or autoinoculation (Scrofuloderma, orificial
tuberculosis and some cases of lupus vulgaris); by hematogenic
dissemination (Lupus vulgaris, tuberculous gumma and acute miliary
tuberculosis));
x Tuberculids (Papulonecrotic tuberculid, Lichen
scrofulosorum);
x Cutaneous tuberculosis secondary to BCG vaccination.
Exogenous cutaneous tuberculosis
Exogenous inoculation of Mycobacterium tuberculosis may
originate tuberculous chancre and tuberculosis verrucosa cutis.
Tuberculous Chancre
It is a rare form of tuberculosis, also called primary tuberculous
inoculation chancre, as it develops in individuals not previously

190
sensitized to the mycobacterium, occurring most often in children in
endemic areas of low vaccination coverage.
Tuberculous chancre develops by direct Mycobacterium
tuberculosis inoculation in the skin after a local trauma, often
unnoticed by the patient. There are reports of injuries developing after
surgical procedures performed with unsterilized materials, and even
after tattoos. After 2 to 4 weeks, a firm, painless, reddish-brown,
slowgrowing papule or nodule, which may develop into an ulcer,
arises. An ulcer is friable, has a tendency to bleeding and a coarse
granular surface.
The lesions measure usually 1 cm or less, the face and extremities
being the most frequently involved sites. Occasionally the result of
lesion growth is a verrucous plaque, or even lesions resembling
scrofuloderma or lupus vulgaris. After 3 to 8 weeks from the onset of
tuberculous chancre, there is often bacilli dissemination through the
lymph and lymph nodes, analogous to what happens in the lungs with
Gohn's complex. Regional lymphadenopathy is evident and
occasionally lymph node involvement results in rupture through the
skin.
The evolution of chancre is variable and healing may occur
between three and 12 months, leaving atrophic scarring and
calcification in the regional lymph nodes. However, if anti-tubercular
medications are not implemented, there is potential risk of developing
complications such as lupus vulgaris, scrofuloderma or dissemination
(acute miliary TB).
Tuberculosis Verrucosa Cutis
Tuberculosis verrucosa cutis, the most common form of
exogenous tuberculosis, is the result of primary inoculation in the
previously sensitized individuals who maintain moderate to high
immunity against Mycobacterium tuberculosis. In the past,
professionals like anatomists and physicians were prone to this type of
cutaneous tuberculosis as a result of direct inoculation of the bacillus
through the injured skin. In tropical zones, tuberculosis verrucosa
cutis is seen more often in children on account of the habit of walking
barefoot on soil contaminated with tuberculous sputum, ankles and
buttocks being the most affected areas in this group.
Lesions are usually solitary, painless and predominate in
anatomical locations that are prone to traumas, such as fingers and
toes). They start as erythematous papules surrounded by a purplish
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inflammatory halo that evolve to asymptomatic verrucous plaques,
with 1 to 5 cm in diameter. Growth happens through peripheral
extension, sometimes accompanied by central atrophy. The lesions
may rarely ulcerate.
Tuberculosis verrucosa cutis tends to persist for many years if
untreated, although spontaneous resolution might also occur. A
secondary bacterial infection and elephantiasis are possible
complications of extensive lesions affecting extremities. Typically
there is a favorable response to anti-tuberculosis therapy.
Endogenous Cutaneous Tuberculosis Forms
By continuity or autoinoculation
Clinical manifestations of cutaneous tuberculosis such as
scrofuloderma, orificial tuberculosis, and lupus vulgaris may arise in
this form of tuberculosis.
Scrofuloderma
Scrofuloderma, also known as tuberculosis colliquativa cutis, was
the most commonly observed form of a cutaneous tuberculosis before
the advent of tuberculostatic drugs and still is the most common form
of a cutaneous tuberculosis in some countries such as Brazil and India
(particularly in children). Persons of any age group can participate.
However, children, teenagers and elders suffer the most because these
are the phases of life when most immunological disorders occur.
This type of tuberculosis penetrates the skin from nearby
structures, such as the lymph nodes, bones, joints, or testicles, where
the infection has developed. The main sites are cervical lymph nodal
chains. Besides these areas, coexistence with pulmonary tuberculosis
is frequent. The occurrence of scrofuloderma after BCG vaccination
has been rarely reported.
The lesions may be single or multiple. Intense inflammation leads
to the formation of painless, cold abscesses, which gradually increase.
The differential diagnosis is carried out with bacterial abscesses,
tumor metastasis, histiocytosis and hydroadenitis. As the lesions
evolve it is possible to observe purplish ulcerated plaques and later the
appearance of fistulae with draining caseous material. Spontaneous
involution may present leaving keloid scars, retractions and atrophic
sequelae. Lupus vulgaris may develop in the scars and next to
scrofuloderma areas.
Orificial Tuberculosis
An orificial tuberculosis or tuberculosis cutis orificialis often
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affects middle-aged adults, and persons who present advanced form of
lung, intestinal or genitourinary tuberculosis or severely impaired
cellular immunity.
The lesions appear as friable, painful, erythematous-to-yellowish
papules and nodules, measuring 1 to 3 cm in diameter, which can lead
to painful ulcers with fibrinous bases in the skin near bodily orifices.
Edema and inflammation are evident in perilesional tissue. Affected
individuals have a poor prognosis, since there is severe underlying
visceral disease. Although there are reports of improvement after
initiating therapy, resistance to tuberculostatic treatment is common. If
the medications are not introduced, lesions progress and contribute to
the development of fatal disease.
By hematogenic dissemination
Hematogenic dissemination from a primary focus of
Mycobacterium tuberculosis infection may lead to tuberculous gumma
(metastatic tuberculous abscesses), acute miliary tuberculosis and
lupus vulgaris.
Lupus Vulgaris is the most common form of cutaneous
tuberculosis in Europe and India. It is a chronic, progressive form of
cutaneous tuberculosis occurring in patients with a high degree of
immunity against the bacillus being thus a paucibacillary form. For
unknown reasons, women are affected 2-3 times more often than men.
In addition to the endogenous source, it may develop upon the
drainage scar of scrofulodermas or rarely be acquired by exogenous
Mycobacterium tuberculosis inoculation.
The clinical finding of lupus vulgaris varies. Usually there are
papules and well-delimited, reddish-brown plaques in facial and
cervical areas, which rarely ulcerate. In tropical countries, the
development of lesions on the legs and buttocks is common. The
plaque grows peripherally, with serpiginous or verrucous borders,
often reaching over 10cm in diameter with central discoloration and
atrophy. Diascopy of non-keratotic areas reveals an "apple jelly"
aspect. This feature is also seen in other granulomatous diseases such
as sarcoidosis and leprosy, and is rarely found in patients with black
skin. The lesions do not always present in typical forms and there are
various descriptions such as nodules, vegetating lesions, ulcerated or
tumoriform lesions, and those mimicking diseases such as discoid
lupus erythematosus, psoriasis, sporotrichosis, actinomycosis and
mycetoma.
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 Untreated, lupus vulgaris lesions persist for years, gradually
growing in size up to tens of centimeters and leading to significant
aesthetic alterations, with ulcerations and tissue destruction. The
incidence of malignant transformation into squamous cell carcinoma
in lupus vulgaris plates ranged from 0.5 to 10.5% and it usually occurs
after 25-30 years of untreated disease. The development of other
malignancies, such as basal cell carcinoma has also been reported.
Tuberculous Gumma
Tuberculous Gumma, also called a metastatic tuberculous
abscess, originates from hematogenous spread especially in the
periods when there is decreased cellular immunity. Typically, it
affects malnourished children and immunocompromised adults, with
rare reports in immunocompetent patients. Tuberculous abscesses
have also been described in individuals with an acute miliary
tuberculosis.
In tuberculous gumma, there are usually few lesions affecting the
trunk and extremities, characterized by fluctuating subcutaneous
nodules. These may ulcerate and drain caseous secretion. Regional
adenopathy is usually not present. Clinically it may resemble
scrofuloderma. The patients diagnosed with tuberculous gumma have
a poor prognosis because of their compromised immunity. In
immunocompetent individuals, abscesses may persist for years
without treatment, and eventually resolve spontaneously.
Acute Miliary Tuberculosis
It is a rare and severe form of tuberculosis that develops in
individuals with impaired cellular immunity and children. Individuals
are systemically compromised with fever, anorexia, asthenia, and
weight loss. Clinically, there is a wide spectrum of cutaneous lesions
such as erythema, erythematous-whitish or erythematous-purplish
papules, upon which small vesicles appear, subsequently breaking
down and resulting in umbilication and crust formation. They tend to
regress in 1 to 4 weeks, leaving depressed and hypochromic scars.
As an acute miliary tuberculosis is usually found in cases of
severe immunosuppression, almost always the tuberculin skin test is
negative, demonstrating anergy. Despite being a rare form of CTB, the
number of cases has been increasing, mainly due to co-infection with
HIV when CD4 count is less than 100 cells/uL.
Tuberculids
It is the most common type of tuberculid often observed in
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children and young people. It presents as a symmetric and recurrent
eruption of erythematous purplish papules that become pustular and
necrotic.
The lesions affect the face, ears, extensor areas of extremities,
trunk and buttocks, associated or not with lymphadenitis.
Constitutional symptoms such as fever and asthenia may precede
cutaneous manifestations.
Eruption may resolve spontaneously after weeks to months,
resulting in formation of depressed varioliform scars. Recurrences are
common without tuberculostatic treatment, however when drugs are
introduced, it is possible to observe clinical improvement in a few
days or weeks.
Lichen Scrofulosorum is a rare tuberculid that most often affects
children and young adults with a lymph node or bone underlying
disease. There are reports on the onset of lichen scrofulosorum after
BCG vaccination and in patients infected with M. avium-
intracellulare. It is characterized by plaques consisting of grouped,
asymptomatic, indurated, and colored from yellow and red to brown-
red follicular or perifollicular papules with 1-5 mm in size, most
commonly observed in the trunks of affected individuals. Anti-
tubercular treatment promotes complete resolution of the lesions in
weeks. Without medication, this dermatosis can regress without
leaving scars, after some months or years.
Erythema Induratum of Bazin is a granulomatous lobular
panniculitis associated with tuberculosis, which affects the lower
limbs of young and middle-aged women. It appears as slightly painful,
erythematous-purplish subcutaneous nodules that persist for several
weeks and are usually distributed in the posterior surface of legs and
thighs. Nodules may reach a few centimeters in diameter and often
rupture, forming deep ulcers that release secretions. The lesions may
regress, even without treatment, after weeks to months, leaving
depressed post-inflammatory hyperpigmentation and scarring,
however, recurrences may occur every 3-4 months.
Differential diagnosis is performed with erythema nodosum.
Histologically, they are different because erythema nodosum is
characterized by septal panniculitis without vasculitis.
One should investigate the possibility of TB through additional
tests and when the disease is evidenced, anti-tuberculosis treatment is
recommended. If the association with tuberculosis is not detected, the
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term "nodular vasculitis" is used to refer to the manifestation of
clinically and histologically similar panniculitis. In this case, hepatitis
C should be suspected and investigated, as it is a potential trigger of
nodular vasculitis.
Cutaneous Tuberculosis Secondary to BCG Vaccination
BCG vaccine is a living virus vaccine derived from attenuated
strains of Mycobacterium bovis. It has been widely used to prevent
serious tuberculosis infections, such as meningoencephalitis and acute
miliary tuberculosis. However, it may cause skin complications like
tuberculids, lupus vulgaris, scrofuloderma and even outbreaks of
tuberculosis in other organs, and nonspecific reactions, such as fever,
local inflammation, abscesses, and lymphadenitis.
Diagnostics
Making diagnosis of cutaneous tuberculosis is very difficult.
There is a reason to believe that 1/3 of patients existing de facto is
only registered.
The causes of insufficient detection of cutaneous tuberculosis are
as follows:
x underestimation of the importance of Mycobacterium
tuberculosis in the etiology of various skin lesions, which doctors
diagnose as non-specific lesions erroneously;
x the problem of detecting Mycobacterium tuberculosis in the
skin lesions (Mycobacterium tuberculosis is determined in 1/5 of the
patients);
x loss of alertness for the detection of tuberculosis by specialists
of the general medical network.
As a result, making the diagnosis of cutaneous tuberculosis often
takes years. Thus, the diagnosis of lupus vulgaris is established in only
5% of patients during the first year of the disease, and for erythema of
Bazin – in 14% of patients. For the remaining 86%, this figure was
9.1±4.2 years. The reason for the low detectability is the similarity of
these skin lesions with rosacea, sarcoidosis, lupus erythematosus,
panniculitis, vasculitis, chromomycosis, and lipoid necrobiosis at the
initial stage of development of these diseases.
Methods to diagnose cutaneous tuberculosis are as follows:
x Histological examination of skin biopsy specimens and
subcutaneous fatty tissue (stained with hematoxylin and eosin) –
detection of tuberculous tubercles consisting mainly of epithelioid
cells with the inclusion of giant multinuclear cells of the Langhans
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type, containing caseous necrosis in the center and surrounded by
monocytes and lymphocytes;
x Immunohistochemical method using monoclonal antibodies to
Mycobacterium tuberculosis complex for the study of biopsy material;
x Molecular genetic methods - polymerase chain reaction (PCR)
for the study of biopsy material and discharge from ulcers;
x Detection of acid resistant mycobacteria in the lesion focus
(Ziehl-Neelsen staining, auramine-rhodamine fluorescent microscopy
test);
x Culture diagnostics, using liquid nutrient media with automatic
registration of culture growth (BACTEC);
x In rare cases (with scientific research) – inoculation of the test
material to a guinea pig (rapid development of generalized
tuberculosis, death of an animal);
x Immunological diagnosis: tuberculin tests, Diaskintest,
T-SPOT. ТВ;
x Ultrasound examination (if there are nodes and infiltrates in the
subcutaneous fatty tissue);
x Chest X-ray and other radiological tests for extrapulmonary
infection;
x Epiluminescent dermatoscopy.
Treatment
Patients with pulmonary or extrapulmonary tuberculosis need to
be treated with anti-tubercular drugs. This usually involves a
combination of antibiotics (isoniazid, rifampicin, pyrazinamide and
ethambutol) given over a period of several months and sometimes
years.
Patients with latent TB infection but not active disease may also
be treated with anti-tubercular drugs to prevent development of an
active disease.
Occasionally a surgical excision of localized cutaneous
tuberculosis is recommended.

