Transcript of "DM Thappa - Essentials in Dermatology, 2nd Edition"
Essentials in Dermatology
(with Multiple Choice Questions)
Essentials in Dermatology
(with Multiple Choice Questions)
Devinder M Thappa MD, DHA, MNAMS, FIMSA
Professor and Head
Department of Dermatology and STD
Jawaharlal Institute of Postgraduate Medical Education and Research
JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD
New Delhi • Ahmedabad • Bengaluru • Chennai • Hyderabad • Kochi
Kolkata • Lucknow • Mumbai • Nagpur • St Louis (USA)
The second edition of Essentials in Dermatology (with Multiple Choice Questions) is being published
6 years after the appearance of the first edition. The encouraging response to the first edition prompted
me to revise the book, keeping in view the comments received, and changing trends in the field of
This new edition incorporates differential diagnosis for each entity or group of entities to further
understand the subject critically. Three new chapters—Skin in Systemic Diseases, Skin Changes of
Pregnancy and Old Age, and Antiretroviral Therapy (ART) have been added. The existing chapters
have been updated and treatment guidelines revised. Newer entities have been included under
various chapters, but not at the cost of brevity and conciseness. For better understanding of the text,
better photographs and clinical illustrations have been incorporated.
The section on multiple choice questions has been considerably expanded, and this section has
been divided into two—for PG entrance examinations and for postgraduates in dermatology.
Additional mnemonics have been included in the useful medical mnemonics section.
The objective of this edition remains the same—to serve as an aid for beginners in dermatology
and those aspiring for PG entrance examinations.
The making of the revised edition of this book involved a number of people besides myself.
Many of the chapters were revised with inputs from my senior residents Dr Rashmi Kumari,
Dr Amiya Kumar Nath and Dr Abarna Devi and junior residents Dr Nidhi Singh, Dr Abhijit
Chougule, Dr Kishan Kumar Agarwal, Dr Balaji Adityan, Dr Sowmya Kaimal and Dr Sakthi Kandan.
The photographs utilized in the book have been possible due to the Medical Illustration Department
of the hospital, and the digital cameras of my postgraduates, making the new edition a colorful
experience. My laboratory technician Mr Samsudeen deserves a mention for his skill in the staining
and preparation of laboratory material for photomicrography. The final making of this edition has
involved the support and cooperation of all my esteemed colleagues, patients and the forgotten
names of residents (who worked for the first edition of the book).
As always, this edition is open to constructive criticism and suggestions for its further
Devinder M Thappa
Preface to the Second Edition
Dermatology, the science of the skin, was one of the many specialties, which evolved from general
internal medicine during the course of the nineteenth century. In India, recognition of dermatology
as a specialty distinct from internal medicine is recent; it has still not grown to its full stature in
practice and teaching. In spite of having some share in the curriculum, dermatology remains a
neglected subject because of its non-inclusion in the qualifying examination at MBBS level. There
has been an explosion of knowledge—easily documented by the size of standard dermatology
textbooks, whose length has increased from an average of 1000 pages to the most recent editions of
Fitzpatrick and of Rook, which are more than 3000 and 3600 pages, respectively. Expansion has
been greater on the surgical and cosmetic side of the specialty, which barely existed 50 years ago.
Such vast knowledge is difficult to grasp in 3 years course of MD dermatology, venereology and
leprology, sometimes may be at the cost of another. So there was need for a short textbook for
postgraduates who have just joined the specialty to have the glimpse of the subject and understand
the basic dermatology before venturing for detailed standard textbooks. There is lack of simple but
up to date book for undergraduates who are preparing for Postgraduate Entrance Examination.
Though market is flooded with a number of books, many of them are not even framed by dermatology
specialty individuals and lack correct and appropriate information. This prompted me to write this
book to fulfill the needs of students aspiring for entering in postgraduate courses in reputed institutes
of India. The material in this book is based on the standard textbooks and latest information from
specialty journals. Introduction to MCQs is a unique section in this book to guide the students. The
multiple choice questions are taken from a number of sources to sensitize the student to know
certain subject areas in this specialty thoroughly and accordingly the book section gives relevant
points highlighted for quick revision of facts. The suggestions and healthy critical remarks will be
very much appreciated to improve this book.
Devinder M Thappa
Preface to the First Edition
I would like to thank those who helped me to update chapters
1. Dr Balaji Adityan for updating
• Principles of Diagnosis in Dermatology
• Bacterial Infections
• Viral Infections
• Fungal Infections
• Skin Changes in Pregnancy and Old Age
2. Dr Sakthi Kandan for
• Disorders of Hair and Nails
• Metabolic and Nutritional Disorders
• Skin in Systemic Diseases
3. Dr Sowmya Kaimal for
• Pediatric Dermatology
• Human Immunodeficiency Virus Infection (HIV) and Acquired Immunodeficiency Syndrome
4. Dr Amiya Kumar Nath for
• Connective Tissue Disorders
• Genetics and Genodermatoses
5. Dr Abhijit Chougule for
• Differential Diagnosis for Leprosy
• Treatment of Leprosy
6. Dr Kishan Kumar Agarwal for
• Urticaria, Angioedema and Pruritus
• Disorders of Sebaceous, Eccrine and Apocrine Glands
7. Dr Nidhi Singh for
• Cutaneous Tuberculosis and Atypical Mycobacterial Infections
• Vesiculobullous Disorders
• Pigmentary Disorders
Following residents helped in framing MCQs for postgraduates
1. Dermatology Basics
• Dr Abhijit Chougule
• Dr Kishan Kumar Agarwal
2. Clinical Dermatology Part -I
• Dr Rashmi Kumari
Essentials in Dermatologyx
• Dr Balaji Adityan
• Dr Ajay Kumar Singh
• Dr Anuradha Priyadarshini
• Dr Tukaram Sori
3. Clinical Dermatology Part -II
• Dr Malathi
• Dr Sathyamoorthy
4. Sexually Transmitted Diseases
• Dr Sowmya Kaimal
• Dr Rajalakshmi
• Dr Abarna Devi
• Dr Sakthi Kandan
“…Most of the dermatology textbooks are too much voluminous for undergraduate students already
overburdened with other heavy weight subjects. Not only undergraduates, beginners at the
postgraduate level also face problem to acquire basic conception from such large books. So there is
always a need for a concise book which can provide clear basic conception and up-to-date knowledge
to the students….will be of immense help to the postgraduate entrance examinees….should be
collected in all undergraduate medical college libraries for the benefit of the students…”
Indian J Dermatol 2003; 48(4): 248.
“…The stated aim of the book is to have a short textbook for new entrants to postgraduate
studies in dermatology which could glimpse of the subject and understand basic dermatology before
venturing for detailed standard textbooks. The second aim stated is to fulfill the needs of students
aspiring for entering in postgraduate courses in reputed institutes….well written and fulfill the
stated aims…An approach to attempting MCQs appears to be a very useful chapter….strongly
recommend this book to the new entrants in specialty training and those preparing for admission to
Indian J Dermatol Venereol Leprol 2004; 70(6): 393.
SECTION 1: DERMATOLOGY
1. Ten Most Influential People in Medicine and Dermatology .................................................... 3
2. History of Dermatology in the World ............................................................................................ 5
3. Microanatomy of the Skin................................................................................................................ 8
4. Physiology, Biochemistry and Immunology of the Skin ......................................................... 13
5. Principles of Diagnosis in Dermatology ..................................................................................... 16
6. Bacterial Infections .......................................................................................................................... 31
7. Viral Infections ................................................................................................................................. 43
8. Fungal Infections ............................................................................................................................. 57
9. Infestations ........................................................................................................................................ 72
10. Papulosquamous Disorders ........................................................................................................... 82
11. Eczema................................................................................................................................................ 99
12. Vesiculobullous Disorders........................................................................................................... 114
13. Cutaneous Tuberculosis and Atypical Mycobacterial Infections ........................................ 127
14. Connective Tissue Disorders (Collagen Vascular Disorders) ............................................... 134
15. Pigmentary Disorders ................................................................................................................... 148
16. Keratinization Disorders .............................................................................................................. 156
17. Urticaria, Angioedema and Pruritus .......................................................................................... 166
18. Drug Eruptions, Erythema Multiforme, Stevens-Johnson Syndrome
and Toxic Epidermal Necrolysis ................................................................................................. 172
19. Disorders of Sebaceous, Eccrine and Apocrine Glands ......................................................... 180
20. Disorders of Hair and Nails ......................................................................................................... 189
21. Metabolic and Nutritional Disorders......................................................................................... 198
22. Genetics and Genodermatoses .................................................................................................... 210
23. Skin in Systemic Diseases............................................................................................................ 222
Essentials in Dermatologyxiv
24. Skin Changes of Pregnancy and Old Age ................................................................................. 237
25. Pediatric Dermatology .................................................................................................................. 240
26. Benign, Pre-malignant and Malignant Tumors of the Skin .................................................. 246
27. Topical Formulary and Key Systemic Drugs............................................................................ 257
28. Dermatosurgical Procedures ........................................................................................................ 272
SECTION 2: SEXUALLY TRANSMITTED DISEASES AND HIV INFECTION
29. Historical Milestones in Sexually Transmitted Diseases ...................................................... 279
30. History Taking and Examination in Sexually Transmitted Diseases (STDs).................... 282
31. Sexually Transmitted Diseases ................................................................................................... 288
32. Human Immunodeficiency Virus Infection (HIV) and Acquired
Immunodeficiency Syndrome (AIDS) ....................................................................................... 309
33. Antiretroviral Therapy (ART) ..................................................................................................... 318
SECTION 3: LEPROSY
34. Historical Milestones in Leprosy ................................................................................................ 327
35. History Taking and Examination in Leprosy ........................................................................... 330
36. Clinical Leprosy ............................................................................................................................. 333
Multiple Choice Questions.................................................................................................................... 351
Some Useful Medical Mnemonics ....................................................................................................... 441
Terminology ............................................................................................................................................. 447
Answers ..................................................................................................................................................... 465
Index ........................................................................................................................................................... 469
Ten Most Influential People in Medicine and Dermatology 3
THE MILLENNIUM AND MEDICINE:
THE TEN MOST INFLUENTIAL
1. Louis Pasteur (1822-1895): Proposed the
“germ theory”. He first associated a specific
micro organism (bacillus) with a specific disease
(anthrax). He developed the method of
pasteurization—a heating process that kills
bacteria in milk, wine and other liquids. He was
also a pioneer in stereochemistry.
2. Robert Koch (1843-1910): The first to isolate
the anthrax bacillus (1876). In 1883, he published
a method of preventive inoculation against this
disease. In 1882, he announced the discovery of
tubercle bacillus and in 1883; he discovered the
cause of cholera. He was awarded the nobel prize
in physiology or medicine in 1905.
