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 Werner Kempf
Markus Hantschke
Heinz Kutzner

Dermatopathology

Second Edition

123
Dermatopathology
Werner Kempf • Markus Hantschke •
Heinz Kutzner

Dermatopathology
Second Edition

123
Werner Kempf Markus Hantschke
Kempf und Pfaltz Histologische Diagnostik MVZ Dermatopathologie Friedrichshafen
Zürich, Switzerland Friedrichshafen, Baden-Württemberg, Germany
Department of Dermatology
University of Zürich
Zürich, Switzerland

Heinz Kutzner
Dermatopathologie Friedrichshafen
Friedrichshafen, Baden-Württemberg, Germany

ISBN 978-3-030-82819-6 ISBN 978-3-030-82820-2 (eBook)

https://doi.org/10.1007/978-3-030-82820-2

1st edition: © Steinkopff Verlag 2008

2nd edition: © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature
Switzerland AG 2022
This work is subject to copyright. All rights are solely and exclusively licensed by the Publisher, whether the whole or
part of the material is concerned, specifically the rights of reprinting, reuse of illustrations, recitation, broadcasting,
reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval,
electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed.
The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not
imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and
regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed
to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty,
expressed or implied, with respect to the material contained herein or for any errors or omissions that may have been
made. The publisher remains neutral with regard to jurisdictional claims in published maps and institutional
affiliations.

This Springer imprint is published by the registered company Springer Nature Switzerland AG
The registered company address is: Gewerbestrasse 11, 6330 Cham, Switzerland
We dedicate this book to our families
Preface

The aim of this book is to provide a structured and easy approach to dermatopathology. To
ensure the clarity of the book for beginners, we have limited ourselves to the histology of the
most common and important skin diseases. Each entity is described in a structured form with
clinical description, histological features, additional examinations (special stains, immuno-
histochemistry, molecular biologic studies) and the differential diagnoses are listed with the
distinguishing features. For each disease or pattern, two representative histologic photographs
show the most important diagnostic key features highlighted with pointers. Clinicopathologic
correlation plays a central role in the diagnosis of inflammatory skin diseases in particular.
This is pointed out in the comments on the corresponding diseases.
The second edition continues the structure and organization of the book. New inflammatory
and infectious dermatoses as well as new diagnostic methods have been included. As in the
first book, we have deliberately omitted references in view of the large number of scientific
papers and widespread access to Internet-based sources of information. Our book cannot and
is not intended to replace the detailed works on dermatopathology. We dedicate the book to
our families and to our friend and co-editor Walter Burgdorf who passed away.
We hope that this book can pass on the authors’s fascination with dermatopathology to the
future generation of dermatologists and dermatopathologists.

Zürich, Switzerland Werner Kempf

Friedrichshafen, Germany Markus Hantschke
Friedrichshafen, Germany Heinz Kutzner
Summer 2021

vii
Contents

Part I Basic Principles

1 Principles of Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3
2 Skin Biopsy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
2.1 Biopsy Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
2.2 Fixation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
2.3 Embedding and Sectioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5
3 Histopathological Techniques . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
3.1 Staining . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
3.2 Immunohistochemical Stains . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
3.3 Immunofluorescence Studies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
3.3.1 Direct Immunofluorescence . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
3.3.2 Indirect Immunofluorescence . . . . . . . . . . . . . . . . . . . . . . . . . . 9
3.3.3 Salt-Split Skin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9
3.4 Molecular Biological Procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
3.4.1 In Situ Hybridization (ISH) . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
3.4.2 Fluorescence in Situ Hybridization (FISH) . . . . . . . . . . . . . . . . 10
3.4.3 Polymerase Chain Reaction (PCR) . . . . . . . . . . . . . . . . . . . . . 10
4 Dermatopathologic Glossary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

Part II Inflammatory and Infectious Dermatoses

5 Epidermis: Spongiosis, Acanthosis and Hyperparakeratosis . . . . . . . . . . . . . . 15
5.1 Dermatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
5.2 Prurigo . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18
5.3 Psoriasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20
5.4 Pustular Psoriasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 22
5.5 Pityriasis Rosea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24
5.6 Cutaneous Fungal Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 26
5.7 Human Papilloma Virus-Associated Acanthopapillomas: Verruca
Vulgaris and Condyloma Acuminatum . . . . . . . . . . . . . . . . . . . . ...... 28
5.8 Molluscum Contagiosum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ...... 30
5.9 Parapoxvirus Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ...... 32
6 Epidermis Acantholysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35
6.1 Darier Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35
6.2 Hailey-Hailey Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 37
6.3 Herpes Virus Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
7 Bullous Diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41
7.1 Pemphigus Foliaceus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41
7.2 Pemphigus Vulgaris . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43