Checkup Questions
1. What is a causative agent of leprosy?
2. How long is an incubation period of leprosy and what ways of
its transmission are known?
3. What are the “facies leonina”
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 4. What does Mitsuda’s test mean?
5. What clinical picture is observed in tuberculoid leprosy?
6. What methods are used for laboratory diagnosis of leprosy?
7. What ways of mycobacterium tuberculosis penetration into the
skin are known?
8. How is cutaneous tuberculosis classified?
9. Does the clinical picture of endogenous forms of cutaneous
tuberculosis differ?
10. How to determine the symptom of "apple jelly"?
11. What principles define the treatment for cutaneous
tuberculosis?

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CHAPTER XVI
FUNGAL INFECTIONS
Unit 1
Tinea corporis
Tinea corporis (also known as ringworm, tinea circinata, and tinea
glabrosa) is a superficial fungal infection (dermatophytosis) of the
arms and legs, especially on glabrous skin, however it may occur on
any part of the body.
Causes
Tinea corporis is caused by a tiny fungus known as
dermatophyte. These tiny organisms normally live on the superficial
skin surface, and when the opportunity is right, they can induce rash
or infection.
The disease can also be acquired by: Person-to-person transfer
usually via direct skin contact with an infected individual. Animal-to-
human transmission is also common. Ringworm commonly occurs on
pets (dogs, cats) and the fungus can be acquired while petting or
grooming an animal. Ringworm can also be acquired from other
animals like horses, pigs, ferrets and cows. The fungus can also be
spread by touching inanimate objects like personal care products, bed
linen, combs, athletic gear, or hair brushes contaminated by an
affected person.
Individuals at high risk of acquiring ringworm include those who:
x Live in crowded, humid conditions.
x Sweat excessively, as sweat can produce a humid wet
environment where the pathogenic fungi can thrive. This is most
common in the armpits, groin creases and skin folds of the abdomen.
x Participate in close contact sports like soccer, rugby, or
wrestling.
x Wear tight, constrictive clothing with poor aeration.
x Have a weakened immune system (e.g., those infected with
HIV or taking immunosuppressive drugs).
Clinical Presentation
It may have a variety of appearance; most easily identifiable are
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the enlarged raised red rings with a central area of healing (ringworm).
The same appearance of ringworm may also occur on the scalp (tinea
capitis), beard area (tinea barbae) or the groin (tinea cruris).
Other classic features of tinea corporis include as follows:
x The edge of the rash appears elevated and is scaly to touch.
x Sometimes the skin surrounding the rash may be dry and flaky.
x Almost invariably, there will be hair loss in the areas of the
infection.
Diagnosis and Testing
x Clinical picture
x Wood's light
x Smear (microscopic examination)
x Culture which is on petri dishes or cotton wool - plugged test
tubes with Sabouraud's dextrose agar.
Prevention
Because fungi prefer warm, moist environments, preventing
ringworm involves keeping skin dry and avoiding contact with the
infectious material. Basic prevention measures include:
x Washing hands after handling animals, soil, and plants.
x Avoiding touching characteristic lesions on other people.
x Wearing loose-fitting clothing.
x Practicing good hygiene when participating in sports involves
physical contact with other people.
Treatment
Most cases are treated by application of topical antifungal creams
to the skin, but in extensive or difficult to treat cases systemic
treatment with oral medication may be required.
In general ringworm responds well to topical treatment. Topical
antifungals are applied to the lesion twice a day for at least 3 weeks.
The lesion usually resolves within 2 weeks, but therapy should be
continued for another week to ensure the fungus is completely
eradicated. The most commonly used antifungal creams are
clotrimazole, ketoconazole, miconazole, terbinafine, tolnaftate, and
butenafine.
If there are several ringworm lesions, and they are extensive,
complications such as secondary infection exist, or the patient is
immunocompromised, oral antifungal medications can be used. Oral
medications are taken once a day for 7 days and result in higher
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clinical cure rates. The antifungal medications most commonly used
are itraconazole and terbinafine.
Prognosis
Tinea corporis is very contagious and can infect everyone in the
household. If a person acquires it, the proper measures must be taken
to prevent its spreading. Young children in particular should be
educated about the infection and how to avoid it. Because of how
easily the condition spreads between individuals, tinea corporis will
keep recurring if preventative measures are not taken. Avoid wearing
tight thick restrictive clothing; fungus thrives in warm humid
conditions. If pets are kept in the household or premises, they should
be checked regularly. It is recommended to get the animal checked for
tinea, especially if hair loss in patches is noticed or the pet is
scratching excessively. The majority of people who have acquired
tinea know how uncomfortable the infection can be. However, the
fungus can easily be treated and prevented in individuals with a
healthy immune system.

Unit 2
Tinea Capitis
T. capitis is a worldwide fungal infection of the scalp. It is
primarily a disease in young children. Boys are affected more often
than girls. This may be due to shortness of the hair, which facilitates
easy reaching the fungal spores on the scalp. Adults are rarely
infected; this is believed to be due to the highly fatty acid of the scalp,
which has dermatophytes inhibiting property. It was established many
years ago that some saturated fatty acids, from adult human hair (and
derived from sebum) were inhibitory to dermatophytes fungi. A fungal
scalp infection may be endemic, sporadic or epidemic, where
involvement of the large number of school children. The tendency of
scalp ringworm to clear spontaneously at puberty was believed to be
due to the change in sebum composition at this age.
Ways of Transmission
x Contact with infected persons or their combs, brushes, or
headgears;
x Contact with infected pets (such as cats, dogs or cattle).
Minor trauma is an important predisposing factor for seeding the
fungi on the scalp to cause infection.
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 Different Fungal Strains Causing infection:
x Microsporum Auduini is the most common strain to cause T.
capitis.
x Microsporum canis is often contracted from animals, can cause
highly inflammatory lesions.
x Trichophyton mentagrophytes causes highly inflammatory T.
capitis.
x Tricophyton Tonsurans causes an exceedingly chronic
infection. The fungal infections are often familiar.
x T. violaceum causes a clinical lesion called "black dot" ring
worm.
x T. Schoenleini causes a clinical type of T. capitis known as
favus.
Clinical Presentation
The clinical picture usually varies according to certain causative
dermatophytes.
Some strains such as M. canis and T. mentagrophytes cause
highly inflammatory lesions, while T. Tonsurans lesions have a very
chronic course.
The clinical picture may be sometimes confusing and cannot be
easily diagnosed except for detection of the dermatophytes through
potassium hydroxide smears.
Different Clinical Types of Tinea Capitis
Dry Type – the lesion may be dry and scaly simulating dandruff
of the scalp, psoriasis and lichen planus.
Black Dot Type – the lesion is usually dry in the site where the
hair is cut short from the stumps, and the bases of infected hairs are
prominent. There is a variable degree of erythema, itching and scaling.
The individual lesion may persist for a long time or resolve
spontaneously.
Kerion – the lesions which may be highly inflammatory and
appear as swollen, edematous, oozing and crusting lesion in the form
of boggy inflammation of the scalp called "kerion". This type may be
misdiagnosed and treated as an abscess of the scalp. Hair loss may be
permanent causing cicatricial alopecia.
Favus – the clinical picture of favus is specific, a solid crust
being formed on the infected area, it may spread to cover the whole
scalp. The scalp has special mouse smell. The condition is very

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chronic and may end with cicatricial alopecia. The infection may
spread to other areas away from the scalp such as to the abdomen and
extremities.
Diagnosis
Diagnosis of T. capitis can be made by different methods:
Clinical presentation – fungi that cause T. capitis feed on keratin
and extend from the center to the periphery. At the periphery of the
lesion there are active edges - papular, vesicular or papulovesicular,
with a scaling surface.
Wood's light – microsporum gives strong green fluorescence.
Trichophyton groups such as T. Schoenleini give dull green
fluorescence under a filtered ultra violet, Wood' light in a dark room.
This is very helpful in rapid screening of the large number of school
children.
Smear – this is a simple method and can be done easily in the
laboratory. Microscopic examination of the specimen can detect the
hyphae of the causative dermatophytes.
Technique
Collection of scrapings from the infected skin should be taken
from the active edge of the lesion using a blunt scalpel blade or by the
edge of a slide. Infected hairs should be depilated from their roots
especially in favus.
The specimen is placed on a slide and a drop of 30 percent
potassium hydroxide is added and covered by a cover slip. This is
heated gently in order to soften and clear the material. Care should be
taken in order not to heat the specimen too much and not to boil.
The specimen is examined under a low power microscope without
staining. This may show the branched septate hyphae.
Hair invasion by dermatophytes is ectothrix in Microsporum and
T. mentagrophytes, while it is endothrix in T. Tonsurans and
T. violaceum.
Culture, which is on petri dishes or cotton wool - plugged test
tubes with Sabouraud's dextrose agar containing antibiotics to inhibit
bacterial and saprophyte contamination. Incubation is kept at 26-30°С
for one to two weeks. Different colonies can be identified
morphologically and microscopically.
Differential Diagnosis
Alopecia areata – The area involved is smooth, hair-free. No short
cut hair. On the surface there are no scales. The shape of the
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exclamation mark in some hairs growing on the periphery of the
lesions helps to diagnose alopecia areata. Detection of a causative
fungi is diagnostic for T. capitis.
Seborrheic dermatitis – the lesion is more diffuse and with greasy
scales, diffuse hair loss and a negative microscopic examination are
important criteria for a differential diagnosis.
Impetigo and carbuncles of the scalp may simulate kerion.
Bacterial lesions are more inflammatory, have shorter course, the hair
is not loose and cut short. Dermatophytes can be detected on
microscopic examination.
Discoid lupus erythematosus: the condition has a chronic course
ending with cicatricial alopecia. The scales are adherent. Other open
areas, such as the face, may be involved. A microscopic examination
for any fungal elements is negative.
Lichen planus: flat topped violaceous papules may be seen in the
lesion, which results in cicatricial alopecia. The extremities and the
buccal cavity may have some specific lesions of lichen planus.
Treatment
x Preventive measures
x Topical treatment
x Systemic treatment
Griseofulvin was discovered in the late 1940s and it was used
after 1958 for treatment of fungal lesions in man. This was the first
oral antimycotic drugs used in the past till nowadays.
Despite it’s a long history as a fungistatic preparation, it has the
most limited spectrum of activity among all the available antifungal
drugs, meanwhile it has no effect on bacteria.
Mode of action:
The mode of action of griseofulvin appears to be partial by
inhibition of microtubules formation and the most apparent in the
active metabolizing cells near the hyphal tip.
In man, griseofulvin is rapidly metabolized and conjugated
with glucuronide in the liver, excreted by the kidney and by the
liver in bile.
Interaction
Griseofulvin interacts with certain drugs such as anticoagulants,
warfarin, cyclosporin, barbiturates and oral contraceptives.
Dose:
Griseofulvin is available in the standard macrocrystalline form as
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125 mg and 500 mg tablets and as a pediatric oral suspension, 125 mg
per 5 ml given after meals preferably after a fatty meal that increases
drug absorption.
In Tinea capitis a single dose, 2 g. of griseofulvin especially in
young children (in order to be sure that an effective dose was given),
is frequently enough to clear most of the lesions.The recommended
daily dose is as follows:
Infants and children:
125 mg/day up to the age of 1 year (one teaspoonful).
187mg/day from I to 5 years (one and a half teaspoonful), and
250-375mg/day (2-3 teaspoonful) from 6 to 12 years divided into two
doses or as one dose after taking a fatty meal.
In children the daily dose is 10 mg/kg/day given in two divided
doses daily. It should be fatty after meals.
The duration of treatment varies from ten to twenty days
according to the type and severity of a fungal infection.
Adult dose:
One to two 500 mg tablet daily. Small adults (55 kg), one tablet
250 mg. twice daily Medium-sized adults, one tablet 250 mg. three
times daily. For large adults (over 100-kg), one tablet 500 mg is taken
twice daily.
Azoles
The newer oral azoles, particularly itraconazole, are effective
substitutes for griseofulvin but more expensive.
Special indications of Azoles:
- Widespread Tinea corporis due to T. rubrum, azoles are the
treatment of choice;
- Type of azoles available
Itraconazole is an effective new anti-fungal preparation.
Dose: Adults – 100-200mg/day for a few weeks in skin fungal
infection and for several months in onychomycosis.
Side effects of itraconazole:
x Gastro-intestinal disturbances;
x Headache;
x Rarely exfoliative dermatitis.
Ketoconazole
Orally active imidazole is a broad-spectrum anti-fungal agent.
Dose: Adult: 200-400 mg/day with meals; it is usually well
tolerated.
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 Side effects: headache and nausea are relatively common minor
side effects. Liver enzymes should be measured at monthly intervals
with prolonged courses. Treatment should be ceased if ALT or SGPT
rise from two to threefold. Ketoconazole may inhibit androgen
biosynthesis.
These are antifungal drugs that act by inhibition of squalene
epoxidase formation of the fungal cell membrane.
The two main compounds are Terbinafine and Naftifine. Both
are active against dermatophytes.
Terbinafine such as Lamisil can be given orally. Children over 20
kg can be given 62.5 mg daily. 20- 40 kg-body weight: 125 mg can be
given daily; over 40 kg – 250 mg daily.
The adult dose is 250 mg daily. Terbinafine is available also as a
topical preparation (Lamisil cream). It produces rapid and long-lasting
remissions in both nail disease and persistent Tinea pedis.
There is some evidence to suggest that the frequency of relapse is
much lower with Terbinafine than that with other antifungal
preparations.