3. Rudolf Virchow (1821-1902): Founded
Cellular pathology. His concept that the basis
of disease is the cell, the essential functional and
structural unit of the body, was of monumental
importance as a basis for understanding the
cause, the process and the results of the disease.
4. Gregor Mendel (1822-1844): Formulated the
laws of heredity. Mendel’s work laid the
mathematical foundation of the science of
1 Ten Most Influential People in
Medicine and Dermatology
5. Francis Crick (1916-) and James Watson
(1928): Accredited with determining the
molecular structure of DNA, the chemical
substrate of heredity, which is regarded as the
most important discovery of the 20th century in
medicine and science. They were awarded the
nobel prize in 1962 sharing it with Maurice
Wilkins (1916). Currently, Crick is associated
with the Salk Institute for biological studies in
San Diego while Watson is the director of the
Cold Spring Harbor lab in southeastern New
6. Marie Curie (1867-1934): Discovered
radioactivity and was given the nobel prize in
1903. The discovery formed the basis of radiation
therapy. In 1911, she was again conferred the
Nobel Prize in chemistry for her discovery of
radium and polonium.
7. Edward Jenner (1749-1823): Introduced the
inoculation for smallpox at the end of the 18th
century, which is considered one of the greatest
triumphs in the history of medicine.
8. Karl Landsteiner (1868-1943): Called the
“father of blood grouping” - a concept without
which blood transfusion would not be possible.
In 1901, he showed that there are at least three
major types of blood. Landsteiner was awarded
the noble prize for his work in 1930.
Essentials in Dermatology4
9. Wilhelm Rontgen (1845-1923): Discoverer of
X-rays in 1895 and nobel prize winner in Physics
in 1901. The value of X-rays in the diagnosis and
treatment was recognised and accepted almost
from the outset of their discovery.
10. Sigmund Freud (1856-1939): Considered the
founder of psychoanalysis, he believed that a
complex of repressed and forgotten expressions
underlies all abnormal mental states and that
infantile mental processes are important in later
TEN MOST INFLUENTIAL PERSONS IN
DERMATOLOGY, VENEREOLOGY AND
1. Dr. JS Pasricha: Pioneer of pulse therapy in
pemphigus, contact dermatitis in India.
2. Dr. LK Bhutani: Clinical dermatology,
“Bhutani’s Colour Atlas of Dermatology”,
3. Dr. Dharmendra: “Father of leprosy” in India.
4. Dr. RV Rajam and Dr. PN Rangaiah:
Monograph on donovanosis.
5. Dr. VN Sehgal: For his literary contribution
in dermatology, venereology and leprosy.
6. Dr. Patrick Yesudian: Clinician par excellence,
known for “Patrick Yesudian sign” for palmar
freckling in neurofibromatosis type 1.
7. Dr. KC Kandhari: Established department of
dermatology at AIIMS.
8. Dr. Gurmohan Singh: contribution to Indian
and community dermatology.
9. Dr. Surinder Kaur: Established department
of dermatology at PGIMER, Chandigarh.
10. Dr. Sardarilal: First editor of Indian Journal
of sexually transmitted diseases, and for
contributions in donovanosis.
TEN MOST INFLUENTIAL PERSONS IN
DERMATOLOGY, VENEREOLOGY AND
1. Dr. Ferdinand Ritter von Hebra– Founder of
the new Vienna school of dermatology, which
set the basis for modern dermatology.
2. Dr. Robert Willan– Founder of dermatology
as a medical specialty.
3. Dr. Josef Jadassohn– Best remembered for his
handbook of skin and venereal disease
(41 volumes), pioneer in allergology, introduced
4. Dr. Johnathan Hunter– Natural history of
syphilis, role of inflammation in healing.
5. Dr. Paul Ehrlich– Developed salvarsan (magic
bullet) as a treatment for syphilis, was the first
to stain tubercle bacilli.
6. Dr. Thomas Bernard Fitzpatrick– Proved that
melanin was produced in melanosomes, first
editor of Dermatology in General Medicine
7. Dr. Arthur Rook (1918-1991), Dr. Darrell
Sheldon Wilkinson and zoologist John Ebling
(1918-1992): Produced their major work,
Textbook of Dermatology (alias The Rook Book)
8. Dr. Paul Gerson Unna, Dr. HKB Pinkus, Dr.
A Bernard Ackerman, and Walter F. Lever:
Contributions to dermatopathology.
9. Heinrich Koebner– Koebner phenomenon,
founder of the dermatology clinic at the
University of Breslau.
10. GHA Hansen– Identified M. leprae as the
causative agent of leprosy in 1873.
History of Dermatology in the World 5
HISTORY OF DERMATOLOGY IN THE
• In Greek and Roman era, Hippocrates
recognized and described many diseases.
Some of the medical facts he observed are as
true today as they were over 2000 years ago.
He rescued medicine from magic and
superstition, therefore rightly so called “the
Father of Medicine”.
• Dermatology, the science of the skin, was
one of the many specialties, which evolved
from general internal medicine during the
course of the nineteenth century. Most
diseases of skin, as ‘external diseases’, had
for many centuries fallen within the province
of the surgeon or of the quack.
• Until the eighteenth century was well-
advanced, physicians with few exceptions
were little concerned with the skin, apart
from the exanthematic eruptions of acute
fevers. However, during the last decades of
that century, many of the great physicians
recorded their observations on diseases of the
skin. The solid contributions of some, such
as Heberden and Cullen, which have
received too little attention from the
historians of dermatology, laid the
foundations on which the pioneer specialist
2 History of Dermatology
in the World
dermatologists of the following century were
able to build.
• Despite developments in 19th century-
vaccination against small pox, recognition
of cellular pathology, Louis Pasteur’s germ
theory of infection, development of
anaesthesia and microscope, the treatment
of most skin diseases was at best
symptomatic and at worst dangerous.
• Amongst the first to specialize in
dermatology was Ferdinand Hebra (1816-
1880) in Vienna, who led the torch of
dermatology, others followed him. The last
half of 19th century saw dermatology and
venereology emerge as a specialty in its own
• The 20th century brought a wealth of new
scientific knowledge that can be used to help
the sick. Perhaps, the most important single
discovery was that of Sir Alexander
Fleming, the British bacteriologist who
found the first antibiotic, penicillin.
• During 20th century, certain turning points
occurred in general sociocultural factors
(welfare—public health, vaccines, hygiene,
clean water, sewerage, etc; war; communi-
cations–books, photography, radio, films,
television, computers; transport), general
scientific developments (genetics- structure
Essentials in Dermatology6
of DNA; inflammation-histamine, prostag-
landins, cytokines, adhesion molecules;
immunology-cell mediated and humoral
immunity; tissue culture; pathogenic agents-
spirochetes, viruses, prion; therapies- x-rays,
antibacterial, immunosuppressive; con-
trolled clinical trials), and strictly
dermatological areas(books- Jadassohn,
Pillsbury, Rothman, Rook; biology-
keratinocyte, melanocyte, Langerhans cell,
basement membrane; diseases- epidermo-
lysis bullosa, pemphigus, toxic epidermal
necrolysis; people- from Unna to Katz;
therapies- local steroids, griseofulvin,
phototherapy, retinoids, Moh’s surgery,
EVOLUTION OF DERMATOLOGY
• In India, recognition of dermatology as a
specialty distinct from internal medicine is
recent; it has still not grown to its full stature
in practice and teaching.
• Therapeutics of dermatoses have been
known and practiced by our ancient
physicians for centuries. Charaka Samhita
contains one chapter on the subject.
• Medical charlatans selling panaceas for
cutaneous ailments and faith healers were
commonly seen all over the country. With the
advent of scientific dermatology, their
number and importance has dwindled.
• In the latter part of the 19th century, the
health authorities in then British India
became aware of the need to have data on
prevalence of dermatoses and venereal
• The first chair of dermatology was
established at Grant Medical College,
Jamshedji Jeejebhoy Hospital (JJ Hospital),
Bombay in 1895.
• The second department, at the School of
Tropical Medicine in Calcutta, was started in
1923, after a gap of nearly 28 years, under
the patronage of Dr Ganpati Panja and
• During the period from 1956 to 1974, the
status of the specialty was further elevated
and steps were taken by state governments
to set up departments of dermatology and
venereology in medical institutions.
• Dr UB Narayan Rao, a pioneer in the
specialty, gets the credit for the creation of
an association of dermatologists and
venereologists in Bombay (July 1, 1947), and
for Indian Journal of Venereology started in
1935, renamed as Indian Journal of Venereal
Diseases and Dermatology in 1940, and later
renamed as Indian Journal of Dermatology
and Venereology in 1955, the first issue of
which was edited by him.
• In 1962, it was decided to affiliate the
association of dermatologists and
venereologists with Association of Physicians
of India (API).
• This continued until 1974, after which this
affiliation was severed and association
became an independent body.
• On January 28, 1973, the present association
the Indian Association of Dermatologists,
Venereologists and Leprologists (IADVL)
came into existence.
• Since 1976 the bimonthly journal is being
published under the title Indian journal of
dermatology, venereology and leprology.
EVOLUTION OF VENEREOLOGY
• Syphilis was first introduced into North India
nearly 500 years ago.
• National STD Control Programme was
started in 1946. This programme continued
to operate till 1991 and with the arrival of HIV
infection in the country, the programme was
History of Dermatology in the World 7
brought under the purview of National
AIDS Control Organization (NACO) in the
• The monograph by Rajam and Rangiah on
donovanosis (granuloma inguinale,
granuloma venereum) is testimony to the
teaching and research standards set by these
two giants at institute of venereology,
• Dr. CN Sowmini founded the Indian
Association for the study of sexually
transmitted diseases (IASSTD) in the year
• In the year 1980, this specialty, under the
banner of IASSTD, started its own exclusive
journal, the Indian Journal of Sexually
• The late Dr. Sardarilal was its founder editor
and guiding force, who had already made a
mark in the field of research, especially in
• Somehow venereology did not prosper as
much, even though it led in front of
dermatology and leprology in teaching and
in the starting of its own journal in early part
of 19th century.
• Unlike in the West, venereology in India has
been combined with dermatology in most of
EVOLUTION OF LEPROLOGY
• There is a great deal of speculation about the
early history of leprosy. The earliest records,
which give accurate descriptions of the
disease, come from India and may have been
written as early as 600 BC.
• In Sushrata Samhita (600 BC), one finds a
reasonably good account of the clinical
features and treatment of the disease.
Sushrata described the different forms of
leprosy, and these forms fit in fairly well with
the forms of the disease as recognized at the
• Sushrata described the treatment of the
disease with Chaulmoogra oil (hydnocarpus
oil), which till 1940s was the mainstay in the
treatment of the disease.
• The first known asylum for leprosy patients
was established in Calcutta early in the 19th
century, followed by another in Varanasi.
