Essentials in Dermatology
(with Multiple Choice Questions)
Essentials in Dermatology
(with Multiple Choice Questions)
Devinder M Thappa MD, DHA, MNAMS, FIMSA
Professor and Head
Depa...
Published by
Jitendar P Vij
Jaypee Brothers Medical Publishers (P) Ltd
Corporate Office
4838/24, Ansari Road, Daryaganj, N...
The second edition of Essentials in Dermatology (with Multiple Choice Questions) is being published
6 years after the appe...
Dermatology, the science of the skin, was one of the many specialties, which evolved from general
internal medicine during...
I would like to thank those who helped me to update chapters
1. Dr Balaji Adityan for updating
• Principles of Diagnosis i...
Essentials in Dermatologyx
• Dr Balaji Adityan
• Dr Ajay Kumar Singh
• Dr Anuradha Priyadarshini
• Dr Tukaram Sori
3. Clin...
“…Most of the dermatology textbooks are too much voluminous for undergraduate students already
overburdened with other hea...
SECTION 1: DERMATOLOGY
1. Ten Most Influential People in Medicine and Dermatology ...........................................
Essentials in Dermatologyxiv
24. Skin Changes of Pregnancy and Old Age ......................................................
Ten Most Influential People in Medicine and Dermatology 3
THE MILLENNIUM AND MEDICINE:
THE TEN MOST INFLUENTIAL
PERSONS
1....
Essentials in Dermatology4
9. Wilhelm Rontgen (1845-1923): Discoverer of
X-rays in 1895 and nobel prize winner in Physics
...
History of Dermatology in the World 5
HISTORY OF DERMATOLOGY IN THE
WORLD
• In Greek and Roman era, Hippocrates
recognized...
Essentials in Dermatology6
of DNA; inflammation-histamine, prostag-
landins, cytokines, adhesion molecules;
immunology-cel...
History of Dermatology in the World 7
brought under the purview of National
AIDS Control Organization (NACO) in the
year 1...
Essentials in Dermatology8
Dermatology may be defined as the study of the
skin and its diseases or is a branch of medical
...
Microanatomy of the Skin 9
STRUCTURE OF THE SKIN
Skin has 3 layers (Fig. 3.1)
1. Epidermis
2. Dermis
3. Subcutaneous fat (...
Essentials in Dermatology10
Fig. 3.2: Diagrammatic representation of shapes of various cells in the epidermis and changes ...
Microanatomy of the Skin 11
Epidermal Appendages Like
a. Pilosebaceous unit
b. Sweat glands.
Pilosebaceous unit: It consis...
Essentials in Dermatology12
Functions of nails are:
1. Protect terminal phalanges
2. Cosmetic function
3. Helps in appreci...
Physiology, Biochemistry and Immunology of the Skin 13
Main functions of the skin are protection,
thermoregulation, sensor...
Essentials in Dermatology14
enhanced by various agents, permitting
increased access of topically applied drugs.
KERATINIZA...
Physiology, Biochemistry and Immunology of the Skin 15
mechanical barrier to penetration of foreign
materials. Apart from ...
Essentials in Dermatology16
Dermatologists often prefer to examine the
patient before obtaining the history and review
of ...
Principles of Diagnosis in Dermatology 17
counter medication, since they are easily
accessible, and since disease is of ch...
Essentials in Dermatology18
Hand lens useful on occasions like identifying:
a. Altered skin markings in tumors.
b. Nail fo...
Principles of Diagnosis in Dermatology 19
Fig. 5.3: Papule—dome shaped papule, a few of
them umbilicated of molluscum cont...
Essentials in Dermatology20
Fig. 5.7: Large well-defined erythematous plaques
of psoriasis vulgaris
Fig. 5.8: Nodule—solid...
Principles of Diagnosis in Dermatology 21
Fig. 5.13: Pustule—numerous tiny pus filled lesions
on erythematous background i...
Essentials in Dermatology22
• Pigmentation: Pigmentation may be hyper,
hypo- or depigmentation of the skin (varies
accordi...
Principles of Diagnosis in Dermatology 23
collagen by ground substance material or
altered quality of collagen.
Special Le...
Essentials in Dermatology24
Figs 5.20A and B: Distribution of skin lesions in
atopic dermatitis in infants
Figs 5.21A and ...
Principles of Diagnosis in Dermatology 25
Figs 5.22A and B: Distribution of skin lesions in
dermatitis herpetiformis
Figs ...
Essentials in Dermatology26
Figs 5.28A and B: Distribution of skin lesions in
children and adults in scabies
Figs 5.29A an...