Unit 3
Tinea Pedis
Tinea pedis is a foot infection due to a dermatophyte fungus.
Tinea pedis thrives in warm humid conditions and is most common in
young adult men.
Tinea pedis is most frequently due to:
x T. rubrum
x T. interdigitale, previously called T. mentagrophytes var.
interdigitale
x Epidermophyton floccosum
Clinical Presentation
Tinea pedis has various patterns and may affect one or both feet.
x Chronic hyperkeratotic tinea refers to patchy fine dry scaling
on the sole of the foot.
x ‘Moccasin’ tinea is extensive hyperkeratotic tinea, in which
the skin of the entire sole, heel and sides of the foot is dry but not
inflamed. The affected area does not include the top of the foot. This
is usually caused by T. rubrum.
x Athlete's foot i.e. moist peeling irritable skin between the toes,
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most often in the cleft between the fourth and fifth toes.
x Clusters of blisters or pustules on the sides of the feet or insteps
(more likely with T. interdigitale).
x Round dry patches on the top of the foot (ringworm like tinea
corporis).
Predisposing Factors
Tinea pedis affects all ages but is more common in adults than in
children. The fungal spores can persist for months or years in
bathrooms, changing rooms and swimming pools. Walking bare foot
on a communal floor or sharing a towel can result in the infection.
Some people are particularly prone to troublesome tinea pedis.
This may be because:
x they are more exposed to the spores at home or during
recreational activities;
x their skin produces less fatty acid (a natural antifungal agent);
x they wear occlusive footwear;
x they wear the same pair of socks or shoes for long periods;
x they sweat excessively (hyperhidrosis);
x they have some form of immune deficiency e.g. medication such
as azathioprine, or infection with human immunodeficiency virus;
x they have poor circulation resulting in cold feet e.g. due to
lymphoedema.
Diagnosis
The diagnosis of tinea pedis is confirmed by microscopy and
culture of skin scrapings.
Treatment
y Correction of the predisposing factors such as excessive
sweating, occlusion of the feet, and proper hygiene to the feet.
y Administration of topical antifungal preparations alone or in
combination with antibacterial ones when secondary infections are
suspected.
y Administration of tolnaftate powder has proven value and the
imidazole are equally effective topical antifungal preparations.
y Administration of potassium permanganate solution 1: 9000 or
aluminium chloride solution 20-30% applied twice daily has
considerable advantages in drying the wet oozing lesions.
y If there is any evidence of bacterial infection, swabs should be
taken for culture and sensitivity.
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 Imidazole, Itraconazole and Terbinafine are effective
medications. There is some evidence that the rate of recovery is higher
and the frequency of relapses is less with these drugs
Other drugs in this group, Miconazole, Isoconazole, Tioconazole
and Sulconazole are equally effective.
Resistance to treatment
Treatment may be unsuccessful due to:
• Untreated infection, such as nails (onychomycosis).
• Reinfection from contact with spores in the surroundings or
clothing.
• Untreated infected family member.
Moccasin tinea is particularly resistant to treatment.

Unit 4
Onychomycosis
Onychomycosis (also known as "dermatophytic onychomycosis"
and "ringworm of the nail") means a fungal infection of the nail. It is
the most common disease of the nails and constitutes about a half of
all nail abnormalities.
This condition may affect toenails or fingernails, but toenail
infections are particularly common. The prevalence of onychomycosis
is about 6-8% in the adult population.
Classification
There are four classic types of onychomycosis:
x Distal subungual onychomycosis is the most common form
of tinea unguium, and is usually caused by Trichophyton rubrum,
which invades the nail bed and the underside of the nail plate.
x White superficial onychomycosis (WSO) is formation of
"white islands" on the plate caused by fungal invasion of the
superficial layers of the nail plate. It accounts for only 10 percent of
onychomycosis cases. In some cases, WSO is a misdiagnosis of
"keratin granulations" which are not a fungus, but a reaction to nail
polish that can cause the nails to have a chalky white appearance. A
laboratory test should be performed to confirm.
x Proximal subungual onychomycosis is fungal penetration of
the newly formed nail plate through the proximal nail fold. It is the
least common form of tinea unguium in healthy people, but is found
more commonly when the patient is immunocompromised.
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 x Candidal onychomycosis is Candida species invasion of the
fingernails, usually occurring in persons who frequently immerse their
hands in water. This is normally due to a prior damage of the nail by
infection or trauma.
Clinical Presentation
The nail plate can have a thickened, yellow, or cloudy
appearance. The nails can become rough and crumbly, or can separate
from the nail bed. There is usually no pain or other bodily symptoms,
unless the disease is severe.
Dermatophytids are fungus-free skin lesions that sometimes form
as a result of a fungus infection in another part of the body. This could
take the form of rash or itch in the area of the body that is not infected
with the fungus. Dermatophytids can be thought of as an allergic
reaction to the fungus. People with onychomycosis may experience
significant psychosocial problems due to the appearance of the nail.
Causes
The causative pathogens of onychomycosis include
dermatophytes, Candida, and nondermatophytic molds.
Dermatophytes are the fungi most commonly responsible for
onychomycosis in the temperate western countries; while Candida and
nondermatophytic molds are more frequently involved in the tropics
and subtropics with a hot and humid climate.
Dermatophytes
Trichophyton rubrum is the most common dermatophyte involved
in onychomycosis. Other dermatophytes that may be involved are T.
interdigitale, Epidermophyton floccosum, T. violaceum, Microsporum
gypseum, T. tonsurans, T. soudanense (considered by some to be an
African variant of T. rubrum rather than a full-fledged separate
species) and the cattle ringworm fungus T. verrucosum. A common
outdated name that may still be reported by medical laboratories is
Trichophyton mentagrophytes for T. interdigitale. The name T.
mentagrophytes is now restricted to the agent of favus skin infection
of the mouse; though this fungus may be transmitted from mice and
their danders to humans, it generally infects skin and not nails.
Other causative agents
Other pathogens include Candida and nondermatophytic molds, in
particular, members of the mold generation Scytalidium (name
recently changed to Neoscytalidium), Scopulariopsis, and Aspergillus.
Candida spp. mainly causes fingernail onychomycosis in people
209
whose hands are often submerged in water. Scytalidium mainly affects
people in the tropics, though it persists if they later move to the areas
of temperate climate. Other molds more commonly affect people over
60 years, and their presence in the nail reflects slight weakening in the
nail's ability to defend itself against fungal invasion.
Risk Factors
Aging is the most common risk factor for onychomycosis due to
the diminished blood circulation, longer exposure to fungi, and nails
which grow more slowly and thicken increasing susceptibility to
infection. Nail fungus tends to affect men more often than women,
and is associated with a family history of this infection. Other risk
factors include perspiring heavily, being in a humid or moist
environment, psoriasis, wearing socks and shoes that hinder
ventilation and do not absorb perspiration, going barefoot in damp
public places such as swimming pools, gyms and shower rooms,
having athlete's foot (tinea pedis), minor skin or nail injury, damaged
nail, or other infection, and having diabetes, circulation problems or a
weakened immune system.
Diagnosis
To avoid misdiagnosis as nail psoriasis, lichen planus, contact
dermatitis, trauma, nail bed tumor or yellow nail syndrome, laboratory
confirmation may be necessary. Three main approaches are potassium
hydroxide smear, culture and histology. This involves microscopic
examination and culture of nail scrapings or clippings. Recent results
indicate the most sensitive diagnostic approaches are direct smear
combined with histological examination, and nail plate biopsy using a
periodic acid-Schiff stain. To identify reliably nondermatophyte
molds, several samples may be necessary.
Treatment
Treatment of onychomycosis is challenging because the infection
is embedded within the nail and is difficult to reach; full removal of
symptoms is slow and may take a year or more.
Most treatments are either systemic antifungal medications, such
as terbinafine and itraconazole, or topical such as nail paints
containing ciclopirox or amorolfine. There is evidence that combining
systemic and topical treatments are beneficial.
For superficial white onychomycosis, systemic rather than topical
antifungal therapy is advised.
Ciclopiroxolamine and butenafine are both effective, but both
210
need to be applied daily for prolonged periods (at least 1 year).
In systemic therapy, terbinafine is more effective than
itraconazole and griseofulvin. The use of terbinafine in combination
with a topical treatment increases the clinical efficacy of treatment.

Unit 5
Candidiasis
Candidiasis or thrush is a fungal infection (mycosis) of any of the
Candida species (all yeasts), of which Candida albicans is the most
common.
Candidiasis encompasses infections that range from superficial,
such as oral thrush and vaginitis, to systemic and potentially life-
threatening diseases. Candida infections of the latter category are also
referred to as candidemia and are usually confined to severely
immunocompromised persons, such as cancer, transplant, and AIDS
patients.
Superficial infections of the skin and mucosal membranes by
Candida causing local inflammation and discomfort are common in
many human populations. While clearly attributable to the presence of
the opportunistic pathogens of the genus Candida, candidiasis includes
a number of different disease syndromes that often differ in their
causes and outcomes.
Classification
Candidiasis may be divided into the following types:
x Oral candidiasis (Thrush)
x Perlèche (Angular cheilitis)
x Candidal vulvovaginitis (vaginal yeast infection)
x Candidal intertrigo
x Diaper candidiasis
x Congenital cutaneous candidiasis
x Perianal candidiasis
x Candidal paronychia
x Erosio interdigitalis blastomycetica
x Chronic mucocutaneous candidiasis
x Systemic candidiasis
x Candidid.
x Antibiotic candidiasis (Iatrogenic candidiasis)

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 Clinical presentation
Most candidial infections are treatable and result in minimal
complications such as redness, itching and discomfort, though
complication may be severe or fatal if left untreated in certain
populations. In immunocompetent persons, candidiasis is usually a
very localized infection of the skin or mucosal membranes, including
the oral cavity (thrush), the pharynx or esophagus, the gastrointestinal
tract, the urinary bladder, or the genitalia (vagina, penis).
Candidiasis is a very common cause of vaginal irritation, or
vaginitis, and can also occur on the male genitals. In
immunocompromised patients, Candida infections can affect the
esophagus with the potential of becoming systemic, causing a much
more serious condition, a fungemia called candidemia.
Thrush is commonly seen in infants. It is not considered abnormal
in infants unless it lasts longer than a couple of weeks.
Children, mostly between the ages of three and nine years of age,
can be affected by chronic mouth yeast infections, normally seen
around the mouth as white patches. However, this is not a common
condition.
Symptoms of candidiasis may vary depending on the area
affected. The infection of the vagina or vulva may cause severe
itching, burning, soreness, irritation, and a whitish or whitish-gray
cottage cheese-like discharge, often with a curd-like appearance.
These symptoms are also present in more common bacterial vaginosis.
The symptoms of the male genitalia infection include red patchy sores
near the head of the penis or on the foreskin, severe itching, or a
burning sensation. Candidiasis of the penis can also have a white
discharge, although uncommon.
Causes
Candida yeasts are commonly present in humans, and their
growth is normally limited by the human immune system and by other
microorganisms, such as bacteria occupying the same locations in the
human body.
C. albicans was isolated from the vaginas of 19% of apparently
healthy women, i.e., those that experienced few or no symptoms of the
infection. External use of detergents or douches or internal
disturbances (hormonal or physiological) can perturb the normal
vaginal flora, consisting of lactic acid bacteria, such as lactobacilli,
and result in an overgrowth of Candida cells causing symptoms of the
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infection, such as a local inflammation. Pregnancy and the use of oral
contraceptives have been reported as risk factors. Diabetes mellitus
and the use of anti-bacterial antibiotics are also linked to an increased
incidence of yeast infections. Diet high in simple carbohydrates has
been found to affect rates of oral candidiases, and hormone
replacement therapy and infertility treatments may also be
predisposing factors. Wearing wet swimwear for long periods of time
is also believed to be a risk factor.
A weakened or undeveloped immune system or metabolic
illnesses such as diabetes are significant predisposing factors of
candidiasis. The diseases or conditions linked to candidiasis include
HIV/AIDS, mononucleosis, cancer treatments, steroids, stress, and
nutrient deficiency. Almost 15% of people with weakened immune
systems develop a systemic illness caused by Candida species. In
extreme cases, these superficial infections of the skin or mucous
membranes may enter into the bloodstream and cause systemic
Candida infections.
Candida species are frequently part of the human body's normal
oral and intestinal flora. Treatment with antibiotics can lead to
eliminating the yeast's natural competitors for resources, and increase
the severity of the condition. Higher prevalence of colonization of C.
albicans was reported in young individuals with tongue piercing, in
comparison to non-tongue-pierced matched individuals.
Diagnosis
Diagnosis of a yeast infection is made either via microscopic
examination or culturing.
For identification by light microscopy, a scraping or swab of the
affected area is placed on a microscope slide. A single drop of 10%
potassium hydroxide (KOH) solution is then added to the specimen.
The KOH dissolves the skin cells but leaves the Candida cells intact,
permitting visualization of pseudohyphae and budding yeast cells
typical of many Candida species. For the culturing method, a sterile
swab is rubbed on the infected skin surface. The swab is then streaked
on a culture medium. The culture is incubated at 37 °C for several
days, to allow development of yeast or bacterial colonies. The
characteristics (such as morphology and colour) of the colonies may
allow initial diagnosis of the organism that is causing disease
symptoms.