• “Leprosy in India”, a journal specific for
leprosy, was started by Dr. Ernest Muir in
1929, initially in the form of quarterly notes,
and later on transformed itself to a full-
fledged scientific journal. Consistent with its
contents and nature, Leprosy in India was
renamed as the Indian Journal of Leprosy in
• Dr. Dharmendra straddled the scene of
leprosy in India like a giant and is known for
lepromin test, Indian classification of types
of leprosy and the journal “Leprosy in India”.
• The National Leprosy Control Programme
(NLCP) was started in 1954-55. In view of
scientific advancement and availability of
highly effective treatment of leprosy, the
programme was redesignated as National
Leprosy Eradication Programme (NLEP) in
• In 1991, the World Health Organization set a
target of elimination of leprosy as a public
health problem by the year 2000. India
achieved this target in 2005.
Essentials in Dermatology8
Dermatology may be defined as the study of the
skin and its diseases or is a branch of medical
science, which deals with systematic study of
skin in health and disease. Since skin conditions
constitute 10 to 30% of outpatient attendance in
any hospital, they are often easily noticed by
others (hence a cause of great social concern to
the patient) and very often, skin diseases offer
diagnostic clue to many major systemic
disorders, makes this subject challenging and
important to study.
FUNCTIONS OF THE SKIN
The skin is the largest organ of the body,
accounting for 16-20% of total body weight. The
skin of an average adult covers an area just under
. It not only gives shape to the body but also
helps it in many ways – the important functions
of the skin are:
1. Protection (Barrier function) from:
a. Physical injuries
b. Chemical injuries
3. Sense organ: A number of sensations –
touch, pressure, warmth, cold and pain are
perceived by the skin.
4. Storage of electrolytes, carbohydrates,
water, fat, vitamins, proteins, etc.
3 Microanatomy of the Skin
5. Vitamin D formation: Vitamin D3 is
essential for skeletal development.
6. Absorption: The skin surface also performs
absorptive function and is the basis of
topical therapy in dermatology.
7. Excretion: Some of the toxins may be
excreted through the skin.
8. Immune surveillance: This immunological
function is performed by Langerhan’s cells,
dendritic cells (intermediate) and keratino-
9. Mechanical function: The mechanical
properties of the skin depend mainly on the
10. Cosmetic function: Colour of the skin and
hair and nails are important for their
decorative value. Hair does not perform a
“vital” physiologic function but it does
provide a sexually attractive ornament.
DEVELOPMENT OF SKIN
Epidermis develops from ectoderm lateral to
neural crest, dermis from mesenchyme and
neural crest cell, subcutaneous fat from
mesenchyme and melanocytes from neural crest.
Foetal skin development occurs in three stages-
specification, morphogenesis and differentiation.
Its specification occurs from 0 to 60 days,
morphogenesis from 2 to 5 months, and
differentiation from 5 to 9 months.
Microanatomy of the Skin 9
STRUCTURE OF THE SKIN
Skin has 3 layers (Fig. 3.1)
3. Subcutaneous fat (Hypodermis).
It is approximately 0.4 mm to 1.6 mm in
thickness. The majority of the cells in the
epidermis are the keratinocytes. These cells are
organized into five layers-stratum corneum,
stratum lucidum (present only in palmar and
plantar skin), stratum granulosum, stratum
spinosum, and stratum basale or stratum
germinatum (Fig. 3.2).
Stratum corneum is the outermost layer
containing flattened anucleated cells without cell
organelles. The thick epidermis of palms and
soles has an additional layer underneath the
stratum corneum that is electron lucent and is
called the stratum lucidum. The stratum
granulosum is so called due to the presence of
intracellular basophilic keratohyaline granules
and consists of 2-5 cells layer. The stratum
spinosum contains 8-10 layers of polyhedral cells
with round nuclei. The stratum basale or stratum
germinativum consists of single layer of cuboidal
or columnar cells.
Keratin filaments are a hallmark of the
keratinocytes and the process by which a
keratinocyte of the basal layer ultimately changes
into keratin is known as keratinization and it
usually takes 4 weeks for its completion. The
epidermal turnover time is about I month.
The other member cells found in the
epidermis are melanocytes (derived from neural
crest, produce melanin), Langerhans cells (origin
from bone marrow, play important role in
cutaneous immune mechanisms), and Merkel
cells (slow adapting type 1 mechanoreceptors).
The Dermal-epidermal Junction
The dermal-epidermal junction (DEJ) is a
basement membrane zone (BMZ) that welds the
epidermis to underlying dermis.
Fig. 3.1: Structure of the skin
Essentials in Dermatology10
Fig. 3.2: Diagrammatic representation of shapes of various cells in the epidermis and changes in them as
they move up from basal cell layer to stratum corneum during the process of keratinization
The dermal-epidermal junction is undulated,
forming dermal papillae (upward projections of
the dermis into the epidermis) and rete ridges
(downward projections of epidermis into the
dermis). The DEJ under electron microscope
consists of four components- plasma membrane
of basal keratinocytes with hemidesmosomes,
lamina lucida (made up of anchoring filaments
and laminin 5), lamina densa ( has type IV
collagen and laminin 5), and lamina
fibroreticularis (containing anchoring fibrils,
dermal microfibrils, and collagen fibers). This
DEJ is weakest at lamina lucida.
The dermis is formed by connective tissue
having fibres (collagen, elastic and reticulin) and
ground substance (made up of proteoglycans
and glycosaminoglycans). It varies in thickness
from about 1 mm on the face to 4 mm on the
back and thigh.
Collagen fibres are the major component of
the dermis, accounting for 75% of dry weight of
the skin. Approximately 80-90% of collagen
fibres in the dermis are of type I collagen. They
are responsible for the mechanical properties of
the dermis. Elastic fibers constitute approxi-
mately 4% of dry weight of dermal matrix
proteins. Due to their elasticity, they maintain
the normal configuration of the skin.
The dermis can be divided into an upper-
papillary dermis that interdigitates between the
rete ridges and the deeper-reticular dermis
recognized by the thicker, aggregated bundles
Microanatomy of the Skin 11
Epidermal Appendages Like
a. Pilosebaceous unit
b. Sweat glands.
Pilosebaceous unit: It consists of a hair follicle
containing hair and sebaceous glands opening
into follicular canal of hair follicle.
Sebaceous glands are lipid secreting
holocrine glands. Their maximum density is in
seborrhoeic areas of the body, i.e. scalp, face,
upper chest, etc. They get activated at puberty
under the influence of androgen hormone.
Functions of sebum are:
1. Barrier function by preventing loss of water
from the skin
2. Emulsification of surface eccrine sweat
3. May have mosquito repellant action
4. Protection against sunburn
5. Has a vitamin D precursor.
Hair structurally consists of a cuticle, cortex
and medulla. These keratinous fibres are of two
types in adults-terminal hair and vellus hair.
Hair grows at the rate of 0.3 mm per day and
they undergo growth cycle. These recurring
cycles consist of anagen (active growth phase),
catagen (static growth phase) and telogen
(shedding phase) phases. On the scalp, 80% to
85% of hair are in anagen phase and 15% to 20%
in catagen and telogen phase. The anagen phase
lasts for two to five years, a short catagen of few
days and a telogen phase of three months.
Functions of hair are:
2. Hair screens entry of irritants to nose
3. Protect scalp from sunrays
4. Shields the eyes
5. Helps in perception of tactile stimuli.
Sweat glands: Two types of sweat glands are
eccrine and apocrine sweat glands.
Eccrine sweat glands: They are tubular
structures, which open on to the skin directly and
have three segments–the secretory coil (consists
of single layer of secretory cells–clear and dark
cells) in the deep dermis, straight intradermal
(has two layers of cuboidal cells lined by
eosinophilic cuticle on luminal side) part and
coiled or spiral intraepidermal (consists of an
inner layer of luminal cells and two to three outer
layer of epithelial cells) part. Sweat glands are
most abundant on the palms, soles, forehead and
axillae. These glands are highly developed and
responsive part of the thermoregulatory
apparatus, innervated by cholinergic nerve
Functions of sweat are:
1. Sweating in heat stress
2. Excretion of heavy metals and drugs.
Apocrine sweat glands: These tubular glands
consists of two main parts – the coiled secretary
gland (consists of single layer of cuboidal or
columnar cells, surrounded by a layer of
myoepithelial cells) and the straight excretory
duct (consists of double layer of cuboidal cells
and inner eosinophilic cuticle) which opens into
follicular canal just above the openings of
sebaceous glands. They are distributed along the
mammary line, i.e. axillae, areolae, periumbilical
area, mons pubis, genital and perianal areas.
Apocrine gland secretion in man serves no
function. Pheromones–its role in humans is
Nail unit: It is yet another epidermal appendage.
It consists of nail matrix just underneath the
proximal nail fold which gives rise to nail plate
– a keratinized structure. The distal portion of
the nail matrix is visible usually in thumbnail as
white crescent or half moon known as lunula.
The rectangular nail plate rests on a nail bed and
is bounded on two sides by lateral nail folds.
The cuticle seals the space between nail folds and
nail plate. The distal portion of nail juts out as a
free end. The space underneath the free end of
the nail plate is called subunguium. In contrast
to hair, nail is a continuously growing structure,
usually at a rate of 0.1 mm per day.
Essentials in Dermatology12
Functions of nails are:
1. Protect terminal phalanges
2. Cosmetic function
3. Helps in appreciation of tactile stimuli
4. Scratching of skin
5. Helps in holding minute objects with finger
Besides the above elements, dermis contains
blood vessels which form two plexuses (other
than providing nutrition to the skin, blood
vessels regulate temperature and blood
pressure), lymphatics roughly parallel the major
vascular plexuses, nerves of the skin are part of
two major systems – somatic sensory and
autonomic motor, smooth muscle occurs in the
skin as arrectores pilorum, as the tunica dartos
of the scrotum and in the areolar around the
nipples and cells – mast cells, fibroblasts,
monocytes, macrophages, dendrocytes and
Subcutaneous Fat (Hypodermis)
The subcutaneous fat layer is constituted by
adipocytes. It is abundant over the breasts,
buttocks, and abdomen, thinner over the nose
and sternum and absent over the eyelids and
male genitalia. It acts as shock absorber, helps
in heat production and hormone conversion,
facilitate mobility of skin over structures that
underlie and acts as an insulator for heat. A
cosmetic role is contributed by the accentuated
distribution of fat in some sites in the sexes. Most
importantly, it stores triglycerides, which serves
as fuel for energy.
Physiology, Biochemistry and Immunology of the Skin 13
Main functions of the skin are protection,
thermoregulation, sensory, storage organ,
vitamin D formation, absorption, excretion,
immune surveillance, mechanical and cosmetic
function. Some important physiological,
biochemical, and immunological processes of the
skin are summarized below.