Principles of Diagnosis in Dermatology 27
Fig. 5.32: Koebner phenomenon in psoriasis
vulgaris over the trunk
Fig. 5.33:Koe...
Essentials in Dermatology28
erection, seen in congenital smooth muscle
hamartoma
• White dermographism: Stroking the skin ...
Principles of Diagnosis in Dermatology 29
If number is more than 5, it is abnormal
capillary fragility.
• Pathergy test: I...
Essentials in Dermatology30
12. VDRL
13. HIV antibody detection test
14. Culture and sensitivity test
15. Patch testing
16...
Bacterial Infections 31
Normal human skin is colonized soon after birth
by a large number of bacteria that live as
commens...
Essentials in Dermatology32
Table 6.2: Non-follicular and follicular pyodermas
A. Non follicular pyodermas include
1. Impe...
Bacterial Infections 33
Complications of Impetigo
• Post-streptococcal acute glomerulonephritis–
S. pyogenes type M-49
• S...
Essentials in Dermatology34
broken or loosened (easy and painless
pluckablity) in the affected area. Loss of hair
is the n...
Bacterial Infections 35
Staphylococcal paronychia: Clinically, skin and soft
tissue of proximal and lateral nail fold are ...
Essentials in Dermatology36
3. Desquamation of palms and soles 1 to 2
weeks after onset
4. Hypotension
5. Involvement of 3...
Bacterial Infections 37
Blistering Dactylitis
• This is nearly always a group A streptococcal
infection in children or tee...
Essentials in Dermatology38
2. Wet compresses: Condy’s compresses for
crusted lesions of pyoderma.
3. Incision and drainag...
Bacterial Infections 39
• Differential diagnosis: Phthiriasis pubis can
be differentiated by its associated pruritis and
c...
Essentials in Dermatology40
Fig. 6.15: Botryomycosis–swelling of the foot with
multiple nodules over it
form granules - my...
Bacterial Infections 41
• A definite diagnosis of actinomycosis cannot
made be on clinical grounds alone.
Demonstration of...
Essentials in Dermatology42
• Differential diagnosis: Carbuncle -
Tenderness is prominent and there is
presence of multipl...
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DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
DM Thappa - Essentials in Dermatology, 2nd Edition
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  1. 1. Essentials in Dermatology (with Multiple Choice Questions)
  2. 2. 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 (JIPMER) Pondicherry, India JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD New Delhi • Ahmedabad • Bengaluru • Chennai • Hyderabad • Kochi Kolkata • Lucknow • Mumbai • Nagpur • St Louis (USA) ® Second Edition
  3. 3. Published by Jitendar P Vij Jaypee Brothers Medical Publishers (P) Ltd Corporate Office 4838/24, Ansari Road, Daryaganj, New Delhi 110 002, India Phone: +91-11-43574357 Registered Office B-3, EMCA House, 23/23B Ansari Road, Daryaganj, New Delhi 110 002, India Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021, +91-11-23245672 Rel: +91-11-32558559 Fax: +91-11-23276490, +91-11-23245683 e-mail: jaypee@jaypeebrothers.com Visit our website: www.jaypeebrothers.com Branches • 2/B, Akruti Society, Jodhpur Gam Road Satellite Ahmedabad 380 015 Phones: +91-79-26926233, Rel: +91-79-32988717 Fax: +91-79-26927094 e-mail: ahmedabad@jaypeebrothers.com • 202 Batavia Chambers, 8 Kumara Krupa Road, Kumara Park East Bengaluru 560 001 Phones: +91-80-22285971, +91-80-22382956, +91-80-22372664 Rel: +91-80-32714073 Fax: +91-80-22281761 e-mail: bangalore@jaypeebrothers.com • 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza, Pantheon Road Chennai 600 008 Phones: +91-44-28193265, +91-44-28194897, Rel: +91-44-32972089 Fax: +91-44-28193231 e-mail: chennai@jaypeebrothers.com • 4-2-1067/1-3, 1st Floor, Balaji Building, Ramkote Cross Road Hyderabad 500 095 Phones: +91-40-66610020, +91-40-24758498 Rel:+91-40-32940929 Fax:+91-40-24758499, e-mail: hyderabad@jaypeebrothers.com • No. 41/3098, B & B1, Kuruvi Building, St. Vincent Road Kochi 682 018, Kerala Phones: +91-484-4036109, +91-484-2395739, +91-484-2395740 e-mail: kochi@jaypeebrothers.com • 1-A Indian Mirror Street, Wellington Square Kolkata 700 013 Phones: +91-33-22651926, +91-33-22276404, +91-33-22276415 Rel: +91-33-32901926 Fax: +91-33-22656075, e-mail: kolkata@jaypeebrothers.com • Lekhraj Market III, B-2, Sector-4, Faizabad Road, Indira Nagar Lucknow 226 016 Phones: +91-522-3040553, +91-522-3040554 e-mail: lucknow@jaypeebrothers.com • 106 Amit Industrial Estate, 61 Dr SS Rao Road, Near MGM Hospital, Parel Mumbai 400012 Phones: +91-22-24124863, +91-22-24104532, Rel: +91-22-32926896 Fax: +91-22-24160828, e-mail: mumbai@jaypeebrothers.com • “KAMALPUSHPA” 38, Reshimbag, Opp. Mohota Science College, Umred Road Nagpur 440 009 (MS) Phone: Rel: +91-712-3245220, Fax: +91-712-2704275 e-mail: nagpur@jaypeebrothers.com USA Office 1745, Pheasant Run Drive, Maryland Heights (Missouri), MO 63043, USA Ph: 001-636-6279734 e-mail: jaypee@jaypeebrothers.com, anjulav@jaypeebrothers.com Essentials in Dermatology (with Multiple Choice Questions) © 2009, Jaypee Brothers Medical Publishers All rights reserved. No part of this publication should be reproduced, stored in a retrieval system, or transmitted in any form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of the author and the publisher. This book has been published in good faith that the material provided by author is original. Every effort is made to ensure accuracy of material, but the publisher, printer and author will not be held responsible for any inadvertent error(s). In case of any dispute, all legal matters are to be settled under Delhi jurisdiction only. First Edition: 2003 Second Edition: 2009 ISBN 978-81-8448-558-5 Typeset at JPBMP typesetting unit Printed at Ajanta