ix
x Contents

7.3 Bullous Pemphigoid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 45

7.4 Dermatitis Herpetiformis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
7.5 Porphyria Cutanea Tarda . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 49
8 Interface Dermatoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51
8.1 Erythema Multiforme . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51
8.2 Pityriasis Lichenoides . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53
8.3 Lichen Planus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55
8.4 Lichen Sclerosus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57
8.5 Lupus Erythematosus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 59
8.6 Pigmented Purpuric Dermatoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
8.7 Incontinentia Pigmenti . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 63
9 Dermis Vascular Disorders . . . . . . . . . . . . . . . . . ........... . . . . . . . . . . . 65
9.1 Leukocytoclastic Vasculitis . . . . . . . . . . . . ........... . . . . . . . . . . . 65
9.2 Granuloma Faciale and Erythema Elevatum et Diutinum . . . . . . . . . . . . . 67
9.3 Polyarteritis Nodosa . . . . . . . . . . . . . . . . . ........... . . . . . . . . . . . 69
9.4 Cryoglobulinemia . . . . . . . . . . . . . . . . . . . ........... . . . . . . . . . . . 71
10 Dermis Granulomatous Inflammation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73
10.1 Granuloma Annulare . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73
10.2 Necrobiosis Lipoidica . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 76
10.3 Interstitial Granulomatous Dermatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . 78
10.4 Sarcoidosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
10.5 Foreign Body Granuloma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 82
10.6 Mycobacterial Infections . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 84
10.7 Syphilis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86
10.8 Leishmaniasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 88
11 Dermis Interstitial Inflammation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
11.1 Borreliosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 91
11.2 Morphea . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 94
12 Dermis Diffuse Mixed Inflammatory Infiltrates . . . . . . . . . . . . . . . . . . . . . . . 97
12.1 Urticaria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
12.2 Acute Febrile Neutrophilic Dermatosis (Sweet Syndrome) . . . . . . . . . . . 99
12.3 Eosinophilic Cellulitis (Wells Syndrome) . . . . . . . . . . . . . . . . . . . . . . . . 101
12.4 Arthropod Assault Reaction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103

13 Dermis - Degenerative and Metabolic Disorders . . . . . . . . . . . . . . . . . . . . . . . 105

13.1 Chondrodermatitis Helicis Nodularis Chronica . . . . . . . . . . . . . . . . . . . . 105
13.2 Pseudoxanthoma Elasticum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107
13.3 Xanthoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
14 Dermis Inflammation of Adnexal Structures . . . . . . . . . . . . . . . . . . . . . . . . . 111
14.1 Folliculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111
14.2 Alopecia Areata . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
14.3 Lupus Erythematosus of the Scalp . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 115
14.4 Folliculitis Decalvans . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117
14.5 Lichen Ruber Planopilaris . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119
15 Subcutaneous Fat - Panniculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121
15.1 Erythema Nodosum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121
15.2 Erythema Induratum and Nodular Vasculitis . . . . . . . . . . . . . . . . . . . . . 123
15.3 Lupus Panniculitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
Contents xi

16 Drug Reactions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127

16.1 Specific Forms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
16.2 Unspecific Forms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129
17 Artifactual Damage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131

Part III Cysts

18 Epithelial Cysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135
18.1 Epidermoid Cyst . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135
18.2 Trichilemmal Cyst . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137
18.3 Steatocystoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139
18.4 Apocrine Hidrocystoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
19 Pseudocysts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143
19.1 Digital Mucous Cyst . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143

Part IV Hamartomas and Neoplasms

20 Epidermal Hamartomas and Neoplasms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147
20.1 Epidermal Nevus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 147
20.2 Nevus Sebaceus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
20.3 Seborrheic Keratosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 151
20.4 Clear Cell Acanthoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 153
20.5 Porokeratosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 155
20.6 Actinic Keratosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157
20.7 Bowen Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 159
20.8 Squamous Cell Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161
20.9 Keratoacanthoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163
21 Melanocytic Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165
21.1 Mucosal Melanotic Macule . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165
21.2 Lentigo Simplex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 167
21.3 Melanocytic Nevi–Junctional and Compound Types . . . . . . . . . . . . . . . . 169
21.4 Melanocytic Nevi–Dermal and Congenital Types . . . . . . . . . . . . . . . . . . 171
21.5 Halo Nevus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 173
21.6 Blue Nevus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 175
21.7 Dysplastic Melanocytic Nevus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 177
21.8 Spitz Nevus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179
21.9 Desmoplastic Spitz Nevus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181
21.10 Pigmented Spindle Cell Nevus (Reed) . . . . . . . . . . . . . . . . . . . . . . . . . . 183
21.11 Clonal Nevus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 184
21.12 Lentigo Maligna and Lentigo Maligna Melanoma . . . . . . . . . . . . . . . . . . 186
21.13 Superficial Spreading Melanoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 188
21.14 Nodular Melanoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190
21.15 Acrolentiginous Melanoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 192
21.16 Desmoplastic Melanoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 194
21.17 Cutaneous Clear Cell Sarcoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 196
22 Adnexal Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 199
22.1 Sebaceous Hyperplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 199
22.2 Sebaceous Adenoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201
22.3 Pilomatricoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203
22.4 Syringoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 205
22.5 Syringocystadenoma Papilliferum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 207
xii Contents