PROTECTIVE FUNCTIONS OF THE SKIN
The innermost region of human skin is the
subcutaneous fat layer. This layer insulates
reduces heat movement into or out of the body,
absorbs energy from blunt mechanical trauma
and is active in general energy metabolism.
Superficial to the fat layer lies the dermis,
composed of collgen-glycosaminoglycan
complexes which also protects the body from
blunt mechanical trauma. Overlying the dermis
is the epidermis which consists of several
stratifying layers of nucleated keratinocytes and
anucleated top layer, the stratum corneum which
performs the major barrier function.
The skin acts as a two way barrier to prevent
the inward or outward passage of water and
electrolytes. The physical barrier is largely
situated in the epidermis, isolated epidermis
being as impermeable as whole skin, whereas
once the epidermis is removed, the residual
dermis is almost completely permeable. The
4 Physiology, Biochemistry and
Immunology of the Skin
epidermal barrier is localized to the stratum
The skin has two barriers to UV radiations:
a melanin barrier in the epidermis; and a protein
barrier concentrated in the stratum corneum.
Both function by absorbing radiation thereby
minimizing absorption by DNA and other
The skin is considered to be a composite
membrane with three anatomically distinct
layers; the stratum corneum (10 µm), the viable
epidermis (100 µm), and the uppermost papillary
layer of the dermis (100-200 µm), each having a
different diffusion constant. Even healthy adult
human skin allows some permeation of almost
every substance, and rates of penetration of
different materials may differ by 10,000 fold.
The efficiency of the barrier differs between
body sites. The scrotum is particularly permeable
and the face, forehead, and dorsa of the hands
may be more permeable to water than the trunk,
arms, and legs. The palms are particularly
impermeable to nearly all molecules except
The barrier is affected by many other factors,
such as age, environmental conditions and
physical trauma, and permeability can be
Essentials in Dermatology14
enhanced by various agents, permitting
increased access of topically applied drugs.
Keratinization is a process of differentiation of
germinative cells in the basal cell layer into the
deceased cornified cells of stratum corneum.
1. Synthesis of distinctive proteins (e.g. keratins,
filaggrins, and involucrin) and lamellar
2. Alterations of nuclei, cytoplasmic organelles,
plasma membranes and desmosomes.
Keratin function is to provide mechanical
strength, cellular structure, and assistance in
adhesion molecule attachment. “Soft” keratin
desquamates as the result of enzymatic action
but the “hard” keratin of the hair and nails
does not, thus requiring periodic cutting.
The epidermis is the prototype of keratinizing
squamous epithelia, also present in the
oesophagus, vagina and oral mucosa.
MELANOCYTES AND MELANOGENESIS
Melanocytes are pigment forming cells in the
epidermis. Each melanocyte supplies pigment,
melanin to approximately 36 keratinocytes and
thus form epidermal melanin unit. Two types of
melanin are synthesized by melanocytes,
eumelanins and pheomelanins. Melanin is
synthesized from tyrosine under the influence
of enzyme tyrosinase through the formation of
various intermediates (dihydroxyphenylalanine
[dopa], dopaquinone, leucodopachrome,
dopachrome, 5’ 6’ dihydroxyindole, indole
5’ 6’-quinone, melanochrome).
FUNCTIONS OF THE MELANIN
1. Protect the skin from harmful effects of
sunlight by scattering and absorbing
2. Melanin may also act as a biochemical
neutralizer of toxic free radical oxygen
derivatives, byproducts of various inflam-
3. Melanocytes situated in the matrix of anagen
follicles impart to hair various colours, e.g.
blond, brunette and red head.
The maintenance of a near constant body core
temperature of 37o
C is a great advantage to
humans, allowing a constancy to biochemical
reactions which would otherwise fluctuate
widely with temperature changes.
The thermoreceptor cells of the skin are
distributed irregularly over the skin, there being
warm- and cold-sensitive thermoreceptors.
Information on changes in their stimulation in
response to changes in the temperature is sent
to the hypothalamus leading to either to
inhibition of sweating or stimulation of
shivering. Skin temperature has a greater role
in mediating the behavior, for example by
turning on the heating or putting on extra
Thermoregulation depends on several
factors, including metabolism and exercise but
the skin plays an important part in control
through the evaporation of sweat and by direct
heat loss from the surface. Heat can be lost
through the skin surface in four ways:
Skin failure is defined as a loss of normal
temperature control with inability to maintain
the core temperature, failure to prevent
percutaneous loss of fluids, electrolytes and
proteins with resulting imbalance and failure of
Physiology, Biochemistry and Immunology of the Skin 15
mechanical barrier to penetration of foreign
materials. Apart from thermal burns, skin failure
can occur as a consequence of a number of
dermatological diseases including Stevens
Johnson syndrome, toxic epidermal necrolysis,
pustular psoriasis and erythroderma of various
COLLAGEN IN THE DERMIS
The closely related proteins of collagen family
are the main fibrillary components of the
connective tissues and the major extracellular
proteins of the human body. The physiological
role of collagen fibers in the skin is to provide
tensile properties that allow the skin to serve as
a protective organ against external trauma.
Collagen is the major structural protein
constituting 70% to 80% of dry weight of the
dermis. The main aminoacids in collagen are
glycine, proline and hydroxyproline.
Elastic Fibers in the Dermis
Elastic fibers of the connective tissue form a
network responsible for the resilient properties
of the skin. In sun protected human skin, elastin
content is about 1% to 2% of the total dry weight
Ground Substance in the Dermis
The ground substance of skin is largely made
up of glycosaminoglycans(GAG) and provide
viscosity and hydration in the dermis. Three
types of GAG are chondroitin sulphate,
dermatan sulphate and hyaluronic acid.
IMMUNOLOGICAL COMPONENTS OF
The immunological functions of the skin depend
both upon cells in the epidermis and on dermal
cellular constituents. Antimicrobial peptides
(AMPs) are a diverse group of proteins that are
involved as first line of immune defense by many
living things. In human skin, AMPs provide a
chemical barrier to potentially pathogenic micro-
organisms. Sebaceous lipids have been reported
to possess antibacterial properties and
glycophospholipids and free fatty acids of
stratum corneum have bacteriostatic effect
selective for pathogenic organisms.
Skin associated lymphoid tissue (SALT) is
langerhans cells, T lymphocytes, mast cells and
keratinocytes. They are involved in various
hypersensitivity reactions of the skin. Hyper-
sensitivity is defined as inappropriate or
exaggerated immune response to a foreign or self
antigen resulting in tissue damage. Main types
of hypersensitivity responses of skin are type I
(immediate), type II (antibody-dependent
cytotoxicity), type III (immune complex disease)
and type IV(cell mediated or delayed). Urticaria
and anaphylaxis is the example for type I
hypersensitivity, transfusion reactions for type
II hypersensitivity, leukocytoclastic vasculitis for
type III hypersensitivity and allergic contact
dermatitis for type IV hypersensitivity.
Essentials in Dermatology16
Dermatologists often prefer to examine the
patient before obtaining the history and review
of systems. This approach is preferred because
diagnostic accuracy is higher when visual
examination is approached without precon-
ceived ideas. Moreover, some dermatologic
lesions are so distinctive that history is not
required to make a diagnosis.
A practical and convenient way to arrive at
a diagnosis may be...
PRELIMINARY GENERAL HISTORY
Biodata: Age, sex, income, occupation, address,
Principles of Diagnosis in
Chief complaints: Limit them to just three only
History of present illness: “What is your skin
This allows patient to point out the lesions and
the area involved.
Three basic questions.
1. Onset and evolution.
3. Treatment taken.
Onset and evolution: To determine the duration
of the disorder, how it evolved over time, initial
site of the disease, mode of spread.
Symptoms: Itching is the most common and
most important symptom in dermatology.
Intense itching, e.g. scabies, atopic dermatitis,
lichen planus, dermatitis herpetiformis.
Pain may predominate in herpes zoster,
furuncles, etc. Loss of sensation points towards
leprosy, or follicular mucinosis. Allodynia
(production of pain by trivial stimuli) occurs in
postherpetic neuralgia. Reversal of hot and cold
sensation may be due to ciguatera fish poisoning.
They may be just asymptomatic as in molluscum
contagiosum, basal cell carcinoma, etc.
Treatment history: Skin lesions are often self-
manipulated by home remedies, or over the
Principles of Diagnosis in Dermatology 17
counter medication, since they are easily
accessible, and since disease is of chronic nature.
Full detailed history of medication used
should be known because
1. Disease may be caused or aggravated by
medication- Fixed drug eruption, dermatitis
2. Patient may have already used the drug
without desired outcome, we planned to
give. Avoid potential embarrassment when
the patient says “I have already tried that and it
Detailed follow-up history: This history is taken
after some diagnosis or conclusion was reached
by initial history and examination, and this
• Past history.
• Family history.
• Review of systems.
• Social history.
• Females- menstrual/obstetric history.
a. History of same disease before.
b. History of prolonged illness– diabetes,
c. Drugs used for other problems (drug rash,
d. Drug allergies– avoid prescribing those
e. Atopic history– asthma, hay fever, eczema.
Family history: It is important for diagnosis,
prognosis, treatment and genetic counseling.
Family history important in:
a. Infectious disorders – scabies
b. Inherited disorders – atopy, psoriasis.
Review of other systems: It is required in
multisystem disorders like SLE, scleroderma, or
Social history: Encounter with potentially
sensitizing materials e.g., in patients with
industrial dermatosis, contact dermatitis. Stress
and strain at work may lead to exacerbation of
psoriasis, neurodermatitis, etc.
Habits: Alcohol induces porphyria cutanea tarda
in predisposed, influences the severity and
therapeutic options in psoriasis. Smoking may
be aggravating factor in palmoplantar
It has been said by Goethe “What is most difficult
of all? It is what appears most simple: To see with
your eyes what lies in front of your eyes” .
Requirements for the Skin to be
Three essential requirements
1. Preferably a completely undressed patient,
clothed only in an examination gown. If not
possible, at least, the affected part should be
2. Adequate illumination: Preferably sunlight
or a bright overhead fluorescent lighting.
Penlight is used in side lighting- to determine
if a lesion is subtly elevated and for
examining the oral cavity.
3. An examining physician ready to see what
is before him.
A complete cutaneous examination should
be made, this includes examining—
• Skin from head to foot.
• Mucous membrane in mouth and genitals
• Hair and nails.
The examination includes inspection and
palpation, besides percussion and auscultation.
Palpation is useful in—
• Assessing the texture and consistency.
• Evaluate whether a lesion is tender or not.
• Reassure a patient that they do not have a
Essentials in Dermatology18
Hand lens useful on occasions like identifying:
a. Altered skin markings in tumors.
b. Nail fold telangiectasia.
c. Burrows in scabies.
d. Wickham‘s striae- for this place a drop of
mineral oil on the area, which makes the
stratum corneum transparent.