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 Treatment
In clinical settings, candidiasis is commonly treated with
antimycotics-the antifungal drugs commonly used to treat candidiasis
are topical clotrimazole, topical nystatin, fluconazole, and topical
ketoconazole. A single dose of fluconazole (150 mg tablet, taken
orally) is effective in 90% of cases in the treatment of vaginal yeast
infection. In severe infections amphotericin B, caspofungin, or
voriconazole may be used. A local treatment may include vaginal
suppositories or medicated douches. Gentian violet can be used for
breastfeeding thrush, but when used in large quantities it can cause
mouth and throat ulcerations in nursing babies, and has been linked to
mouth cancer in humans. Chlorhexidine gluconate oral rinse is not
recommended to treat candidiasis but is effective as prophylaxis;
chlorine dioxide rinse was found to have similar in vitro effectiveness
against candida.

Checkup Questions
1. What are the causes of tinea corporis?
2. What symptoms are characteristic of tinea corporis?
3. How is tinea capitis transmitted?
4. What clinical types of tinea capitis exist?
5. What methods are used to diagnose tinea capitis?
6. What clinical manifestations are characteristic of tinea pedis?
7. How is onychomycosis treated?
8. What is a causative agent of candidiasis?

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CHAPTER XVII
ALLERGIC VASCULITIS AND
REACTIVE ERYTHEMAS
Allergic vasculitis is an extreme reaction to a drug, infection, or
foreign substance that leads to inflammation and damage to blood
vessels of the skin.
Vasculitis refers to a heterogeneous group of disorders that are
characterized by inflammatory destruction of blood vessels. Both
arteries and veins are affected. Lymphangitis is sometimes considered
a type of vasculitis. Vasculitis is primarily due to leukocyte migration
and a resultant damage.
Classification
There are many ways to classify vasculitis.
It can be classified by an underlying cause. For example, the
cause of syphilitic aortitis is infectious (aortitis simply refers to
arteritis of the aorta, which is an artery.) However, the cause of many
forms of vasculitis is poorly understood. There is usually an immune
component, but the trigger is often not identified. In these cases, the
antibody found is sometimes used in classification, as in ANCA-
associated vasculitis.
It can be classified by the location of the affected vessels. For
example, ICD-10 classifies "vasculitis limited to skin" with skin
conditions using with letter "L", and "necrotizing vasculopathies" with
musculoskeletal system and connective tissue conditions (under) letter
"M". Arteritis/phlebitis on their own are classified with circulatory
conditions (under "I").
Vasculitis can be classified by the type or size of the blood
vessels that predominantly affect. Apart from the arteritis/phlebitis
distinction mentioned above, vasculitis is often classified by the
caliber of the vessel affected. However, there can be some variations
in the size of the vessels affected.
According to the size of the vessel affected, vasculitis can be
classified as:
x When large vessels affected – Behçet's syndrome, giant cell
215
arteritis, polymyalgia rheumatica, Takayasu's arteritis;
x When medium vessels affected – cutaneous vasculitis,
polyarteritis nodosa, Kawasaki disease, Berger disease;
x When small vessels affected – Churg-Strauss syndrome,
cutaneous vasculitis, Henoch-Schönlein purpura, microscopic
polyangiitis, Wegener's granulomatosis.

Unit 1
Erythema nodosum
Erythema nodosum (red nodules) is an inflammation of the fat
cells under the skin (panniculitis) characterized by tender red nodules
or lumps that are usually seen on both shins. Erythema nodosum is an
immunologic response to a variety of different causes.
Epidemiology
Erythema nodosum is the most common form of panniculitis
(inflammation of the subcutaneous fat). The peak incidence of
erythema nodosum occurs between 18–36 years of age. Women are 3-
6 times more affected than men.
Classification
Erythema nodosum may be divided into the following types:
x Acute erythema nodosum
x Chronic erythema nodosum
Clinical Presentation
Erythema nodosum usually resolves itself 3–6 weeks after
occurrence on either the internal or external surfaces of the body, that
initiates a hypersensitivity reaction in subcutaneous fat. Erythema
nodosum is frequently associated with fever, malaise, joint pain and
inflammation. It presents as tender red nodules on the shins which are
smooth and shiny. The nodules may occur anywhere where there is fat
under the skin, including the thighs, arms, trunk, face, and neck. The
nodules are 1–10 cm in diameter, and individual nodules may coalesce
to form large areas of hardened skin.
As the nodules age, they become bluish purple, brownish,
yellowish, and finally green, similar to the color changes that occur in
a resolving bruise. The nodules usually subside over a period of 2–6
weeks without ulceration or scarring.
Causes
In about 30-50% of cases, the cause of erythema nodosum is
216
unknown. Erythema nodosum may be associated with a wide variety
of diseases, including infections (e.g., hepatitis C, tuberculosis,
streptococcal, Mycoplasma pneumoniae, Yersinia, and Epstein-Barr
virus), Coccidioides immitis, sarcoidosis, autoimmune disorders (e.g.,
inflammatory bowel disease or Behçet's disease), pregnancy,
medications (sulfonamides, oral contraceptives, bromides),
vaccinations, and cancer. Erythema nodosum may also be due to
excessive antibody production in lepromatous leprosy leading to
deposition of immune complexes. There is an association with the
HLA-B27 histocompatibility antigen, which is present in 65% of
patients with erythema nodosum.
Diagnosis
Diagnosis is clinical. A deep punch biopsy or an incisional biopsy
may be performed in cases when the diagnosis is unclear. A
microscopic examination will reveal a septal panniculitis with acute
and chronic inflammation in the fat and around blood vessels.
Once erythema nodosum is diagnosed, additional evaluation is
required to be performed for determination of an underlying cause. A
complete blood count, erythrocyte sedimentation rate (ESR),
antistreptolysin-O (ASO) titer, urinalysis, throat culture, intradermal
tuberculin test, and chest x-ray are part of the initial examination.
The ESR is initially very high, and falls as the nodules fade. The
ASO titer is high in cases associated with a streptococcal throat
infection. A chest X-ray should be performed to rule out pulmonary
diseases. Hilar lymphadenopathy may be due to tuberculosis,
sarcoidosis, or Löfgren syndrome (a form of acute sarcoidosis with
erythema nodosum, bilateral hilar adenopathy, fever which is often
accompanied by joint symptoms).
Treatment
Erythema nodosum is self limiting and usually resolves itself within
3–6 weeks. A recurring form does exist, and in children it is attributed to
repeated infections due to streptococcus. Treatment should focus on the
underlying cause. Symptoms can be treated with bed regimen, leg
elevation, compressive bandages, wet dressings, and nonsteroidal anti-
inflammatory agents (NSAIDs). NSAIDs are usually more effective at
the onset of erythema nodosum versus with a chronic disease.
Potassium iodide can be used for persistent lesions whose cause
remains unknown. Corticosteroids and colchicine can be used in
severe refractory cases.
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 Unit 2
Henoch-Schonlein purpura
Henoch–Schönlein purpura (HSP, also known as anaphylactoid
purpura, purpura rheumatica, and Schönlein–Henoch purpura) is a
disease of the skin and other organs that most commonly affects
children. In the skin, the disease causes palpable purpura (small
hemorrhages), often with joint and abdominal pain. When kidney
involved, there may be a loss of small amounts of blood and protein in
the urine, but this usually goes unnoticed; in a small proportion of
cases, the kidney involvement proceeds to chronic kidney disease.
HSP is often preceded by an infection, such as pharyngitis.
HSP is a systemic vasculitis (inflammation of blood vessels) and
is characterized by deposition of immune complexes containing the
antibody IgA; the exact cause for this phenomenon is unknown. It
usually resolves within several weeks and requires no treatment apart
from the symptom control, but may relapse in a third of the cases and
cause irreversible kidney damage in about one in a hundred cases.
Multiple standards exist for defining Henoch–Schönlein purpura,
including the American College of Rheumatology (ACR)
classification (in1990) and the Chapel Hill Consensus Conference
(CHCC) in 1994. Some investigators have reported the ACR criteria
to be more sensitive than those of CHCC.
More recent classifications, the European League Against
Rheumatism (EULAR, 2006) and Pediatric Rheumatology Society
(PReS) classification, include palpable purpura as a mandatory
criterion, together with at least one of the following findings: a diffuse
abdominal pain, predominant IgA deposition (confirmed by skin
biopsy), acute arthritis in any joint, and renal involvement (as
evidenced by the presence of blood and/or protein in the urine).
Pathophysiology
Henoch-Schönlein purpura is a small-vessel vasculitis in which
complexes of immunoglobulin A (IgA) and complement component
3 (C3) are deposited on arterioles, capillaries, and venules. As with
IgA nephropathy, serum levels of IgA are high in HSP and there are
identical findings on renal biopsy; however, IgA nephropathy has
predilection for young adults while HSP is more predominant
among children. Further, IgA nephropathy typically affects only the
kidneys while HSP is a systemic disease. HSP involves the skin
218
and connective tissues, scrotum, joints, gastrointestinal tract and
kidneys.
Clinical Presentation
Purpura, arthritis and abdominal pain are known as a "classic
triad" of Henoch–Schönlein purpura. Purpura occurs in all cases,
joint pains and arthritis in 80%, and abdominal pain in 62%. Some
scholars include gastrointestinal hemorrhage as a fourth criterion;
this occurs in 33% of cases, sometimes, but not necessarily always,
due to intussusception. The purpura typically appears on the legs
and buttocks, but may also be seen on the arms, face and trunk. The
abdominal pain is colicky in character, and may be accompanied by
nausea, vomiting, constipation or diarrhea. There may be blood or
mucus in the stools. The joints involved tend to be ankles, knees,
and elbows, but arthritis in the hands and feet is possible; arthritis
is nonerosive and hence causes no permanent deformity. Forty
percent have evidence of kidney involvement, mainly in the form of
hematuria (blood in the urine), but only a quarter will have this in
sufficient quantities to be noticeable without laboratory tests.
Problems in other organs, such as the central nervous system (brain
and spinal cord) and lungs may occur, but is much less common
than in the skin, bowel and kidneys.
Of the 40% of patients who develop kidney involvement,
almost all have evidence (visible or in urinalysis) of blood in the
urine. More than half also have proteinuria (protein in the urine),
which is severe enough to cause a nephrotic syndrome (generalized
swelling due to low protein content of the blood) in one eighth of
the patients. While abnormalities in urinalysis may continue for a
long time, only 1% of all HSP patients develop a chronic kidney
disease. Hypertension (high blood pressure) may develop. Protein
loss and high blood pressure, as well as the signs on biopsy of the
kidney if performed, may predict progression of an advanced kidney
disease. Adults are more likely than children to develop an
advanced kidney disease.
Diagnosis
The diagnosis is based on the combination of the symptoms, as
very few other diseases cause the same symptoms together. Blood
tests may show elevated creatinine and urea levels (in kidney
involvement), raised IgA levels (in about 50%), and raised CRP or
erythrocyte sedimentation rate (ESR) results; none are specific for
219
Henoch–Schönlein purpura. The platelet count may be raised, and
distinguishes it from the diseases where low platelets are the cause
of purpura, such as idiopathic thrombocytopenic purpura and
thrombotic thrombocytopenic purpura.
If there is a doubt about the cause of the skin lesions, a biopsy
of the skin may be performed to distinguish the purpura from other
diseases that cause it, such as vasculitis due to cryoglobulinemia; on
microscopy there are the signs of a hypersensitivity vasculitis, and
immunofluorescence demonstrates IgA and C3 (a protein of the
complement system) in the blood vessel wall. However, overall
serum complement levels are normal.
Biopsy of the kidney may be performed both to establish the
diagnosis and to assess the severity of already suspected kidney
disease. The main findings on kidney biopsy are enlarged cells and
Ig deposition in the mesangium (part of the glomerulus, where
blood is filtered), white blood cells, and the development of
crescents. The changes are indistinguishable from those observed in
IgA nephropathy.
HSP can develop after infections caused by streptococci (β-
haemolytic, Lancefield group A) hepatitis B virus, herpes simplex
virus, parvovirus B19, Coxsackievirus, adenovirus, Helicobacter
pylori, measles, mumps, rubella, Mycoplasma and numerous others.
Drugs linked to HSP, usually as an idiosyncratic reaction, include
antibiotics (vancomycin and cefuroxime), ACE inhibitors (enalapril
and captopril), anti-inflammatory agent (diclofenac), as well as
ranitidine and streptokinase. Only in about 35% of cases HSP can be
traced due to any of these causes.
The exact cause of HSP is unknown, but most of its features are
due to the deposition of abnormal antibodies, leading to vasculitis,
in the wall of blood vessels. These antibodies are of the subclass
IgA1 in polymers; it is uncertain whether the main cause is
overproduction (in the digestive tract or the bone marrow) or
decreased removal of abnormal IgA from the circulation. It is
suspected that abnormalities in the IgA1 molecule may provide an
explanation for its abnormal behaviour in both HSP and the related
condition IgA nephropathy. One of the characteristics of IgA1 (and
IgD) is the presence of an 18 amino acid-long "hinge region"
between complement-fixating regions 1 and 2. Among the amino
acids, a half is proline, while the others are mainly serine and
220
threonine. The majority of the serines and the threonines have
elaborate sugar chains, connected through oxygen atoms
(O-glycosylation). This process is thought to stabilize the IgA
molecule and make it less prone to proteolysis. The first sugar is
always N-acetyl-galactosamine (GalNAc), followed by other
galactoses and sialic acid. In HSP and IgAN, these sugar chains
appear to be deficient. The exact reason for these abnormalities is not
known.
Treatment
Pain killers may be required for the abdominal and joint pains. It
is uncertain whether HSP needs treatment beyond controlling the
symptoms. Most patients do not receive therapy because of a high
spontaneous recovery rate. Steroids are generally avoided. However,
if they are given in the early stage of the disease, the duration of
symptoms may be shortened, and abdominal pain can improve
significantly. Moreover, the threat of severe kidney problems is
reduced.
Treatment may be indicated on the basis of the appearance of the
biopsy sample; various treatments may be used, ranging from the use
of oral steroids to a combination of intravenous methylprednisolone
(steroid), cyclophosphamide and dipyridamole followed by
prednisone. Other regimens include steroids/azathioprine, and
steroids/cyclophosphamide (with or without heparin and warfarin).
Intravenous immunoglobulin (IVIG) is occasionally used.
Prognosis
Recovery and recurrence
Overall prognosis is good in most patients, with one study
showing recovery occurring in 94% and 89% of children and adults,
respectively (some having needed treatment).
In children under ten, the condition recurs in about a third of all
cases and usually within the first four months after an initial attack.
Recurrence is more common in older children and adults.