  4. 4. 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 dermatology. 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 improvement. Devinder M Thappa Preface to the Second Edition
  5. 5. 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
  6. 6. 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 • Infestations • 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 (AIDS) 4. Dr Amiya Kumar Nath for • Eczema • 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 Acknowledgements
  7. 7. 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 5. Leprosy • Dr Abarna Devi • Dr Sakthi Kandan
  8. 8. “…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 postgraduate courses…” Indian J Dermatol Venereol Leprol 2004; 70(6): 393. Reviews
  9. 9. 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 Contents
  10. 10. 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
  11. 11. Ten Most Influential People in Medicine and Dermatology 3 THE MILLENNIUM AND MEDICINE: THE TEN MOST INFLUENTIAL PERSONS 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 genetics. 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 York. 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.
  12. 12. 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 development. TEN MOST INFLUENTIAL PERSONS IN DERMATOLOGY, VENEREOLOGY AND LEPROSY: INDIA 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”, photobiology. 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 LEPROSY: WORLD 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 patch testing. 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 (1965). 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) in 1968. 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.
  13. 13. History of Dermatology in the World 5 HISTORY OF DERMATOLOGY IN THE WORLD • 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 right. • 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
  14. 14. 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, laser, cryotherapy). 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 diseases. • 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 Colonel Acton. • 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
  15. 15. History of Dermatology in the World 7 brought under the purview of National AIDS Control Organization (NACO) in the year 1992. • 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, Chennai. • Dr. CN Sowmini founded the Indian Association for the study of sexually transmitted diseases (IASSTD) in the year 1975. • In the year 1980, this specialty, under the banner of IASSTD, started its own exclusive journal, the Indian Journal of Sexually Transmitted Diseases. • The late Dr. Sardarilal was its founder editor and guiding force, who had already made a mark in the field of research, especially in donovanosis. • 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 the universities. 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 present time. • 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 1984. • 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 1983. • 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.
  16. 16. 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 2 m2 . 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 c. Infections 2. Thermoregulation 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- cytes. 9. Mechanical function: The mechanical properties of the skin depend mainly on the dermis. 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.
  17. 17. Microanatomy of the Skin 9 STRUCTURE OF THE SKIN Skin has 3 layers (Fig. 3.1) 1. Epidermis 2. Dermis 3. Subcutaneous fat (Hypodermis). Epidermis 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
  18. 18. 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. Dermis 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 of collagen.
  19. 19. 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: 1. Cosmetic 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 fibers. 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 debated. 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.
  20. 20. 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 tips. 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 pericytes, etc. 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.