Subtle genital warts- ‘aceto-whitening’,
gauze soaked with 5% acetic acid applied in
suspected area for 3 minutes, warts turn white.
Actually individual skin lesions are
analogous to the letters of the alphabet, and
groups of lesions can be analogous to words or
phrases. Basis of morphological lesions is given
in the form of table for clear understanding.
Basis of morphological lesions in dermatology
1. Impalpable change- Macule
2. Palpable change-
• Solid change-Papule, plaque, nodule, wheal
• Superficial visualized free fluid collection-
• Superficial free pus collection-Pustule, abscess
• Deep free fluid/semisolid material collection-Cyst
3. Loss of skin-Erosion, ulcer
4. Healing stage- Scale, crust
5. End stage- Atrophy, scar
Ultimately, diagnosis may rest on recognition
of lesions and their distribution and
arrangement, whether they are primary,
secondary or some special lesions. Describe their
shape, size, color and distribution. Take the
help of diagnostic tools for further details.
These are the lesions, which appear first in any
skin disease. They are the best clues to the
diagnosis. They are:
• Macule: The macule is a discrete, flat,
circumscribed lesion that differs from
surrounding skin because of its color
(Fig. 5.1). It may be a small or a large macule.
Earlier used term “patch” is now obsolete.
Macule may be erythematous, hypo-
pigmented, hyperpigmented or of any other
• Papule: It is a discrete, circumscribed, solid
elevated lesion of less than 0.5 cm in size (Figs
5.2 to 5.5). So, it is a palpable lesion. A papule
may be dome shaped, verrucous, umbi-
licated, pedunculated, etc.
Fig. 5.1: Macule—depigmented flat lesions of variable
size and shape of vitiligo vulgaris and lip tip type
Fig. 5.2: Papule—solid elevated lesions of verruca
vulgaris of less than 0.5 cm
Principles of Diagnosis in Dermatology 19
Fig. 5.3: Papule—dome shaped papule, a few of
them umbilicated of molluscum contagiosum
Fig. 5.4: Typical umbilicated papule of molluscum
Fig. 5.5 Violaceous colored papules of lichen
planus over the genitalia and thigh
• Plaque: A plaque is a circumscribed solid
raised lesion with a flat top. It is formed due
to coalescence of papules (Figs 5.6 and 5.7).
It may be a lichenified plaque, eczematous
plaque, psoriasiform plaque, flat smooth
• Nodule: A nodule is a discrete circumscribed
solid elevated lesion, which is more felt than
seen from the top (Figs 5.8 and 5.9). It may
develop from a papule.
terms used for circumscribed elevated lesions
containing free clear fluid, called blister. If it is
less than 0.5 cm, it is called vesicle (Fig. 5.10)
and if more than this, it is a bulla (Figs 5.11 and
5.12). They may be tense or flaccid.
Fig. 5.6: Plaque—flat elevated lesions covered with
silvery white micaceous scales of psoriasis vulgaris
Essentials in Dermatology20
Fig. 5.7: Large well-defined erythematous plaques
of psoriasis vulgaris
Fig. 5.8: Nodule—solid deep-seated elevated
lesion due to secondaries in the skin
Fig. 5.9: Erythematous tender nodules of furuncle
over the face and neck
Fig. 5.10: Vesicle—cluster of tiny blisters of herpes
labialis over the lips
Fig. 5.12: Large tense bulla of bullous pemphigoid
on an erythematous base
Fig. 5.11: Bulla—small blisters on erythematous
bases of bullous pemphigoid
Principles of Diagnosis in Dermatology 21
Fig. 5.13: Pustule—numerous tiny pus filled lesions
on erythematous background in a case of pustular
• Pustule: A pustule is a circumscribed
elevated lesion containing visible pus
(Fig. 5.13). It results from an epidermal or
upper dermal accumulation of pus.
• Cyst: A cyst is a sac that contains liquid or
• Wheal: Wheal is a pale or erythematous
edematous, transient, evanescent lesion.
• Diffuse thickening of skin: It may result
from edema of dermis (pitting edema or
nonpitting edema) or infiltration of dermis
(e.g. myxoedema, lepromatous leprosy).
Secondary or Consecutive Lesions
They are due to the subsequent changes, which
takes place on the primary lesions, either as a
part of natural evolution or due to manipulation
of the patient.
• Oozing: It is due to the rupture of vesicles or
• Crust: It is dried up exudate like serum, pus
or blood (Fig. 5.14). It may be thick or thin,
friable or adherent. It occurs in many
inflammatory and infectious diseases.
• Scale: Scales are thin, dry plates of heaped
up desquamating epithelial cells formed as
a result of either increased or abnormal
keratinization (Fig. 5.15).
• Excoriation: An excoriation is a superficial
erosion or ulcer caused by scratching. So,
it will be linear or have a geometric outline
• Erosion: It is a superficial ulceration
involving epidermis only which heals
without scarring (Fig. 5.17).
• Ulcer: It is a break in continuity of epithelium,
which involves epidermis, and dermis of the
skin (Fig. 5.18). It has length, breadth as well
as depth. It heals with scar formation.
• Fissure: Fissure is a linear crack in the skin,
which may be superficial or deep to the
• Lichenification: It is characterized by
thickening of the skin (becomes leather
like) with increased skin markings and
pigmentation. It is seen in chronic dermatitis.
• Scar: A scar is an evidence of destruction of
the skin with fibrotic tissue replacement. It
occurs wherever ulceration has taken place
and reflects the pattern of healing in those
Fig. 5.14: Crust—dried out oozed material over the
face in impetigo contagiosa
Essentials in Dermatology22
• Pigmentation: Pigmentation may be hyper,
hypo- or depigmentation of the skin (varies
according to the quantity of melanin).
• Atrophy: Atrophy refers to a diminution
in the size of a cell, tissue, organ or part of
the body. The skin becomes thin, shiny and
wrinkled. Atrophy may be of epidermal,
dermal or subcutaneous fat.
• Sclerosis: Sclerosis means a circumscribed or
diffuse hardening or induration in the skin.
It occurs as a result of an increase in the
amount of dermal collagen, expansion of the
Fig. 5.15: Scale—face and trunk covered with moist
scales of pemphigus foliaceous
Fig. 5.16: Excoriation—multiple linear scratch
marks due to itching over psoriatic plaques
Fig. 5.17: Erosion—multiple superficial eroded
areas in herpes genitalis
Fig. 5.18: Ulcer—single, painless, indurated
ulceration of extragenital primary chancre
Principles of Diagnosis in Dermatology 23
collagen by ground substance material or
altered quality of collagen.
These lesions are given below:
• Comedone: It is a plug of keratin and sebum
formed in the follicular canal of
pilosebaceous unit. Comedones may be
closed or open.
• Burrows: These are serpentine caves of
scabies mite at the level of stratum
granulosum. They are visible as S-shaped
brownish-black lesions, which at their distal
end have a papule housing the mite.
• Alopecia means loss of hair.
• Telangiectasia: It refers to individually
visible dilated vessels.
• Poikiloderma: It is a combination of atrophy,
pigmentation and telangiectasia.
• Purpura: It is visible extravasated blood
(Fig. 5.19). It may occur as tiny pinpoint spots
(petechiae) or larger spots (ecchymoses). The
term hematoma refers to an area of massive
bleeding into the skin and underlying tissues.
“Pinch purpura” hemorrhage induced by
mild often subclinical trauma is a charac-
teristic presentation of primary systemic
amyloidosis of the skin. Similar periorbital
hemorrhage following proctoscopy or
pulmonary function testing, postproctoscopic
purpura also typifies the vascular fragility
induced by systemic amyloidosis.
• Livedo: Blue red discoloration of the skin of
skin due to passive congestion of the vessels
often with net-like pattern
• Exanthem: Abrupt appearance of diffuse or
generalized similar skin lesions (usually
represents viral infections or drug reactions)
• Enanthem: Abrupt appearance of mucosal
lesions similar to exanthems.
• Nits: They are glistening white ovoid bodies
attached to shafts of hair.
Fig. 5.19: Purpura—multiple, small, erythematous non-blanchable lesions of purpura
Essentials in Dermatology24
Figs 5.20A and B: Distribution of skin lesions in
atopic dermatitis in infants
Figs 5.21A and B: Distribution of skin lesions in
atopic dermatitis in children and adults
DISTRIBUTION OF SKIN LESIONS IN SOME DERMATOLOGICAL DISORDERS
Disease Classical sites of involvement
1. Acne vulgaris Face, upper trunk, proximal parts of upper extremities
2. Atopic dermatitis Infants -face and extensor aspects of limbs (Figs 5.20A and B)
Children and adults-flexures (Figs 5.21A and B).
3. Dermatitis herpetiformis Scalp, extensor aspects of limbs, shoulder and buttocks (Figs
5.22A and B).
4. Lichen planus Flexor aspect of upper extremities (wrists), trunk (lumbosacral
area), shins, glans penis (Figs 5.23A and B).
5. Neurodermatitis Nape of neck, wrist, ankle, genitalia, and perianal area (Figs
5.24A and B).
6. Pityriasis rosea Herald patch-trunk. Daughter patches-Christmas tree pattern
over the trunk (Figs 5.25A and B).
7. Psoriasis vulgaris Extensor aspects of limbs, scalp, lumbosacral area (Figs 5.26A
8. Scabies Infants-Face, intertriginous area of fingers, palms and soles,
extensor aspect of limbs, around umbilicus, genitalia and
gluteal area (Figs 5.27A and B). Children and adults-finger
web spaces, wrist, elbows, axillary fold, around areola and
umbilicus, genitalia, and gluteal area (Figs 5.28A and B).
9. Seborrhoeic dermatitis Infants-Cradle cap over scalp (Figs 5.29A and B). Adolescence
and adults- scalp, eyebrows, nasolabial folds, presternal and
interscapular area, axilla and groin (Figs 5.30A and B).
10. Tinea versicolor Upper trunk (Figs 5.31A and B).
Principles of Diagnosis in Dermatology 25
Figs 5.22A and B: Distribution of skin lesions in
Figs 5.23A and B: Distribution of skin lesions in
Figs 5.24A and B: Distribution of skin lesions in
neurodermatitis (lichen simplex chronicus)
Figs 5.25A and B: Distribution of skin lesions in
Figs 5.26A and B: Distribution of skin lesions in
Figs 5.27A and B: Distribution of skin lesions in
infants in scabies
Essentials in Dermatology26
Figs 5.28A and B: Distribution of skin lesions in
children and adults in scabies
Figs 5.29A and B: Distribution of skin lesions in
seborrhoeic dermatitis in infants
Figs 5.30A and B: Distribution of skin lesions in
seborrhoeic dermatitis in adolescence and adults
Figs 5.31A and B: Distribution of skin lesions in
Certain phenomenon and signs are there to be
seen and observed; others need to be elicited by
• The Koebner phenomenon: The Koebner
phenomenon is the development of
morphologically identical lesion/s in the
traumatized uninvolved skin of patients who
have cutaneous diseases. It is also known as
isomorphic phenomenon, a self-explanatory
term. This phenomenon is observed in a number
of dermatological disorders such as psoriasis
(Fig. 5.32), lichen planus, vitiligo, eczema,
dermatitis herpetiformis, bullous pemphigoid,
warts (Figs. 33 and 34), molluscum contagiosum
(Fig. 5.35), etc.