Checkup Questions
1. What is allergic vasculitis?
2. What criterion is used to classify vasculitis?
3. What forms of erythema nodozum exist?
4. What clinical manifestations are typical of erythema
nodosum?
221
 5. What causes may lead to the development of erythema
nodozum?
6. What methods of diagnosis are used to define erythema
nodozum?
7. How is erythema nodozum treated?
8. What are the causes of Henoch–Schönlein purpura?
9. How does it develop?
10. What clinical manifestations does Henoch–Schönlein purpura
have?

222
CHAPTER XVIII
SKIN TUMOURS
Unit 1
Actinic Keratosis
The term actinic (solar) keratosis (AK) was coined in 1958 and
means literally thickened scaly growth (keratosis) caused by sunlight
(actinic).
Actinic keratosis is an extremely common disorder, with a small
malignant potential. AK is seen in fair-skinned persons in areas of
long-term sun exposure, like Australia, where about half of the
population over the age of 40 years are affected. Although the
condition is very similar to Bowen's disease or carcinoma in situ, most
lesions do not progress to malignant change. However, recognition
and simple treatment help to prevent progression.
Pathophysiology
Cells within actinic keratoses (AKs) show characteristic UV-
induced gene mutations. Histologically AKs share features with
squamous cell carcinoma (SCC). AK is an epidermal lesion
characterized by collections of atypical, pleomorphic keratinocytes in
the basal layer which can extend to the upper granular and cornified
layers.
The epidermis is abnormal in architecture, with acanthosis,
parakeratosis, and dyskeratoses. Cellular atypia is present with
keratinocytes varying in size and shape. Mitotic figures are present as
well.
It has some features of Bowen's disease or carcinoma in situ:
x They can be distinguished more by the degree of cellular
change and the extent of the lesions rather than differences in the
features of individual cells.
x Often, marked hyperkeratosis and areas of parakeratosis with
loss of the granular layer are present.
x A dense inflammatory infiltrate is usually present.
AK is considered by some to be the earliest manifestation of SCC
and should be regarded as such rather than as a precancerous lesion.

223
 Epidemiology
Actinic keratosis (AK) is most common in people with fair skin at
a rate corresponding to the total exposure to ultraviolet radiation.
Frequency increases according to a number of risk factors:
x Increasing age, as the dose of UV is cumulative.
x Proximity to the equator as this affects UV dosage and
cumulative exposure.
x Lifestyle and time spent outdoors. Outdoor lifestyles, whether
with work or recreation and sport, will increase risk.
x Other specific practices such as use of tanning booths.
Artificial sunlight is a risk factor and may produce lesions in unusual
places.
Skin is graded from Fitzpatrick type I to VI according to
sensitivity to sunlight, as displayed by a tendency to burn or to tan.
These lesions are almost entirely confined to fair skin types I and II.
Patients who are immunosuppressed following organ
transplantation have a markedly increased risk of developing AKs and
of developing malignant change in AKs.
AKs are more common in men than in women. Traditionally men
are more likely due to work and recreational activities to spend time
outdoors. AK has also been associated with a high-fat diet. They tend
to present at the age from 30 to 60 years but can present earlier or
later.
Clinical Presentation
Lesions occur in fair-skinned people in parts of the body exposed
to long-term sun exposure, such as the head area (face, ears and
scalp), forearms, and backs of the hands. Other areas repeatedly
exposed to the sun include the back, chest, and legs.
The first lesion is usually a single plaque on the face in the 20s or
30s but, with time and further exposure to strong sunlight, they tend to
progress on the nose, forehead and cheeks.
Actinic keratoses (AKs) begin as small rough spots. Over several
years, lesions enlarge, often becoming red and scaly. From small 3-10
mm lesions they can enlarge to several centimeters.
Variations of them include brown (pigmented AK), lichen planus-
like areas, and exaggerated hyperkeratosis (the hornlike projection
known as a cutaneous horn for example).
They flare and become more erythematous when immunity is
suppressed. This may be in a systemic disease or its treatment, such as
224
chemotherapy for malignancy, but it can also be the result of much
UV light.
As the years pass, and especially with continued exposure to
strong sunlight, about 10% patients will undergo malignant change.
This is more likely in those who are erythematous, elevated and
indurated. It may be necessary to remove the layer of keratin to see
this.
Clinical Forms
The most frequently misdiagnosed variant is an almost flat,
erythematous or telangiectatic type which may be mildly scaly and
rather diffuse. This is most frequently found on the forehead or temple
skin, and is often incorrectly diagnosed as eczema.
Hypertrophic actinic keratoses, which have a thickened, fleshy
base, cause concern as they resemble a slowly growing squamous cell
carcinoma. These often have a large and firmly adherent horn arising
from the fleshy base.
The risk of squamous cell carcinoma arising from actinic
keratoses is uncertain, as it is impossible in retrospect to know
whether a precursor keratosis was actually a small squamous cell
carcinoma or an actinic keratosis, but the risk of transformation is
probably in about 1:500 to 1:1000.
Pigmented actinic keratoses are uncommon, and may resemble
seborrheic keratoses or even malignant melanoma. Extensive diffuse
actinic keratoses may occur, often with a history of extensive use of
tanning sunbeds, and are often very itchy and confused with eczema.
Actinic cheilitis
This is a variant of actinic keratosis which usually affects the
more sun-exposed lower lip.
Diagnosis
This is made according to clinical features. Skin biopsy is used
where there are features which are at a high risk for malignant change.
The roughness is more easily felt than seen, and occurs on the
sites which have had a considerable exposure to the sun, such as a
bald scalp, face, dorsum of the hands, and the lower legs.
There must be signs of a solar damage such as solar elastosis
shown by yellow thickening of the skin with increased wrinkles.
Seborrheic warts are not so rough and keratin is more easily
picked off.
Squamous cell carcinomas (SCCs) may arise from solar keratosis
225
but, under the keratin surface there is a feeling that the dermis has
been infiltrated.
Differential Diagnosis
Basal cell carcinoma (BCC) and squamous cell carcinomas (SCC)
are indurated nodular lesions reflecting more rapid growth and tend to
be eroded or ulcerated on the surface. They must be differentiated
with some similar diseases.
Seborrheic keratosis produces greasy, brown crusts with sharply
demarcated borders and a non-erythematous base. They may occur in
the areas that are not exposed to the sun.
Bowen's disease (tends to be a large plaque with a sharp outline).
Discoid lupus erythematosus shows abnormal pigmentation,
dilated follicles and atrophy.
Investigations
No specific investigations are required unless there is suspicion
that the lesion may be malignant, when biopsy is needed.
This includes:
x Lesions with pronounced hyperkeratosis, increased erythema,
or induration;
x Lesions that recur;
x Lesions which are unresponsive to treatment;
x Large confluent lesions;
x Lesions in transplant recipients;
x Lesions in patients with a history of squamous cell carcinoma
(SCC).
Treatment
Many options are open to patients with actinic keratoses (AKs).
Prevention of SCC is the main reason for therapy.
Treatment options for actinic keratosis:
The first part of management is education of the patient about the
nature of the lesion and the need to avoid excessive exposure to
sunlight. Both sunscreens and protective clothing should be worn. No
therapy or emollient acceptable for mild AKs.
Topical treatments:
Sunblock applied twice daily for 7 months may prevent
development of AKs.
Topical 5-fluorouracil (5-FU) can be used. The 5% cream is
applied twice daily for 3 to 4 weeks for facial lesions but lesions on

226
the other parts of the body need 6 to 8 weeks.
Other treatments:
x Cryosurgery
x Photodynamic therapy (PDT)
x Curettage or excisional surgery
x Cryotherapy with liquid nitrogen
x Dermabrasion and chemical peels
x Systemic retinoids in very high-risk patients, such as transplant
patients, may be justified.
PDT is another treatment option. Topical 5-aminolevulinic acid
accumulates preferentially in the dysplastic cells. Exposure to
irradiation with light of an appropriate wavelength generates oxygen
free radicals that kill the cells. There is pain in the areas treated,
similar to that from topical 5-FU. One treatment with PDT appears to
be as effective as 5-FU and may be considered in patients with contact
sensitivity to 5-FU. The cosmetic result can be better and patients
prefer it.
Complications
The most important complication is progression to a malignant
change.
Prognosis
Progression to squamous cell carcinoma (SCC) occurs slowly and
affects about 10% of sick people. When it does undergo malignant
change it tends to be of low aggression and distant metastases are rare.

Unit 2
Keratoacanthoma
Keratoacanthoma (KA) is a rapidly growing tumor that eventually
involutes, and may be a self-healing variant of SCC. Keratoacanthoma
may serve as a marker for an important autosomal dominant familial
cancer syndrome, the Muir-Torre syndrome. It is a pseudo-
carcinomatous hyperplasia, sort of transition between benign keratosis
and definite epitelioma.
Etiology
The etiology is as for SCC.
Risk Factors
x Sunlight and chemical carcinogens have been implicated.
x Trauma, genetic factors and immunocompromised status have
227
 also been associated.
x Industrial workers exposed to pitch and tar have a higher
incidence of both keratoacanthoma and SCC.
Epidemiology
x Incidence is estimated as1:1,000.
x Peak incidence occurs in those aged over 60 years. It is rare in
young adults.
x It is uncommon in darker-skinned patients.
x Males are twice as often affected as females.
x Epidemiological data are similar to squamous cell carcinoma
(SCC) and Bowen's disease in terms of age, sex and the site of lesions.
Clinical Presentation
x Typically rapid growth persists over a few weeks to months
followed by a slow spontaneous resolution over 4-6 months (but it
may take up to 1 year).
x Most growths occur on the sun-exposed areas, i.e. the face,
neck, and dorsum of hands and forearms.
x They are usually solitary and begin as firm, round, skin-colored
or reddish papules that rapidly progress to dome-shaped nodules with
a smooth shiny surface. A central crater of ulceration may develop, or
keratin plaques that may project like a horn.
x It leaves a residual scar if not excised.
x Occasionally it presents as multiple tumors and may enlarge up
to 15 cm, become locally aggressive and metastatic.
Differential Diagnosis:
x Squamous cell carcinoma (SCC)
x Basal cell carcinoma
x Actinic keratosis
x Seborrheic keratosis
Investigations
x Shave biopsy of keratoacanthoma is indistinguishable from an
invasive squamous cell carcinoma (SCC). Therefore, excisional or
deep incisional biopsy is required.
Treatment
x Complete excision is the treatment of choice for all the skin
neoplasms thought to be keratoacanthoma.
x Medical treatment continues when surgical intervention is not
possible, e.g. multiple lesions are not amenable to surgery because of
228
their size or location.
x Treatments that have produced certain effect include
administration of systemic retinoids (e.g. isotretinoin, intralesional
methotrexate and 5- fluorouracil).
x As keratoacanthomas are radiosensitive and respond well to
low doses of radiation, radiation therapy may be useful in selected
patients with large tumors when resection will result in a cosmetic
deformity, or for tumors that have recurred following attempted
excision.
x Both laser therapy and cryotherapy have been used successfully
in small keratoacanthomas.
Complications
Progress to invasive or metastatic carcinoma, although rarely is
reported.
Prognosis
Prognosis is excellent following excisional surgery.