  21. 21. 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 corneum. 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 cellular constituents. PERCUTANEOUS ABSORPTION 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 water. The barrier is affected by many other factors, such as age, environmental conditions and physical trauma, and permeability can be
  22. 22. Essentials in Dermatology14 enhanced by various agents, permitting increased access of topically applied drugs. KERATINIZATION Keratinization is a process of differentiation of germinative cells in the basal cell layer into the deceased cornified cells of stratum corneum. It involves: 1. Synthesis of distinctive proteins (e.g. keratins, filaggrins, and involucrin) and lamellar granules, and 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 ultraviolet light. 2. Melanin may also act as a biochemical neutralizer of toxic free radical oxygen derivatives, byproducts of various inflam- matory processes. 3. Melanocytes situated in the matrix of anagen follicles impart to hair various colours, e.g. blond, brunette and red head. THERMOREGULATION 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 clothing. 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: 1. Radiation 2. Convection 3. Conduction 4. Evaporation SKIN FAILURE 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
  23. 23. 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 causes. 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 of dermis. 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 SKIN 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.
  24. 24. 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, marital status. Principles of Diagnosis in Dermatology Chief complaints: Limit them to just three only History of present illness: “What is your skin problem?” This allows patient to point out the lesions and the area involved. Three basic questions. 1. Onset and evolution. 2. Symptoms. 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 5
  25. 25. 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 medicamentosa. 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 didn’t work”. Detailed follow-up history: This history is taken after some diagnosis or conclusion was reached by initial history and examination, and this includes. • Past history. • Family history. • Review of systems. • Social history. • Females- menstrual/obstetric history. Past history: a. History of same disease before. b. History of prolonged illness– diabetes, hypertension. c. Drugs used for other problems (drug rash, urticaria). d. Drug allergies– avoid prescribing those drugs. 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. c. Genodermatoses. Review of other systems: It is required in multisystem disorders like SLE, scleroderma, or lepromatous leprosy. 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 pustulosis. PHYSICAL EXAMINATION 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 Properly Examined 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 properly exposed. 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 contagious disease.
  26. 26. 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- Vesicle, bulla • 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. Primary Lesions 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 color. • 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
  27. 27. 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 contagiosum 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 plaque, etc. • 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. • Vesiclesandbullae:Vesicleandbullaearetwo 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
  28. 28. 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
  29. 29. Principles of Diagnosis in Dermatology 21 Fig. 5.13: Pustule—numerous tiny pus filled lesions on erythematous background in a case of pustular psoriasis • 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 semisolid material. • 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 bullae. • 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 (Fig. 5.16). • 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 dermis. • 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 areas. Fig. 5.14: Crust—dried out oozed material over the face in impetigo contagiosa
  30. 30. 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
  31. 31. Principles of Diagnosis in Dermatology 23 collagen by ground substance material or altered quality of collagen. Special Lesions 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
  32. 32. 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 and B). 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).
  33. 33. Principles of Diagnosis in Dermatology 25 Figs 5.22A and B: Distribution of skin lesions in dermatitis herpetiformis Figs 5.23A and B: Distribution of skin lesions in lichen planus Figs 5.24A and B: Distribution of skin lesions in neurodermatitis (lichen simplex chronicus) Figs 5.25A and B: Distribution of skin lesions in pityriasis rosea Figs 5.26A and B: Distribution of skin lesions in psoriasis vulgaris Figs 5.27A and B: Distribution of skin lesions in infants in scabies
  34. 34. 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 tinea versicolor Certain phenomenon and signs are there to be seen and observed; others need to be elicited by tools. • 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 graft sites.
  35. 35. 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 contagiosum • 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 disease). • Pseudo-Darier’s sign: Here stroking of skin produces transient induration with pilo-
  36. 36. Essentials in Dermatology28 erection, seen in congenital smooth muscle hamartoma • 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 epidermis. • Auspitz’s sign: This sign if present is diagnostic of psoriasis. It has three components. 1. On scraping with glass slide, initially silvery white micaceous scales come out. 2. Removal of the scales is followed by a thin membranous structure. 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.
  37. 37. Principles of Diagnosis in Dermatology 29 If number is more than 5, it is abnormal capillary fragility. • 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, candidiasis, etc. 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 infections. 4. Gram’s stained pus smear: Indicated for pyogenic infections, vaginal and urethral discharge. 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 treponemes. 7. Wet preparation: It is utilized for diagnosis of trichomonal infestation of the genital tract. 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 planus). 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.
  38. 38. Essentials in Dermatology30 12. VDRL 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 20. Immunofluorescence 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 diagnoses. 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 friends.