• Reverse Koebner phenomenon: Area of
psoriasis clears of following injury.
• Remote reverse Koebner phenomenon is the
spontaneous repigmentation of vitiligo
patches distant from the autologous skin
Principles of Diagnosis in Dermatology 27
Fig. 5.32: Koebner phenomenon in psoriasis
vulgaris over the trunk
Fig. 5.33:Koebner phenomenon in
plane warts over the wrist
Fig. 5.34: Koebner phenomenon
in verruca vulgaris
Fig. 5.35: Koebner phenomenon in molluscum
• Dermographism: It can be elicited with the
help of blunt instrument like key. Firm
stroking of skin may result in exaggerated
triple response of Lewis, which persists for
more than 5 minutes. Stroking causes hista-
mine to be released, leading to localised
redness and edema (Wheal). Dermographism
can occur in urticaria.
• Darier’s sign: When the above phenomenon
is limited to skin overlying a lesion (macule
or papule), it is called as Darier’s sign and is
diagnostic of urticaria pigmentosa (Mast cell
• Pseudo-Darier’s sign: Here stroking of skin
produces transient induration with pilo-
Essentials in Dermatology28
erection, seen in congenital smooth muscle
• White dermographism: Stroking the skin of
atopic patients produces a characteristic
white line in the involved area.
• Grattage test: It is done on a scaly lesion to
look for types of scales. Scraping of the lesion
is done with a glass slide. Fine powdery
scales of tinea versicolor can be made out if
you examine the glass slide against light after
scraping the lesion.
• Candle sign and last cuticle sign: In
psoriasis, if the silvery-white scales are
scraped off, they detach from the lesions as
small flakes, similar to wax scraped from
candle. With continued scraping, one can
remove a coherent moist sheet from the lesion
corresponding to the lowest layers of
• Auspitz’s sign: This sign if present is
diagnostic of psoriasis. It has three
1. On scraping with glass slide, initially
silvery white micaceous scales come out.
2. Removal of the scales is followed by a thin
3. On its removal by glass slide, minute
pinpoint bleeding spots are seen.
• Diascopy (Vitropression): It is based on the
principle that vascular lesions will blanch in
response to pressure with a glass slide
whereas purpuric lesions, in which blood and
blood pigments have leaked from the
cutaneous vessels, will not blanch. Diascopy
is most useful in detection of nonblanchable-
raised purpura, the clinical hallmark of
cutaneous vasculitis. It is useful in
differentiating nevus anemicus from nevus
depigmentosus. Nevus anemicus (a localised
area of vasoconstriction) on diascopy of
adjacent skin reveals an identical color to
depigmented area. By contrast diascopy of
skin adjacent to nevus depigmentosus or
vitiligo, the affected area still remains paler.
Apple jelly nodules in lupus vulgaris active
edge of the lesion, appear as translucent
brownish color granulomatous nodules, a
distinctive feature of the disease.
• Ollendorf’s sign: If touching of the papule
of secondary syphilis with the head of pin is
exquisitely tender, then Ollendorf’s sign is
said to be present.
• Nikolsky’s sign: A frictional force is applied
with a finger or thumb over the apparently
normal skin, usually overlying a bone like the
clavicle or perilesional skin in a patient with
vesiculo-bullous lesions. If epidermis or
surface of the skin breaks down or peels off
leaving raw moist erosion, it is called positive
Nikolsky’s sign. Various disorders, in which
Nikolsky’s sign is positive, are pemphigus,
staphylococcal scalded skin syndrome, toxic
epidermal necrolysis, etc. This test is based
on the fact that in certain diseases, even the
normal looking skin has a weak cohesion
between its different layers.
• Bulla spread sign: It can be demonstrated by
marking the boundary of the bulla and then
applying pressure with a finger on the edge
of the bulla. In pemphigus, bulla spreads
beyond the marked line showing that active
process of acantholysis has weakened the
cohesion between keratinocytes.
• Button holing sign: In neurofibromatosis, if
fingertip is pressed over neurofibroma, the
finger gapes in due to defect in the dermis.
• Dimple sign: It distinguishes dermato-
fibroma from malignant melanoma.
Applying lateral pressure with thumb and
index finger –results in formation of a dimple
in dermatofibroma, whereas melanoma
protrudes above its original plane.
• Hess test or Capillary fragility test: A blood
pressure cuff is applied to upper arm
between systolic and diastolic pressure for
5 minutes. The number of petechiae in
predetermined area of 5 cm circle is counted.
Principles of Diagnosis in Dermatology 29
If number is more than 5, it is abnormal
• Pathergy test: Inject 0.1 ml of physiologic
saline intradermally with fine needle over the
forearm. Read after 24-48 hours. Pustules or
papules suggest the diagnosis of Behcet’s
disease. Histology shows neutrophilic
infiltrate or vasculitis.
• Testing sensation and palpation of
peripheral nerves may be required to fulfil
one of the cardinal features of leprosy and
thus help in its diagnosis.
LABORATORY AND SPECIAL TESTS
They may be needed to confirm the diagnosis:
1. Wood’s light examination: It is useful in
detecting fungal infections of the scalp
(bluish-green fluorescence in tinea capitis
caused by Microsporum species—Micros-
porum canis and Microsporum audouinii),
tinea versicolor (yellow fluorescence),
erythrasma (coral red fluorescence),
porphyrins in patients with porphyria
cutanea tarda (Urine will produce bright red
fluorescence), trichomycosis axillaris
(orange fluorescence), Pseudomonas in-
fection (green fluorescence), etc. In scabies,
fluorescein solution fills burrows. In
pigmentary disorders, vitiligo, piebaldism,
and ash leaf macules of tuberous sclerosis,
the lesions become prominent.
2. KOH preparation: Indicated when
infection with fungi or yeast is suspected,
e.g. dermatophytosis, tinea versicolor,
3. Tzanck test: It is used in the diagnosis of
various skin disorders characterised by
vesicles, pustules, bullae and erosions and
in particular in viral infections like herpes
simplex, herpes zoster and varicella
4. Gram’s stained pus smear: Indicated for
pyogenic infections, vaginal and urethral
5. Tissue smear: It is used for diagnosis of
donovanosis (granuloma inguinale).
6. Dark field (ground illumination) test:
Primary and secondary syphilis can be
easily diagnosed by demonstrating
7. Wet preparation: It is utilized for diagnosis
of trichomonal infestation of the genital
8. Slit skin smear: This test is performed on
leprosy patients to demonstrate acid-fast
bacilli in skin smears.
9. Lepromin test: It is useful for classification
of leprosy and is strongly positive in
tuberculoid leprosy and mildly positive in
borderline tuberculoid leprosy. It is negative
in borderline borderline, borderline
lepromatous and lepromatous leprosy.
10. Dermatoscopy (Epiluminescence micros-
copy, dermoscopy): Method of observing
superficial layers of skin using 10-100 X
magnification with oil immersion. Both
hand held and computer assisted
instruments are available. It is used for
differential diagnosis of pigmented skin
lesions, melanoma, for detailed
examination of nail fold capillaries,
Wickham’s striae, scabies burrows (hang
glider sign), surface of verrucae and the
scalp surface (cadaver hairs and
exclamation point hairs suggest alopecia
areata, loss of follicular openings indicates
scarring alopecia and follicular
hyperkeratosis point towards lichen
11. Biopsy: Most frequently skin biopsy is taken
to confirm a clinical diagnosis or to aid in
the establishment of a diagnosis where
clinical diagnosis is not apparent.
Essentials in Dermatology30
13. HIV antibody detection test
14. Culture and sensitivity test
15. Patch testing
16. Prick testing
17. Intradermal testing
18. LE cell phenomenon
19. Mouse foot pad inoculation
21. Hair examination and counts
22. Trichogram- method for analyzing hair
bulbs to identify in what stage hairs are
being lost and thus to distinguish between
different types of hair loss.
23. Electron microscopy
Five Thoughts for the Students in the
Field Of Dermatology
1. Diagnosis is the art of recognition, not the
science of cognition
2. The best diagnosticians are the ones with the
best visual memories
3. The best history is taken by one who already
knows the diagnosis
4. If puzzled, limit yourself to three working
5. A good colour atlas (a memory of 75 diseases
allows you to immediately recognize 95% of
all the skin lesions you will ever see) and a
good dermatopathologist are your best
Bacterial Infections 31
Normal human skin is colonized soon after birth
by a large number of bacteria that live as
commensal on the epidermis and epidermal
appendages. Coagulase negative staphylococci
(S. epidermidis) are inoculated during vaginal
passage; coryneform bacteria take up residence
on neonatal skin shortly after birth; and within
several weeks after birth, the flora of neonatal
skin is similar to that of adults. Staphylococcus
aureus is persistent member of the microbial
flora in 10 to 20% of the population. As many as
84% of healthy individuals have occasional
carriage of S. aureus in their anterior nares.
Pyoderma is a common purulent infection of the
skin caused by staphylococcal or streptococcal
organisms. They can be classified as primary
6 Bacterial Infections
Primary pyodermas are further divided into
non-follicular and follicular for clinical
application (Table 6.2) and on the basis of
organism involved (Table 6.3).
Non-bullous impetigo (Impetigo contagiosa of
• It is caused by S. aureus or group A
Streptococcus or both
• Occurs in children of all ages, common
in preschool and young school children
• Commonly over the face (especially
around nares) or extremities after trauma
• The initial lesion is a transient vesicle or
pustule that quickly evolves into a honey
coloured crusted plaque (Fig. 6.1)
• Surrounding erythema may be present
Table 6.1: Distinctive features of pyodermas
Primary pyodermas Secondary pyodermas
1. Invasion of normal skin by bacteria 1. Develop in areas of already damaged/compromised skin
2. Single species of bacteria involved 2. Mixture of organisms involved
3. Appearance of lesions is characteristic 3. Not characteristic
e.g., impetigo, erysipelas, furuncle
4. Treatment is clear cut – Drugs aimed 4. Role of antibacterial treatment less defined.
at the microorganism Here, the aim is to treat the underlying process
Essentials in Dermatology32
Table 6.2: Non-follicular and follicular pyodermas
A. Non follicular pyodermas include
B. Follicular pyodermas include
Table 6.3: Cutaneous diseases caused by
staphylococci and streptococci
1. Cutaneous diseases caused by
A. Direct infection of skin:
Impetigo, ecthyma, folliculitis, furunculosis,
B. Due to effect of bacterial toxin:SSSS, TSS.
2. Cutaneous diseases caused by streptococcus:
A. Direct infection of skin:
Impetigo, ecthyma, erysipelas, cellulitis,
vulvovaginitis, perianal infection, blistering
dactylitis, necrotizing fasciitis.