Unit 3
Bowen's Disease
Intraepidermal squamous cell carcinoma (intraepidermal SCC)
is often known as Bowen’s disease or cutaneous squamous cell
carcinoma in situ. It was first described by John Bowen in 1912.
In the past it has been thought of as indicative of an underlying
malignancy but more recent surveys of better methodology have
suggested that it is not a paraneoplastic disease.
Epidemiology
When associated with sunlight, the risk is much higher in white
races. Some sources state that there is no difference in incidence
between the genders whilst others state that it is 3 times as common in
women as in men. It tends to appear at the age of 60 to 70.
Risk Factors
x Exposure to sunlight (especially with fair skin) is a strong risk
factor.
x Exposure to inorganic arsenic is less important than it was.
Arsenic used to be found in Fowler's solution – applied to treat
psoriasis, in Gay's solution – administered to treat asthma, in water
from a contaminated well and in some pesticides.
x Ionizing radiation: intraepidermal SCC was common on the
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hands of radiologists early in the 20th century.
x Viral infection has been implicated, particularly human
papillomavirus (usually HPV-16 but more rarely HPV-2).
x Suppression of the immune system appears to be a risk.
Malignant and premalignant skin tumors are more common in patients
who have received organ transplants. The risk is higher for heart
recipients than for kidney recipients, perhaps as they are more
strongly immunosuppressed. The literature also contains a number of
reports on Bowen's disease, quite often extensive, in patients with HIV
infection.
Clinical Presentation
It presents as a slowly growing erythematous patch or plaque. It is
sharply demarcated, scaling or hyperkeratotic with a pink or red
surface. There may be small erosion or it may be crusted.
Lesions are usually asymptomatic but can bleed. There may be a
solitary lesion or multiple lesions. Two thirds are solitary.
They are often found on the sites exposed to the sun and are most
common on the head and neck, then on the limbs; however, they may
occur elsewhere – for example, as a disorder of the vulva. When it
arises on the glans penis, it is referred to as Queyrat's erythroplasia.
They vary in size from a few millimeters to a few centimeters. They
are rarely pigmented. Diagnosis is often delayed, as it is asymptomatic
and may appear similar to benign skin lesions.
Differential diagnosis
A characteristic feature is that it is well demarcated.
x Discoid eczema, other forms of eczema
x Psoriasis
x Lichen planus
x Seborrhoeic (solar) keratosis
x Superficial basal cell carcinoma
x Malignant melanoma
x Mammary Paget's disease
Investigations
A shave or punch biopsy is required for histological diagnosis.
Where it is possible, include a hair follicle in biopsy.
Treatments
Pharmacological
Topical 5-fluorouracil cream may be used. It may be preceded by
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keratolytic therapy or cryotherapy. It can be used under occlusion or
with ionophoresis, where an electrical current drives it into the tissues.
Imiquimod 5% cream appears to be an effective treatment for
Bowen's disease on the lower limbs.
Photodynamic therapy
Radiological
Superficial X-ray treatment may be best for patients unsuitable
for surgery, especially with multiple lesions.
Surgical
Cautery, curettage and cryotherapy may be satisfactory but they
do not give histological diagnostic findings and may fail to reach all
the affected tissue.
Surgical excision is usually satisfactory for small lesions but not
on the face or the digits. Although the lesion looks clearly demarcated
it may extend beyond the apparent boundary and so at least 5 mm of
clearance should be allowed.
Prognosis
This is excellent, especially with treatment. Untreated, 3 to 5%
progress to invasive squamous cell carcinoma, but metastases are rare.

Unit 4
Sebaceous Naevus
Nevus sebaceous, also known as nevus sebaceous of Jadassohn, a
hamartoma of the skin and its adnexa, is characterized by epidermal,
follicular, sebaceous, and apocrine gland abnormalities.
Epidemiology
Nevus sebaceous occurs in approximately 0.3% of all newborn
infants. Both sexes are equally affected. There is no racial and/or
ethnic predominance. Recent studies suggest a possible link with
mothers positive for human papillomavirus. The occurrence of the
nevus is usually sporadic, although familial cases have rarely been
reported. An autosomal dominant mode of inheritance has also been
described.
Histopathology
The early infantile stage is characterized by papillomatous
epithelial hyperplasia. The epidermis is only slightly acanthotic. The
hair follicles are underdeveloped and the sebaceous glands are not
prominent. Apocrine glands are rarely seen. During puberty,

231
sebaceous glands become numerous and hyperplastic, apocrine glands
become hyperplastic and cystic, and the epidermis becomes verrucous.
The hair follicles remain small and primordial and may disappear
altogether. During adulthood, epidermal hyperplasia, large sebaceous
glands, and ectopic apocrine glands are characteristic histological
findings. Normal hair follicles are characteristically absent. This stage
is also distinguished by the potential development of a variety of
adnexal tumors.
Clinical Presentation
Approximately two thirds of cases are present at birth and the rest
develop in early childhood. At birth, nevus sebaceous typically
presents as a solitary, well-circumscribed, smooth to velvety, yellow
to orange, round, oval, or linear, flat or minimally raised, plaque.
Lesions on the scalp are typically hairless. The lesions are often
distributed along Blaschko’s lines and are arrayed in a linear
configuration. This may be difficult to appreciate if the lesion is small.
The scalp and face are sites of predilection, although the trunk and
extremities may also be affected. Rare intraoral extension may present
as a linear whitish plaque. Characteristically, the lesion grows
proportionally with the size of the patient until puberty.
Diagnostics
The diagnosis is usually based on clinical manifestations. In some
cases, a biopsy is required.
Treatment
Excision of the lesion may be considered at any age for cosmetic
reasons. Ablative laser and photodynamic therapy may be supposed
for the occasional cases with inoperable lesions.

Unit 5
Malignant melanoma
Normal melanocytes are found in the basal layer of the epidermis.
Melanocytes are found in equal numbers in black and in white skin,
but the melanocytes in black skin produce much more melanin. People
with dark brown or black skin are very much less likely to be
damaged by ultraviolet (UV) radiation than those with white skin.
Non-cancerous growth of melanocytes results in moles (benign
melanocytic naevi) and freckles (ephelides and lentigines).
Most skin melanomas spread out within the epidermis. If all the

232
melanoma cells are confined to the epidermis then the lesion is a
melanoma in situ, which can be cured by excision because it has no
potential to spread around the body. When the cancer has grown
through the dermis it is known as invasive melanoma. Four clinical
types of skin melanoma exist.
Lentigo maligna melanoma is located where a patch of lentigo
maligna develops a papule or nodule, signaling an invasive tumor.
Superficial melanoma is a large flat irregularly pigmented lesion
which grows laterally before vertical invasion develops.
Nodular melanoma is the most aggressive type. It presents as a
rapidly growing pigmented nodule which bleeds or ulcerates. Rarely,
they are amelanotic (non-pigmented) and can mimic pyogenic
granuloma.
Acral lentiginous malignant melanoma arises as pigmented
lesions on the palm, sole or under the nail and it usually manifests
late.
Once the melanoma cells have reached the dermis, they may
spread to other tissues via the lymphatic system to the local lymph
nodes or, via the bloodstream to the other organs. Metastases can
occur virtually anywhere and at any time. Common sites for
metastases are lymph nodes, liver, lungs, bone and brain.
A malignant melanoma is more common in women than men. A
malignant melanoma is much less common than non-melanoma skin
cancers (e.g. basal cell carcinoma, squamous cell carcinoma of skin).
A malignant melanoma is rare in children. The incidence of
melanoma increases with age in both men and women. The median
age of diagnosed melanoma in men is 62 years and in women – 60
years.
A superficial spreading melanoma (SSM) is the most common
subtype and occurs in approximately 70% of patients with a
melanoma. It is most common on the trunk in men and on the legs in
women. Most often, it presents in individuals aged 30-50 years.
A nodular melanoma represents 15-30% of all malignant
melanomas.
Risk factors are as follows:
x Previous personal primary invasive melanoma;
About 3 to 5% of all the patients with a malignant melanoma will
develop a further lesion or a different type of skin cancer.
Naevi are the most powerful predictor of the risk of melanoma.
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An individual with more than 100 common naevi or more than two
atypical naevi has a 5- to 20-fold increased risk of melanoma.
x Sun exposure;
The host response to UV radiation appears to be more important
than a dose of sun exposure.
x Past sunbed use, especially under the age of 30;
x Skin pigmentation i.e., having fair skin (skin type 1 or 2) with
a poor ability to tan, or a freckled complexion with or without red or
blond hair, doubles a person's risk of melanoma.
x Family history of melanoma and genetic factors
People with a first-degree relative with melanoma are at increased
risk of developing melanoma. 5-10% of individuals with melanoma
have a family history of melanoma. Patients with numerous atypical
lesions and a personal or family history of malignant melanoma are at
increased risk. They tend to develop the disease about 10 years earlier
than others and they have a greater risk of multiple lesions. In some
families with melanoma, susceptibility to some other cancers, such as
pancreas, brain and breast increases.
Skin manifestations that may indicate melanoma:
x A new mole appearing after the onset of puberty, which is
changing in shape, color or size;
x A long-standing mole which is changing in shape, color or size;
x Any mole which has three or more colors or has lost its
symmetry;
x A mole which is itching or bleeding;
x Any new persistent skin lesion, especially if growing, if it is
pigmented or vascular in appearance;
x A new pigmented line in a nail, especially where there is
associated damage to the nail;
x A lesion growing under a nail.
Primary investigation is visual inspection and taking specimen for
(removal) histological analysis where necessary. Diagnosis should be
based on a full thickness excisional biopsy. All pigmented lesions that
are not viewed as suspicious of melanoma but are excised should have
a lateral excision margin of 2 mm of clinically normal skin and cut to
include subcutaneous fat. All excised lesions should be sent for
histology. A dermatoscope can be used to examine skin lesions and
may make distinguishing benign from malignant pigmented lesions
234
more accurate.
Sentinel lymph node biopsy (SLNB), identifying and removing
the lymph node(s) immediately draining the area of the primary
tumour for histological analysis, provides prognostic information. An
SLNB for pathological staging is particularly important for primary
tumours greater than, or equal to, 1 mm depth.
Further investigations include CXR and liver ultrasound, or CT
scan of the chest, abdomen and pelvis.
Blood tests include FBC, LFTs and lactate dehydrogenase (LDH).
However, CXRs and LDH lack significant impact on early
detection of metastases and survival. They should therefore not be part
of a routine investigation and staging.
Bone scans should only be performed if there is indication of
bone disease.
Treatment
All patients with a suspicious pigmented skin lesion or a
malignant melanoma, or where the diagnosis is uncertain should be
referred to a doctor trained in the specialist diagnosis of skin
malignancy.
The primary treatment for malignant melanoma is wide local
excision. Re-excision should be performed for proven melanomas if
the margins are inadequate.
Completion lymphadenectomy (regional lymph nodes are
removed when a sentinel node biopsy is positive) has not been shown
to improve overall survival.
Chemotherapy has limited benefit and response rates are limited.
Dacarbazine remains the standard of care. It has a response rate of 5-
15% and improves progression-free survival by a few months at best.
Patients with elevated LDH are less likely to benefit from currently
available systemic treatment.
Radiotherapy has only a limited role in the management of
patients with melanoma but it may be useful and potentially curative
in some patients with lentigo maligna and is occasionally used in the
palliative treatment of symptomatic metastases, especially in brain and
bone.
For some patients with advanced disease, management may
consist entirely of supportive palliative care.
Prevention
Avoiding sunburn and excessive sun exposure without protection
235
seems to be the most important message in skin cancer prevention.
Current recommendations are that sunbed should be avoided,
especially in relation to premature skin ageing. Individuals with red
hair and freckles, or multiple atypical naevi, should avoid sunbeds
since their risks of developing both melanoma and non-melanoma
skin cancer is already significantly increased.
Secondary prevention with early detection of melanoma saves
lives. Educating the public and health professionals to recognize
melanoma early is crucial. Rapid referral for surgery and further
management are imperative to improve outcomes.
Individuals with multiple atypical naevi, a family history of
melanoma, and/or multiple cancers should be referred to a
dermatologist for screening, as their risk of melanoma is significantly
high.

Unit 6
Squamous Cell Carcinoma of the Skin
Primary cutaneous squamous cell carcinoma (SCC) is a malignant
tumor that arises from the keratinising cells of the epidermis or its
appendages. It is locally invasive and has the potential to metastases
across the other organs of the body.
Epidemiology
Skin cancers are the most common cancers diagnosed and
incidence is rising across the world despite the knowledge and
education about prevention.
Squamous cell carcinoma (SCC) is the second most common skin
cancer after basal cell carcinoma (BCC).
There is a rising incidence with age. Men are more commonly
affected, probably because of greater head and neck exposure to
ultraviolet radiation (UVR).
Risk Factors
Chronic UVR exposure is the most important risk factor. This
helps to explain very high rates of skin cancer in countries like
Australia, where fair-skinned, susceptible people are put at risk by sun
exposure. The rise in UVR exposure produces more cases of SCC in
populations in equatorial zones.
UV light as there is increased risk at resting in the sun, having
outdoor occupations and leisure pursuits, and using tanning beds.