  39. 39. 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. PYODERMAS Pyoderma is a common purulent infection of the skin caused by staphylococcal or streptococcal organisms. They can be classified as primary pyodermasandsecondarypyodermas(Table6.1). 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). Staphylococcal Pyodermas Impetigo Non-bullous impetigo (Impetigo contagiosa of Tilbury Fox): • 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
  40. 40. Essentials in Dermatology32 Table 6.2: Non-follicular and follicular pyodermas A. Non follicular pyodermas include 1. Impetigo 2. Ecthyma 3. Cellulitis 4. Erysipelas 5. SSSS B. Follicular pyodermas include 1. Folliculitis 2. Furuncle 3. Carbuncle Table 6.3: Cutaneous diseases caused by staphylococci and streptococci 1. Cutaneous diseases caused by staphylococcus include: A. Direct infection of skin: Impetigo, ecthyma, folliculitis, furunculosis, carbuncle, sycosis. 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 infection • 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). Bullous Impetigo • Earlier bullous impetigo in neonates was popularly known as pemphigus neonatorum. • S. aureus (phage group II) is the causative agent. • Occurs commonly in the newborn and in older infants. • 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 associated feature. 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
  41. 41. Bacterial Infections 33 Complications of Impetigo • Post-streptococcal acute glomerulonephritis– S. pyogenes type M-49 • Scarlet fever • Urticaria • Erythema multiforme Rheumatic fever in not a complication of streptococcal skin infection (but of streptococcal sore throat). Ecthyma • 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 elderly patients • Poor hygiene and neglect are key elements in pathogenesis. • Dirty grayish-yellow crust surmounts a “punched out” ulcer (Fig. 6.3). Folliculitis Pyoderma affecting the hair follicles, classified according to depth of invasion. Superficial folliculitis • Also known as follicular or Bockhart’s impetigo • 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 Deep folliculitis Sycosis barbae is a deep folliculitis with perifollicular inflammation occurring in the bearded areas of the face (Fig. 6.4) and upper lip. Differential diagnosis 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 ulcerated lesions Fig. 6.4: Sycosis barbae– grouped follicular based crusted lesions in the beard area of the face
  42. 42. 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 persistent lesions 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 accompany. 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 periphery Fig. 6.6: Furuncle–a red tender suppurated nodule in a case of erythroderma
  43. 43. 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 folds. 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 S. aureus. • 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
  44. 44. Essentials in Dermatology36 3. Desquamation of palms and soles 1 to 2 weeks after onset 4. Hypotension 5. Involvement of 3 or more other organ systems • 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- preserved. 2. Scarlet fever– not usually associated with hypotension and shock. 3. Kawasaki’s syndrome– prolonged fever, cardiac involvement, generalized lymphadenopathy and absence of peripheral shock. Streptococcal Pyodermas 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 implicated. • 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 subcutaneous tissue. • 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 symptoms. • 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
  45. 45. Bacterial Infections 37 Blistering Dactylitis • 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. Streptococcal Vulvovaginitis • 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 gangrene) • 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- nisms). Diagnosis 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 cells. 4. Histopathology: Histopathological exami- nation is hardly required for the diagnosis. Treatment 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
  46. 46. 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 definite fluctuation. 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. NON-PYODERMAS Erythrasma • 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 aerobic condition • A short course of systemic erythromycin is the easiest method of treatment. Topical imidazole creams are also effective. Trichomycosis Axillaris • 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 centimetres. • 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
  47. 47. 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 disinfectant. 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 Pitted Keratolysis • 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 considered. • Topical erythromycin solution or benzoyl peroxide gel can be applied once or twice daily. Remove aggravating factors, if possible. Botryomycosis • 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 multiple pits
  48. 48. 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 (Fig. 6.15). • 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 • 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 cutaneous. • 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 mass. • Pelvic actinomycosis occurs in women and is usually associated with the use of intrauterine device. • 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
  49. 49. 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 infiltrate. • Actinomycosis may resemble various chronic inflammatory diseases such as tuberculosis, syphilis, etc. • Dramatic response to penicillin therapy occurs. Cutaneous Anthrax • Causative agent- Bacillus anthracis, gram positive bacillus, • 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 forms also. • 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 the infection. 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
  50. 50. 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 bacteriological examination. • 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. Bacillary Angiomatosis • Causative agent: Bartonella henselae (organism also causes Cat Scratch disease); rarely Bartonella quintana. • 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 starry staining. • The mainstay of treatment is erythromycin. Alternatively, doxycycline or ciprofloxacin can be used.

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