B. Due to effect of bacterial toxin:
Scarlet fever, toxic shock like syndrome
• Regional lymphadenopathy in up to 90%
of patients with prolonged untreated
• In severe cases, there may be fever,
adenitis and constitutional symptoms
• Differential diagnosis: 1.Tinea corporis –
has dry, scaly, advancing edge with
central clearing. 2. Ecthyma- charac-
terized by crusted ulcers (not erosions).
• Earlier bullous impetigo in neonates was
popularly known as pemphigus
• S. aureus (phage group II) is the causative
• Occurs commonly in the newborn and in
• Bullae (flaccid) rapidly evolve from
vesicles on areas of grossly normal skin
(Fig. 6.2) due to local production of
exfoliative toxin A and B.
• Differential diagnosis: Pemphigus
vulgaris-Generally occurs in young
adults. Erosions show no tendency to
heal, Nikolsky’s sign and bulla spread
sign are positive. More importantly,
mucosal erosions are more commonly
Fig. 6.1: Impetigo contagiosa–honey colored
crusted lesions over the face of a child
Fig. 6.2: Bullous impetigo–large pus filled blisters
over the trunk of a child
Bacterial Infections 33
Complications of Impetigo
• Post-streptococcal acute glomerulonephritis–
S. pyogenes type M-49
• Scarlet fever
• Erythema multiforme
Rheumatic fever in not a complication of
streptococcal skin infection (but of streptococcal
• Consequence of neglected impetigo
• S. aureus and/ or group A Streptococcus
are causative agents
• Most commonly occurs on the lower
extremities of children or neglected
• Poor hygiene and neglect are key
elements in pathogenesis.
• Dirty grayish-yellow crust surmounts a
“punched out” ulcer (Fig. 6.3).
Pyoderma affecting the hair follicles, classified
according to depth of invasion.
• Also known as follicular or Bockhart’s
• A small fragile dome shaped pustule
occurs at the infundibulum of a hair
follicle, often on scalps of children and in
the beard area, axilla, extremities and
buttocks of adults.
• Differential diagnois: Miliaria pustulosa
– non follicular pustules are wide spread,
which occur in hot and humid conditions
Sycosis barbae is a deep folliculitis with
perifollicular inflammation occurring in the
bearded areas of the face (Fig. 6.4) and upper
1. Pseudofolliculitis– Papules/pustules are
irregularly scattered at the site of ingrowing
beard hairs. Neck and angle of jaw (vs.
sycosis barbae– upper lip and below angles
of jaw) are preferentially involved.
2. Tinea barbae– Site involved is usually
submaxillary region or the chin. Hairs are
Fig. 6.3: Ecthyma–crusted lesion over the leg with
Fig. 6.4: Sycosis barbae– grouped follicular based
crusted lesions in the beard area of the face
Essentials in Dermatology34
broken or loosened (easy and painless
pluckablity) in the affected area. Loss of hair
is the norm. Suppurative or granulomatous
nodules rather than pustules characterize this
condition. Spores and hyphae can be demon-
strated in the hair by KOH examination.
3. Herpetic sycosis is usually limited for a few
days and invariably shows vesicles even in
4. Acne vulgaris is polymorphous condition
mainly of glabrous skin of the face where
comedones are the hallmark of that condition
Lupoid sycosis is deep, chronic form of
sycosis barbae associated with scarring usually
occurring as circinate lesion. Pustules and
papules surround a central scar (Fig. 6.5).
Differential diagnosis: Lupus vulgaris is
characterized by areas of scarring on one side
and progression on the other side. There is
absence of pustules in the lesions but it
demonstrates apple jelly nodules on diascopy.
Furuncles and Carbuncles
• A furuncle or boil is a deep-seated
inflammatory nodule that develops about a
hair follicle, often evolving into an abscess
(Fig. 6.6). They arise in hair bearing areas,
particularly in regions subject to friction,
occlusion, and perspiration.
Differential diagnosis: Folliculitis-
Inflammatory change is confined within the
follicle without any surrounding inflam-
mation – hence presents as a pustule whereas
furuncle presents as a nodule. There is less
pain and it heals without scar formation.
Cystic acne- Associated with other lesions of
acne – comedones, papules and pustules and
acne scars and it is confined to face and trunk.
• A carbuncle is a cluster of furuncles, more
extensive, deeper, communicating, in
filtrated lesion that develops when
suppuration occurs in elastic skin. It usually
involves the nape of the neck, back or thighs
and usually occurs in the setting of under-
lying diabetes mellitus, alcoholism, malnu-
trition, blood dyscrasias, iatrogenic or other
immunosuppression including HIV
infection. Fever, malaise, prostration
Differential diagnosis: Anthrax – charac-
terized by painless, hemorrhagic crusted
(blackish eschar) lesion with surrounding
gelatinous edema out of proportion to the
extent of the lesion.
Fig. 6.5: Lupoid sycosis–scarring alopecia in the
beard area showing active pustular lesions at the
Fig. 6.6: Furuncle–a red tender suppurated nodule
in a case of erythroderma
Bacterial Infections 35
Staphylococcal paronychia: Clinically, skin and soft
tissue of proximal and lateral nail fold are red,
hot and tender, and if not treated, can evolve to
abscess formation. In contrast, chronic or
recurrent paronychia caused by Candida albicans
is an infection of the space underneath the nail
Toxin Mediated Syndromes
Staphylococcal scalded skin syndrome
(SSSS) (Ritter’s disease)
• This is the most severe form of skin disease
due to the exfoliative exotoxins (A and B)
produced by S. aureus of group II, phage type
71 or 55 and is characterized by generalized
bulla formation and exfoliation. Most
commonly involves neonates and young
children, but also in adults with renal
compromise. Typically, the patient has fever
and is irritable. The changes usually begin
periorificially or in body folds (Figs 6.7 and
6.8). Then they spread rapidly. Nikolsky’s
sign is positive even on apparently normal
skin. One should culture the perineum, eyes,
ears, nose and throat, looking for S. aureus as
the focus of infection is located at a distant
site. The bacteria can not be cultured from
the skin. For differential diagnosis Table 6.4.
Toxic Shock Syndrome
• TSS is a multiorgan systemic illness due to
exotoxin (TSS-Toxin 1) producing strains of
• Case definition
1. Temperature of 38.9o
C or higher
2. Erythematous eruption
Figs 6.7 and 6.8: SSSS–typical periorificial and body fold involvement with peeling skin
Table 6.4: Differential diagnosis of SSSS from toxic epidermal necrolysis (TEN)
Staphylococcal scalded skin syndrome (SSSS) TEN
1. Age – less than 5 years 1. More than 40 years
2. Skin shows marked tenderness 2. Mild to moderate tenderness
3. Distribution – face, neck , axilla, groin 3. No clear distribution
4. Mucoca – not involved 4. Involved
5. Prognosis – good 5. Poor
6. Histology – subgranular split due to acantholysis 6. Necrosis of epidermis
Fig. 6.7 Fig. 6.8
Essentials in Dermatology36
3. Desquamation of palms and soles 1 to 2
weeks after onset
5. Involvement of 3 or more other organ
• About 85 to 90 percent of cases of TSS have
occurred in women at the time of mens-
truation; almost all had been tampon users
(particularly of super absorbent types).
• Differential diagnosis:
1. SSSS– It has the presence of bullae,
Nikolsky’s sign is positive with skin
tenderness, but systemic organs are not
involved and patient appears well-
2. Scarlet fever– not usually associated with
hypotension and shock.
3. Kawasaki’s syndrome– prolonged fever,
cardiac involvement, generalized
lymphadenopathy and absence of
The major pathogen belongs to group A and is
referred to as Streptococcus pyogenes. Streptococci
colonise damaged skin, although less frequently
than staphylococci. Major complications
following streptococcal infection are rheumatic
fever (following Streptococcal pyogenes
pharyngitis), acute glomerulonephritis (both
throat and skin infection), erythema nodosum
and guttate psoriasis, and scleredema of Buschke
(following throat infection).
Impetigo and Ecthyma already discussed.
Crowding, poor hygiene, and neglected minor
skin trauma contribute to the spread of
streptococcal impetigo in families.
Cellulitis and Erysipelas
• Predominantly streptococcal disease,
Staphylococcus aureus is occasionally
• Cellulitis is an acute, subacute or chronic
infection of loose connective tissue, mainly
of subcutaneous tissue whereas erysipelas is
a bacterial infection of the dermis and upper
• Erythema, warmth, swelling and tenderness
are constant features (Fig. 6.9). In erysipelas,
the edge of the lesion is well defined and
raised, but in cellulitis it is diffuse.
• In erysipelas, blistering is common.
• Except in mild cases, there are constitutional
• The leg is the commonest site; the next most
frequent site for classical streptococcal
erysipelas is face.
• Milian’s sign – cellulitis of the face does not
involve pinna, unlike erysipelas (as there is
no subcutaneous tissue there).
• Without effective treatment, complications
are common-fasciitis, myositis, subcutaneous
abscesses, septicaemia, and nephritis.
• For presumed streptococcal infection,
penicillin is the treatment of choice.
Fig. 6.9: Cellulitis–lower leg showing shiny
erythema and edema
Bacterial Infections 37
• This is nearly always a group A streptococcal
infection in children or teenagers.
• A large blister containing thin seropurulent
fluid forms on the distal phalanx, usually of
a finger, typically on a phalangeal pad.
Perianal Streptococcal Infection
• It occurs in children aged 1-10 years and is
characterized by intense perianal erythema,
perianal soreness, pain on defecation, faecal
retention and blood-streaked stools.
• Streptococcus pyogenes accounts for 10% of
cases of vulvovaginitis in prepubertal girls.
Toxin Mediated Streptococcal Disease
• Scarlet fever and streptococcal toxic shock
like syndrome are due to toxins.
• Scarlet fever is a diffuse erythematous
eruption resulting from the production and
subsequent circulation of pyrogenic
exotoxins A, B, C (erythrogenic toxin)
produced by group A streptococci usually
located in pharynx. Incubation period – 2 to
5 days – starts with an acute tonsillitis. Rash
appear on the 2nd day as finely punctuate
erythema “Sunburn with goose-pimples”.
Other features include Pastia’s lines
(transverse streaks in the skin folds due to
capillary fragility), pallor around mouth, red
strawberry tongue, and high fever.
Myocarditis may complicate this condition.
• Group A streptococci cause an acute
multisystemic syndrome coined toxic-shock
–like syndrome (TSLS) resembling that
caused by S. aureus.