236
 Susceptibility to UV light exposure i.e., having fair skin (skin that
tans poorly), blonde or red hair;
Chemical carcinogens: arsenic and chromium, soot, tar and pitch
oils;
Human papillomavirus infection;
Ionising radiation exposure;
Immunodeficiency;
Chronic inflammation around chronic ulcers, around chronic
sinuses (e.g. osteomyelitis), lupus vulgaris (chronic form of cutaneous
tuberculosis);
Genetic conditions, such as xeroderma pigmentosum and
albinism;
Pre-malignant conditions such as Bowen's disease and the areas
of the skin showing actinic damage;
Multiple actinic keratoses are associated with an estimated 10%
lifetime risk of skin cancer. Keratoacanthomas may rarely progress to
SCC.
Clinical Presentation
Squamous cell carcinoma (SCC) usually presents as an indurated
nodular keratinizing or crusted tumor that may ulcerate, or it may
present as an ulcer without evidence of keratinization.
Typically, SCC presents as a non-healing ulcer or growth in one
of the higher-risk sun-exposed areas. About 70% of SCCs appear on
the skin of the head and neck.
A small nodule enlarges and the center becomes necrotic and
sloughs, developing into an ulcer. The tumor therefore usually
presents as an ulcerated lesion with hard, raised edges. Slow-growing
ulcer or reddish skin plaque can appear. Bleeding may occur from the
tumor. SCC may give rise to local metastases or spread to local lymph
nodes.
Differential Diagnosis
There is a number of serious conditions which can produce
similar-looking skin lesions:
x Keratoacanthoma (can be difficult to differentiate even
histologically).
x Basal cell carcinoma (BCC).
x Malignant melanoma (particularly amelanotic malignant
melanomas).
x Solar keratosis.
237
 x Pyogenic granuloma.
x Seborrheic warts (especially if traumatized or infected).
x Plantar warts or veruccas.
Investigations
Investigations are primarily by visual inspection and removal for
histology (histologically) where necessary.
Skin biopsy
Excisional biopsy (whole lesion excised): small lesions which are
accessible and not in cosmetically sensitive areas or near to vital
structures can be removed completely. The excision should be well
wide of the margins to achieve clearance.
Shave biopsies should not be performed.
Incisional or punch biopsy (part of the lesion excised) is
appropriate if the lesion is large, located in cosmetically sensitive
areas or closely to the vital structures.
Further surgery is performed according to histological results.
Further investigations
In the advanced stages of the disease, further investigations to
assess the extent of disease may be required.
Imaging including CT scanning (bone or soft tissue involvement,
particularly cervical lymph nodes) and MRI scanning (particularly for
the head and neck involvement as well as perineural invasion).
Clinically enlarged nodes should be examined histologically, e.g.
by fine needle aspiration or excisional biopsy.
Treatment
The standard effective treatment is complete surgical excision and
all the excised specimens should be sent for histopathological
examination. Other surgical and nonsurgical treatments include
several procedures.
Curettage and cautery/electrodessication is performed using a
curette to remove soft material from the tumor. The base of the tumor
is then destroyed, using cautery. This may be used to treat small (less
than 1 cm) in situ SCCs and precancerous lesions. It is safe and well
tolerated, and usually produces a good cosmetic outcome. It is suitable
for patients with multiple lesions. The histology may be difficult to
interpret, as the lesion may be incompletely removed and margins of
the excision cannot be assessed optimally.
Cryotherapy/cryosurgery is a cost-effective treatment and is
well performed for small in situ SCCs and precancerous lesions.
238
Histology is not available unless an incisional biopsy is taken first.
Photodynamic therapy (PDT) involves the use of light therapy
in combination with a topical photosensitizing agent to destroy cancer
cells. It is used in the treatment of SCCs in situ and actinic keratosis.
Evidence of efficacy for treatment of invasive SCCs is limited,
recurrence rates are high, there is a risk of metastasis and retreatment
may be necessary.
Mohs' micrographic surgery is a precise technique in which
excision of the skin lesion is carried out in stages and each stage is
checked histologically. It is advocated for use in cases where it is
critical to obtain a clear margin while preserving the maximum
amount of normal surrounding tissue. This procedure is more often
used in the treatment of basal cell carcinomas (BCCs).
Radiotherapy is a useful treatment for patients who cannot be, or
do not prefer to be treated surgically. The cure rates are over 90% for
most skin lesions, but the long-term cosmetic outcome, particularly
for young patients, is inferior to that following other treatments. The
same area cannot be treated twice and so, if there is a recurrence,
surgery is required, which may be more difficult than if the lesion had
been removed surgically to start with. Radiotherapy can also be used
in cases when the margins of excision appear to be incomplete on
histopathological examination. Radiotherapy is curative for some
cases of advanced inoperable disease. Radiotherapy also has a role in
the palliative treatment of patients with large, inoperable and recurrent
SCC, or if there are inoperable metastases in lymph nodes or
elsewhere.
Prognosis
In individual cases, even with similar tumor characteristics, the
prognosis can vary with a range of other factors, e.g. age, degree of
sun exposure, other diseases co-existing with the squamous cell
carcinoma (SCC).
With increasing depth of invasion of the primary tumor, the risk
of nodal metastasis increases and survival decreases. Early-stage
tumors will have more than 90% of 5-year survival. Patients with
metastatic lymph node disease have around 30% of 5-year survival.
Prevention
Avoiding sun exposure is the key to prevention.
Secondary prevention by early detection and effective
management is also very important.
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 Unit 7
Basal Cell Carcinoma
Basal cell carcinomas (BCCs) are slow-growing, locally invasive
malignant epidermal skin tumors which are thought to arise from hair
follicles. The tumor infiltrates local tissues through the slow irregular
growth of subclinical finger-like outgrowths and morbidity results
from local tissue invasion and destruction, especially on the areas of
chronic sun exposure, such as the face, head and neck.
Metastasis is relatively rare with a metastasis rate of 0.0028% to
0.5%. However, there is a 2% incidence of metastasis for tumors
larger than 3 cm in diameter, 25% for tumors larger than 5 cm and
50% for tumors larger than 10 cm in diameter.
Epidemiology
BCC is the most common cancer in Europe, Australia and the
USA and is showing a worldwide increase in incidence. Superficial
BCCs occur at a younger age than other BCC variants, particularly in
women.
Risk Factors
The most significant etiological factors appear to be genetic
predisposition and exposure to ultraviolet (UV) radiation.
The sun-exposed areas of the head and neck are the most
commonly involved sites. Sun exposure in childhood may be
especially dangerous.
Increasing age, male sex, skin types I and II (skin that always
burns and never/only sometimes tans), immunosuppression and
arsenic exposure are other recognized risk factors. A high dietary fat
intake may also be relevant.
People diagnosed with one BCC are at an increased risk of
developing further BCCs. The risk of developing a second BCC
within three years after the first presentation is approximately 44%.
The incidence rates of BCC increase with age and, over the age of
55, the age-specific incidence rates are higher in males than females.
Clinical Presentation
The sun-exposed areas of the head and neck are the most
commonly involved sites. Approximately 80% occur on the head and
neck, with the rest mainly on the trunk and lower limbs. Early lesions
are often small, translucent or pearly and have raised areas with
telangiectasia. It is slow-growing but can spread deeply to cause
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considerable destruction.
It often presents late and may become very large and then require
extensive plastic surgical reconstruction. It may infiltrate cutaneous
nerves (perineural spread) and is prone to recurrence after treatment.
Differential diagnosis
Nodular basal cell carcinoma:
x Intradermal nevus
x Sebaceous hyperplasia
x Fibrous papule
x Molluscum contagiosum
x Keratoacanthoma
Superficial BCC:
x Discoid eczema.
x Psoriasis.
x Actinic keratosis (solar keratosis).
x Lichen simplex.
x Bowen's disease.
x SCC.
x Seborrheic keratosis.
Pigmented BCC:
x Melanoma.
Morphoeic BCC:
x Scar tissue.
x Localised scleroderma.
Investigations
Investigation is primarily by visual inspection and removal for
histology where necessary.
All excised specimens should be sent for histopathological
examination.
When nonsurgical treatments are used, an incisional biopsy must
be sent before treatment for confirmation of the diagnosis.
Biopsy is also indicated when clinical doubt exists or when the
histological subtype of basal cell carcinoma (BCC) may influence
treatment selection and prognosis.
CT or MRI scan are indicated in cases where bony involvement is
suspected or where the tumor may have invaded major nerves, the
orbit or the parotid gland.

241
 Treatment
Surgery and radiotherapy appear to be the most effective
treatments, with surgery showing the lowest failure rates. There is
only limited evidence of the effectiveness of other treatment
modalities compared with surgery. Recurrent BCC is more difficult to
cure than primary lesions.
Surgery
Excision with primary closure, flaps and grafts
An excision margin of 4 mm around the tumor is recommended
where possible, especially for all high-risk BCCs.
Mohs' micrographic surgery
Excision of BCC is carried out in stages and each stage is checked
histologically. It is advised for use in cases where it is critical to
obtain a clear margin while preserving the maximum amount of
normal surrounding tissue, especially for recurrent and high-risk
aggressive growth pattern BCCs such as morphoeic BCCs.
Morphoeic and recurrent tumors are best treated by Mohs'
micrographic surgery. Overall cure rates for primary BCC are almost
100% and 95% for recurrent BCC.
Curettage and cautery/electrodesiccation
It is not recommended for recurrent, large, morphoeic tumors or
tumors on the face. The overall cure rate is over 90% for low-risk
BCCs. It is performed using a curette to remove soft material from the
tumor. The base of the tumor is then destructed, using cautery. This
may be used to treat small (less than 1 cm) primary BCCs. It is safe
and well tolerated, and usually produces a good cosmetic outcome. It
is suitable for patients with multiple lesions. The histology may be
difficult to interpret, as the lesion may be incompletely removed and
margins of excision cannot be assessed optimally.
Cryotherapy/cryosurgery
Cryotherapy is well applied for treating small low-risk lesions,
including superficial BCCs. Histology is not available unless an
incisional biopsy is taken first.
Nonsurgical:
Topical treatment
Imiquimod 5% cream is an immune response modifying agent
that has been licensed for the treatment of small superficial BCCs.
Imiquimod has been shown to achieve clearance rates ranging from
70% to 100% but relapse rates appear higher than with other
242
conventional treatments and there are some difficulties with side-
effects (e.g. pruritus). It is more effective for superficial than nodular
tumors.
Topical fluorouracil 5% cream is useful in the management of
multiple superficial BCC on the trunk and limbs. Cure rates are about
80%.
Photodynamic therapy (PDT)
It involves the use of light therapy in combination with a topical
photosensitizing agent to destroy cancer cells. Its use has been well
described in the treatment of superficial BCC. Evidence of efficacy is
adequate to support its use. The average clearance rate for superficial
BCC is about 85% but is lower in nodular BCC. Advantages of PDT
include a low rate of adverse effects and good cosmetic outcome.
The disadvantages are that the patient has to be available for a
period of at least 3-4 hours for treatment, and that the photosensitizer
and equipment are relatively expensive. There is currently little
information available on long-term cure rates.
Radiotherapy
It is useful treatment for patients with non-melanoma skin cancer
(NMSC) who cannot be, or prefer not to be treated by surgery.
The cure rates are over 90% for most skin lesions, but the long-
term cosmetic outcome, especially for young patients, is worse than
for other treatments. The same area cannot be treated twice and so
surgery is required for any recurrence. Radiotherapy can also be used
in cases when the margins of excision appear to be incomplete on
histopathological examination. Sometimes, especially in the very
elderly and debilitated, it may be appropriate to provide no treatment
(given the slow growth and low risk of many superficial BCCs) or
palliative (debulking or radiotherapy) treatment if the tumor is
symptomatic.
Prognosis
Mortality is low because basal cell carcinomas (BCCs) rarely
metastasize.
Recurrent tumors have poorer cure rates than primary tumors.
Following development of a BCC, patients are at significantly
increased risk of developing subsequent BCCs at other sites.1
Patients with BCC also have an increased risk of developing
squamous cell carcinoma (SCC) and malignant melanoma.
There may also be a small increased risk of other malignancies,
243
such as cancer of lung, thyroid, mouth, breast, and cervix and also
non-Hodgkin's lymphoma.
Prevention
Recommendations on sun avoidance:
x Avoid UV exposure in susceptible individuals, particularly
children and adolescents.
x Stay out of the sun between 10 am and 4 pm.
x Use high-factor sunscreens.
x Wear wide-brimmed hats, long-sleeved shirts and trousers.

Checkup Questions
1. What skin tumors are premalignant?
2. What clinical signs are characteristic of actinic keratosis,
keratoacanthoma, intraepidermal carcinoma, and sebaceous naevus?
3. What tactics is used in the management and treatment of
patients with premalignant skin tumors?
4. What skin tumors are malignant?
5. What is the clinical picture of malignant melanoma, squamous
cell carcinoma and basal cell carcinoma?
6. What tactics is used in the management of patients with
malignant skin tumors?