Necrotizing Fasciitis (Streptococcal
• It represents cellulitis that has progressed to
gangrene of subcutaneous tissue followed by
necrosis of overlying skin (Fig. 6.10).
• It is not only caused by group A streptococci
but also due to other bacterial species
(mixture of anaerobes/facultative orga-
1. Gram’s stained smear from the purulent
material may demonstrate streptococci or
staphylococci or both.
2. Culture and sensitivity: Swabs taken from
infected sites may be sent for culture and
sensitivity, so that appropriate antibiotic may
be instituted to treat the condition.
3. Tzanck smear in SSSS shows acantholytic
4. Histopathology: Histopathological exami-
nation is hardly required for the diagnosis.
1. General measures such as improved
hygiene, loose light weight porous clothing,
regular bathing, use of antiseptics in bath,
antibacterial soaps, etc.
Fig. 6.10: Necrotizing fascitis—cellulitis progressing
to gangrene over the leg
Essentials in Dermatology38
2. Wet compresses: Condy’s compresses for
crusted lesions of pyoderma.
3. Incision and drainage is indicated when
furuncle has become localized and shows
4. Topical antibacterial agents such as gentian
violet, neomycin, fusidic acid or mupirocin.
5. Systemic antibacterial agents: Systemic
antibiotic therapy is indicated–
i. For extensive lesions of pyoderma
ii. For erysipelas, cellulitis, carbuncle,
furunculosis, SSSS, etc.
Penicillin is preferred for streptococcal
infection whereas penicillinase resistant
penicillin such as cloxacillin and cephalosporins
are required for staphylococcal infections. Oral
antibiotics (e.g., rifampicin 600 mg orally daily
for 10 days) have been effective in eradicating S.
aureus from most nasal carriers for periods of up
to 12 weeks in cases having recurrent
furunculosis. Intranasl application of 2%
mupirocin ointment for 5 days can eliminate S.
aureus nasal carriage in 70% of healthy
individuals for up to 3 months.
• Causative agent-Corynebacterium minutis-
simum, diphtheroids bacillus, gram positive,
non spore forming rod shaped organism.
• Bacterial infection of the intertriginous areas
like axilla, groin, gluteal cleft, inframammary
folds, umbilicus and toe web spaces.
• Usually manifest with asymptomatic red
brown macules with sharp border (Fig. 6.11).
• The best way to make the diagnosis is Wood’s
light examination for coral red fluorescence.
• Differential diagnosis: Hyperpigmented
tinea versicolor (asymptomatic in nature)
may appear like erythrasma. It predo-
minantly affects upper trunk, individual
lesions are small, but not erythematous and
satellite lesions are more commonly seen than
erythrasma. KOH examination and culture
from the lesions may clinch the diagnosis.
Tinea cruris is characterized by pruritic well
defined annular plaques with peripheral rim
of papulopustules, and satellite lesions.
• C. minutissimum can be cultured under
• A short course of systemic erythromycin is
the easiest method of treatment. Topical
imidazole creams are also effective.
• Causative agent- Corynebacterium tenuis.
• Collections of this bacteria forms concretions
on hairs, usually in the axilla.
• The axillary hairs are surrounded by white-
yellow (Fig. 6.12), red or black, difficult to
remove concretions that extend for several
• Diagnosis is established by examining hair
under microscope (Fig. 6.13), if necessary to
culture the organism.
Fig. 6.11: Erythrasma–asymptomatic brownish
macular lesion with fine scaling in the axilla
Bacterial Infections 39
• Differential diagnosis: Phthiriasis pubis can
be differentiated by its associated pruritis and
crawling sensation. Piedra can be
differentiated by its gritty hard feeling and
by doing a KOH examination.
• The easiest treatment is to shave the area and
treat the regrowing hairs with any topical
Fig. 6.12: Trichomycosis axillaris–yellow
discoloration of axillary hairs due to concretions
Fig. 6.13: Trichomycosis axillaris–same patient's
axillary hair under light microscope showing
concretions over the hair shaft
• Causative agent- Corynebacterium species,
Streptomyces species, Dermatophilus congo-
lensis and Micrococcus sedentarius.
• Multiple pitted defects, 2-5 mm in size occur
in thick horny layer of soles (Fig. 6.14).
• The key factor is maceration, usually arising
from hyperhidrosis, prolonged wearing of
shoes and improper hygiene.
• Differential diagnosis: The lesions are easily
recognizable, but simple hyperhidrosis,
erythrasma and tinea pedis have to be
• Topical erythromycin solution or benzoyl
peroxide gel can be applied once or twice
daily. Remove aggravating factors, if
• Botryomycosis is a chronic suppurative,
granulomatous disorder of bacterial origin.
True non- filamentous aerobic and anaerobic
bacteria such as Staphylococcus aureus,
Pseudomonas species, Proteus vulgaris,
Escherichia coli or Micrococcus cause it.
• Botryomycosis needs to be differentiated
from two other granulomatous diseases that
Fig. 6.14: Pitted keratolysis–soles demonstrating
Essentials in Dermatology40
Fig. 6.15: Botryomycosis–swelling of the foot with
multiple nodules over it
form granules - mycetoma and actino-
mycosis, since clinically it has similar features
• Effective treatment of botryomycosis
depends on various factors such as the
causative agent, location of the lesion and
immune status of the host. Various drugs,
mostly as single agents given for several
weeks, have been successfully used in
botryomycosis including trimethoprim-
sulfamethoxazole, minocycline, erythro-
mycin and cefazolin. In addition to
antibiotics, surgical excision and drainage of
lesions may be useful in certain patients.
• Actinomycosis is a chronic suppurative
infection caused by anaerobic Actinomyces
species. Actinomycetes are bacteria producing
filamentous and branching hyphae.
• Pathogenic organisms of these genera,
namely Actinomyces israelii exists as a
commensal in the oral cavity, tonsillar crypts
and genital mucosa.
• This organism gains entry when there is a
disruption of mucosal barrier in the form of
trauma or surgery. The resultant disease,
actinomycosis is characterized by an early
inflammatory phase which resembles
cellulitis and a more typical chronic phase,
which presents as single or multiple
indurated swellings (usually fibrosis).These
swellings become soft and fluctuant and later
suppurate, sometimes forming sinus tracts
discharging yellow colour granules. These
so called “sulphur granules” are lobulated
masses of intertwining filaments.
• Human infections are categorized based on
anatomical sites, namely cervicofacial (lumpy
jaw), thoracic, abdominal, pelvic and primary
• Cervicofacial actinomycosis is the most
common clinical presentation. It commonly
follows dental extraction and presents as
painful, indurated soft tissue swelling located
at the angle of the jaw.
• Thoracic infection occurs due to aspiration
and it involves lungs and pleura.
• Actinomycosis of gastrointestinal tract most
commonly develops in ileocecal region and
presents as appendicitis or slow growing
• Pelvic actinomycosis occurs in women and
is usually associated with the use of
• Primary cutaneous actinomycosis is a rare
type and probably occurs due to direct
implantation of the organism. It usually
occurs on the exposed skin (Fig. 6.16).
Fig. 6.16: Actinomycosis–scalp showing ulcerated
indurated nodules with sulphur granules
Bacterial Infections 41
• A definite diagnosis of actinomycosis cannot
made be on clinical grounds alone.
Demonstration of sulphur granules, grams
stain and culture from the appropriately
obtained specimen is needed to confirm the
diagnosis. Histopathology reveals granular
colonies from which delicate mycelial
filaments radiate. These colonies are
surrounded by a chronic inflammatory
• Actinomycosis may resemble various chronic
inflammatory diseases such as tuberculosis,
• Dramatic response to penicillin therapy
• Causative agent- Bacillus anthracis, gram
• The most common form of infection with
Bacillus anthracis is an acute cutaneous lesion
called “malignant pustule.”
• Anthrax is primarily a disease of domestic
and wild animals, but humans become
accidentally involved through exposure to
animals and their products.
• Human anthrax occurs in three clinical forms:
1) cutaneous anthrax due to direct contact
with contaminated meat, carcasses, hides,
hair, wool or bone, 2) inhalational anthrax
(Woolsorter’s disease) due to inhalation of
spores and 3) gastrointestinal anthrax due to
ingestion of contaminated meat or milk.
Anthrax meningitis occurs secondary to skin
lesions, but it can complicate the other two
• Cutaneous anthrax usually begins as a
painless, pruritic papule within 3 to 10 days
of inoculation. It rapidly progresses into a
serous or serosanguineous vesicles, which
ulcerate with a central black eschar,
surrounded by a ring of vesicles within 36
hours (Figs 6.17 and 6.18). Perilesional
oedema can be extensive. Toxic features
occur in 50% of cases only and healing occurs
in 1 to 3 weeks with variable scarring.
• The following clinical features are strongly
suggestive of cutaneous anthrax -
1. The presence of edema out of proportion
to the size of the lesion.
2. Lack of pain during the initial phases of
3. The rarity of polymorphonuclear
leucocytes from vesicular fluid on gram’s
stain and distinctive box car arrangement
of bacillus anthracis (Fig. 6.19).
Figs 6.17 and 6.18: Cutaneous anthrax (Malignant pustule)–typical painless lesion with central blackish
eschar surrounded by wreath of erythema, edema and vesiculation
Fig. 6.17 Fig. 6.18
Essentials in Dermatology42
• Differential diagnosis: Carbuncle -
Tenderness is prominent and there is
presence of multiple furuncles in a group.
Cow pox and sporotrichosis are other
differential diagnoses. The history, rapid
course, clinical appearance and lack of
lymphangitis should suggest the diagnosis
of anthrax which should be confirmed by
• Since 20% of untreated cases of cutaneous
anthrax develop bacteraemia, which leads to
rapid death, cutaneous anthrax should be
treated energetically with penicillin.
Fig. 6.19: Anthrax–"Box car" arrangement of
bacillus anthracis in gram's stained smear
Ciprofloxacin, erythromycin, tetracycline
and chloramphenicol are alternative drugs
for penicillin sensitive patients.
• Causative agent: Bartonella henselae (organism
also causes Cat Scratch disease); rarely
• Infection is most common in HIV/AIDS
patients, causes endothelial proliferation and
produces vascular tumors.
• Clinically, lesions are rapidly growing
pyogenic granuloma like papules and
nodules, which often ulcerate.
• Purple, papular and nodular vascular lesions
may resemble Kaposi’s sarcoma.
• Diagnosis is based on demonstration of
organism in the skin biopsy tissue section by
Warthin Starry staining. Blood cultures are
positive in half of the cases.
• Differential diagnosis: Pyogenic granuloma
and Kaposi’ sarcoma are close differential
diagnosis, differentiation can be made by
histopathological examination and
demonstration of the organism by Warthin
• The mainstay of treatment is erythromycin.
Alternatively, doxycycline or ciprofloxacin
can be used.