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CHAPTER XIX
GENODERMATOSIS
Unit 1
Ichthyosis
Ichthyosis – a rare disease with a genetic predisposition,
characterized by disorder of the skin keratinization. More than 20
types of ichthyosis range in severity of symptoms, outward
appearance, underlying genetic cause, and mode of inheritance.
The severity of symptoms can vary enormously, from the mildest,
most common, types such as ichthyosis vulgaris, which may be
mistaken for normal dry skin, up to the life-threatening conditions
such as harlequin-type ichthyosis.
Clinical Presentation
Ichthyosis vulgaris accounts for more than 95% of cases, that is
characterized by extremely dry skin (xerosis) involving most of the
skin surface. The condition follows an autosomal dominant pattern.
This means that only one parent needs to possess a mutated gene in
order to pass it onto his or her child. It’s one of the most common of
all inherited skin disorders. It may be found in patients with atopic
dermatitis. Ichthyosis vulgaris produces large scales in the skin that
can resemble fish scales, hence the term ichthyosis. Patients with this
condition have a defective skin barrier, which permits the evaporation
of water at an elevated rate. It develops not earlier than the first year
of life, typically at the ages of 2 to 5. Ichthyosis vulgaris is often
called a fish scale disease because the scales that characterize the
condition look like fish scales. Among men and women ichthyosis
occurs equally. The disease is characterized by dryness and peeling of
the skin, most pronounced on the extensor surfaces of the extremities.
The dryness is usually mild and symptoms are few. Extremely dry,
scaly skin is known as xerosis.
Clinical presentation of ichthyosis vulgaris include:
x flaky scalp;
x itchy skin;
x polygon-shaped scales on the skin;
x brown, gray, or white scales;
245
 x rather dry skin;
x thickened skin.
Symptoms of ichthyosis vulgaris are typically worse in winter,
when the air is colder and drier. The patches of dry skin typically
appear on the elbows and lower legs. It most frequently affects the
shins in thick, dark segments. In severe cases, ichthyosis vulgaris may
also cause deep, painful cracks to develop on the soles of the feet or
palms of the hands.
Treatment and Prevention of Ichthyosis
Since the condition is rare, there are few well-controlled treatment
trials. There is no way of replacing the defective filaggrin molecule.
Living in a humid environment is very helpful in controlling the
disease. Patients usually do well in places like Southeast Asia as
opposed to Northern Europe.
The primary means of general therapy of ichthyosis is vitamin A,
which is prescribed in high doses over 2-3 months, repeated cycles
(2-3 times a year) and tigazon. It is recommended the combination of
vitamin A with tocopherol acetate (especially aevitum. Frequent warm
(38-39°C) bath, preferably with the addition of baking soda
(50-100 g), milk (0.5 l), olive oil (1-2 tablespoonfulls), salt (100-200
g), are useful. Using emollients on the skin that tend to suppress the
evaporation of water can be very helpful. Topical medications that
contain 10% lactic acid, 10% urea, and/or 10% glycerol (AmLactin,
Lac-Hydrin, Lactinol, Lactinol-E, LactiCare, Ureacin-10).
Oral retinoids display an impressive antikeratinizing action in
ichthyosiform dermatoses. Etretinate (1 mg/kg/d) and isotretinoin
(2 mg/kg/d) have been shown to reduce scaling, discomfort, and
disfigurement. However, when these drugs are discontinued, the
ichthyotic skin recurs, thereby necessitating long-term use.
Prognosis
Ichthyosis vulgaris may be either mild or severe depending on the
precise genetic defect (more than one mutation affecting filaggrin
production), as well as ambient environmental factors (average
relative humidity and temperature). A mild disease has an excellent
prognosis, whereas a severe disease may be difficult to control.

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 Unit 2
Epidermolysis Bullosa
Epidermolysis bullosa is a group of rare hereditary genetic skin
diseases caused by mutations in a number of genes that are
responsible for the synthesis of skin structural proteins. The disease
is characterized by the tendency of the skin and mucous membranes
to form blisters, mainly at the places of insignificant mechanical
impact, due to the intercellular connections in the epidermis or the
dermoepidermal junction. Patients with epidermolysis bullosa are
recorded most often between the ages of 1 and 5 years. The
dystrophic variant accounts for more than half of patients from the
total number of all forms of epidermolysis bullosa. Diagnosis and
treatment of epidermolysis bullosa remain one of the main problems
in medicine. Epidermolysis bullosa is severe in any form, disability
occurs in the early years of the disease.
The development of epidermolysis bullosa is caused by
mutations of the genes encoding structural proteins of the skin, which
provide a link between the epidermis and the dermis. More than 1000
mutations have been identified in 15 genes of structural skin proteins
that can lead to the development of various clinical types of
congenital epidermolysis bullosa.
Changes in protein synthesis are associated with mutations: lack
of protein, synthesis of a functionally defective protein, protein
synthesis with impaired structures, facilitating access to the protease
protein, which leads to its rapid destruction. Keratins 5 and 14,
desmoplakin, plakofilin-1, plectin, integrin α6β4, laminin 332,
collagens type VII and XVII and kindlin are proteins that are
associated with the development of the disease. These proteins have
different localization in the skin: keratins 5 and 14 are localized in
keratinocytes, α6β4 integrin, laminin 332, type XVII collagen –
inside the lamina lucida of the basement membrane, type VII
collagen – under the dark lamina (lamina densa) of the basement
membrane, kindlin – at different levels of the epidermis.
Classification
There are several main types of epidermolysis bullosa based on
the mechanism of blister formation and its clinical picture:
epidermolysis bullosa simplex, junctional epidermolysis bullosa,
dystrophic epidermolysis bullosa and Kindler syndrome (a different
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level of blistering).
Epidermolysis Bullosa Simplex
Epidermolysis bullosa simplex is characterized by the formation
of intraepidermal blisters as a result of the disintegration and
cytolysis of keratinocytes without scarring, atrophy and the
formation of milium. The type of inheritance is autosomal dominant.
The first signs of the disease usually appear in the first year of life,
sometimes they may already be at birth. Blisters of various sizes
(from 0.5 to 7 cm and more) with a dense tire and transparent
contents appear at the site of mild trauma, more often in the area of
the hands, feet, back, elbow and knee joints, occipital region on
intact skin. Nikolsky's symptom is negative. Acantolytic cells in the
contents of the blisters are absent. Blisters open in a few days,
forming erosions that become crusted and quickly epithelialize. Any
scar or atrophy does not remain. Blisters are usually more in the
warm period of the year with severe hyperhidrosis. With age, the
lesions are localized mainly on the limbs, especially on the feet and
hands. Great trauma to these areas of the skin, tight, poorly chosen
shoes, as well as tight clothing contributes to this. Blisters appear
throughout life, but in the post pubertal period their number
decreases. Mucous membranes and nails are not affected or their
changes are minimal. The general condition of the patient does not
change. Prenatal diagnosis of this form of the disease is possible by
the high content of α-fetoprotein in the serum of a pregnant woman
in the second trimester.
Junctional epidermolysis bullosa
Junctional epidermolysis bullosa is characterized by the formation
of subepidermal blisters due to the damage of lamina lucida, located
between the plasma membrane of the basal keratinocytes and the
basement membrane of the skin. This leads to the development of skin
atrophy. A prenatal diagnosis is possible using a skin biopsy of an 18-
week fetus based on the detection of these changes. The type of
inheritance is autosomal recessive. The process is characterized by the
appearance of blisters and erosion at the birth of a child or soon after
it. The process is generalized within a few days. The main localization
of the rash is the skin of the chest, head, and mucous membranes of
the mouth, larynx and trachea. The nails are dystrophic, although the
skin of the hands and feet is intact. Anonychia and acroosteolysis
develop. The erosive surfaces formed at the site of the blisters heal
248
slowly. In their place there are areas of skin atrophy. Scars and milia
are absent. Many children die in the first months of life from sepsis
and anemia.
Dystrophic Epidermolysis Bullosa
Dystrophic epidermolysis bullosa is characterized by the
formation of blisters due to dermatolysis – the death of collagen fibrils
in the papillary dermis below the lamina densa. Formed erosive-
ulcerative surfaces, healing scars, characterized by the formation of
milia, changes in nails, hair, teeth and other anomalies.
Epidermolysis bullosa dystrophic recessive generalized
(epidermolysis bullosa dystrophic polydysplastic) is characterized by
the formation of blisters in the papillary dermis as a result of
dermatolysis – lysis of collagen fibrils with their phagocytosis by
macrophages. The pathological process is associated with the
increase in the level and activity of the enzyme collagenase, which
destroys the main component of the supporting collagen fibrils –
collagen VII (collagenolysis). A prenatal diagnosis of the disease is
possible according to the results of fetal skin biopsy on the 21st week
of development and identification of previously described changes.
The first signs of the disease appear at birth (60% of patients) or in
the first weeks of life. Large blisters, often with hemorrhagic
contents, occur spontaneously anywhere on the skin and mucous
membranes. Extensive, non-healing erosive-ulcerous surfaces that
form when they are opened make it difficult to care and feed
newborns. Vegetations develop on erosive-ulcerative, often bleeding,
painful areas. Their healing occurs slowly, with the formation of
malformed atrophic scars. Cicatricial changes of the esophagus,
pharynx and oral mucosa can impede food intake, obliterate the
excretory ducts of the salivary glands, restrict the mobility of the
tongue and lead to the development of leukoplakia. Damage to the
eyes (erosive-ulcerative keratitis, followed by scarring) leads to loss
of vision, cicatricial ectropion, and obliteration of the lacrimal ducts.
Acrocyanosis, scleroderm-like changes in the skin of the hands and
feet, with the formation of joint flexion contractures, acroosteolysis
and the characteristic deformation of the hands as a result of
accretion and deformation of the fingers are also observed.
Dystrophy of nails, hair, teeth is also characteristic. Disturbances of
the endocrine (hypofunction of the thyroid gland, pituitary), nervous
(epilepsy, mental retardation) systems are possible. There is a high
249
mortality rate in early childhood from sepsis, anemia, eating
disorders, and in older children from malignant tumors of the skin,
esophagus, and oral organs.
Epidermolysis bullosa dystrophic dominant (epidermolysis bullosa
dystrophic hyperplastic) is characterized by the formation of blisters in
the dermis (dermatolysis) below the lamina densa due to the death of
supporting collagen fibrils. Prenatal diagnosis is possible (by analogy
with dystrophic polydisplastic epidermolysis bullosa). The type of
inheritance is autosomal dominant. The first manifestations of the
disease appear in early childhood or later (4-10 years). Blisters occur
after a minor injury, often in the limbs. They are tense, dense, with
serous or hemorrhagic contents. When opened, they form erosive-
ulcerous surfaces that heal slowly with the formation of a soft or keloid-
like cicatricial atrophy, first pink, then white. Scar tissue with multiple
epidermal cysts (milia) forms in the area of the joints at the site of the
blisters. The nails involved in the process are thickened, dystrophic.
Mucous membranes are rarely affected. Hair, teeth, and general
development do not usually change, but association with ichthyosis,
follicular keratosis, and hypertrichosis is often noted.
Diagnosis
The diagnosis of epidermolysis bullosa is based on clinical and
histological data. A prenatal diagnosis of the disease is possible.
The differential diagnosis in early childhood is carried out with:
x epidermolytic ichthyosis, which is dominated by keratosis;
x epidemic pemphigus of newborns, which is characterized by an
acute onset with fever, intoxication and inflammatory blisters as a
result of necrotic processes in the epidermis caused by
staphylococcus.
In older children, some forms of epidermolysis bullosa
differentiate from benign bullous pemphigoid, which is characterized
by a linear deposition of IgA along the nasal membrane.
A laboratory diagnosis is required to clarify the diagnosis in most
cases.
The following diagnostic methods are used:
x skin biopsy;
x immunofluorescent antigen mapping;
x transmission electron microscopy;
x genetic analysis (molecular or DNA diagnostics).

250
 A prenatal diagnosis and genetic counseling are particularly
important at the planning stage for a family at risk of inheriting this
pathology. Improvement of molecular diagnostic methods allowed
for prenatal diagnostics is based on the analysis of fetal DNA,
which can be obtained from amniotic fluid and/or chorionic villi.
Chorionic villus biopsy and amniocentesis can significantly reduce
the risk of premature termination of pregnancy as compared with
fetoscopy. A prenatal diagnosis is possible only when it is planned
in advance. Before the onset of pregnancy, it is necessary to
establish precisely the genetic defect in the ailing family member. If
a defective gene is known, then the search for the same damage to
the fetus takes only a few days.
A non-invasive method of prenatal diagnosis – ultrasound
diagnosis. This method allows you to visualize some features of the
development of the fetus with a limited number of severe pathologies,
as well as other structures of the contents of the uterus, which can be
identifiers of some congenital diseases.
Treatment
Effective methods for the treatment of epidermolysis bullosa have
not been developed to date. In the neonatal period, observation and
symptomatic therapy of patients with congenital epidermolysis bullosa
is carried out in the conditions of the intensive care unit of the
pediatric hospital.
Patients with epidermolysis bullosa should avoid physical
exertion associated with increased sweating, traumatic situations and
sudden movements. Clothes, closed shoes minimize skin trauma. With
the damage of the oral cavity special attention must be paid to
nutrition. The diet should be mechanically, thermally and chemically
gentle (wiped and semi-liquid, not hot). Food of patients should be
rich in proteins, carbohydrates, fats, and also contain vitamins,
minerals, dietary fiber and a large amount of fluid. It is recommended
to take multivitamin-mineral complexes. Vitamins A, B, C, D, E and
minerals – iron, zinc, selenium and calcium are important.

Checkup Questions
1. What symptoms and signs does ichthyosis vulgaris manifest?
2. What is the treatment for ichthyosis vulgaris?
3. What does the prognosis of ichthyosis vulgaris depend on?
251
 4. What causes epidermolysis bullosa?
5. What forms does epidermolysis bullosa have?
6. What is the typical clinical picture in various forms of
epidermolysis bullosa?
7. What are the diagnostic methods and treatment guidelines for
epidermolysis bullosa?

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 Учебное издание

Белазарович Анастасия Александровна

Новоселецкая Алевтина Ивановна

ДЕРМАТОЛОГИЯ
Рекомендовано учебно-методическим объединением
по высшему медицинскому, фармацевтическому образованию в
качестве пособия для студентов учреждений высшего образования,
обучающихся по специальности 1-79 01 01 «Лечебное дело»

Ответственный за выпуск В. В. Воробьев

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