22.6 Poroma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209

22.7 Hidradenoma Synonyms: Nodular Hidradenoma, Clear Cell
Hidradenoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
22.8 Spiradenoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 213
22.9 Cylindroma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215
22.10 Paget Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 217
22.11 Digital Papillary Adenocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 219
22.12 Trichoblastoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 221
22.13 Desmoplastic Trichoepithelioma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223
22.14 Basal Cell Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225
22.15 Fibroepithelioma of Pinkus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 227
22.16 Mixed Tumor of the Skin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229
23 Soft Tissue Proliferations and Neoplasms . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231
23.1 Scar . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231
23.2 Hypertrophic Scar and Keloid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
23.3 Skin Tag Synonym: Fibroma Molle . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235
23.4 Dermatofibroma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
23.5 Dermatofibrosarcoma Protuberans . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
23.6 Atypical Fibroxanthoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241
23.7 Leiomyoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 243
23.8 Nevus Lipomatosus Superficialis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 245
23.9 Lipoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 247
23.10 Neurofibroma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 249
23.11 Schwannoma Synonym: Neurilemmoma . . . . . . . . . . . . . . . . . . . . . . . . 251
23.12 Merkel Cell Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253
24 Vascular Tumors . . . . . . . . . . . . . . . . . . . . . . . ................... . . . . 255
24.1 Hemangioma . . . . . . . . . . . . . . . . . . . . . ................... . . . . 255
24.2 Pyogenic Granuloma (Synonyme: Lobular Capillary Hemangioma) . . . . . 257
24.3 Angiokeratoma . . . . . . . . . . . . . . . . . . . . ................... . . . . 259
24.4 Kaposi Sarcoma . . . . . . . . . . . . . . . . . . . ................... . . . . 261
24.5 Angiosarcoma . . . . . . . . . . . . . . . . . . . . ................... . . . . 263
25 Lymphomas and Pseudolymphomas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 265
25.1 Mycosis Fungoides . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 265
25.2 Primary Cutaneous CD30-positive Lymphoproliferative Disorders . . . . . . 268
25.3 Primary Cutaneous Marginal Zone Lymphoma . . . . . . . . . . . . . . . . . . . . 270
25.4 Primary Cutaneous Follicle Center Lymphoma . . . . . . . . . . . . . . . . . . . . 272
25.5 Cutaneous Diffuse Large B-cell Lymphoma, Leg Type . . . . . . . . . . . . . . 274
25.6 Cutaneous B-cell Pseudolymphoma Syn.: Lymphocytoma Cutis,
Lymphadenosis Cutis Benigna When Caused by Borrelial Infections . . . . 276

26 Histiocytoses and Mastocytoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279

26.1 Langerhans Cell Histiocytoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
26.2 Juvenile Xanthogranuloma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281
26.3 Cutaneous Mastocytoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 283
27 Cutaneous Metastases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285

Direct Immunofluorescence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 287

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 289
 Part I
Basic Principles
 Principles of Diagnosis
When starting, the simplest approach is to examine the
epidermis, then the dermis and finally the subcutaneous fat.
This approach reduces the likelihood of overlooking some-
thing. For this reason, we have arranged this book, starting
with epidermal changes and moving down through dermal
and subcutaneous lesions.
Inflammatory dermatoses are best approached by identi-
fying first the pattern of inflammation (superficial vs.
superficial and deep vs. subcutaneous; with and without
epidermal involvement) and studying the cellular composi-
tion (lymphocytes, macrophages, neutrophils, eosinophils,
and mast cells). Cutaneous tumors are approached just like
all other tumors considering the pattern (symmetry, cir-
cumscription, level of invasion) and cytomorphology (nu-
clear pleomorphism and mitotic activity). Increasingly the
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022
W. Kempf et al., Dermatopathology,
https://doi.org/10.1007/978-3-030-82820-2_1
1
final answer is based on the expression of a pattern of
specific tumor antigens (immunohistochemical profile).
Clinicopathologic correlation: This is the crux and beauty
of dermatopathology; no other branch of medicine has so many
different names for the appearance of an organ and in many
cases, each of the peculiar names has a histological correlate.
On the other hand, the skin can only react in so many ways, so
that some patterns such as “superficial lymphocytic perivas-
cular infiltrate with sparse admixture of eosinophils” can be
associated with many different diagnoses ranging from viral
exanthem to drug reaction or bullous pemphigoid. The digital
age has made it convenient to provide the dermatopathologist
not only with a detailed clinical history but also with clinical
pictures (e.g., digital images), both of which increase the
chances of the clinician receiving a helpful diagnosis.
3
 Skin Biopsy
2.1 Biopsy Techniques
There are several ways of obtaining a skin biopsy; each has
advantages and disadvantages.
Excision. An excision is preferred when removing skin
tumors as it allows an adequate evaluation of the margins to
determine completeness of excision. An excisional biopsy is
required for deep inflammatory processes, especially pan-
niculitis, and is ideal for studying a disease process at all
levels of the skin.
Punch biopsy. Punch biopsies usually 3–4 mm in diam-
eter produce a cylindrical plug. They can be done rapidly,
heal satisfactory without suturing and are thus efficient; their
downside is the risk of sampling error, especially for larger
lesions.
Shave biopsy. The shave biopsy is the quickest way to
sample or remove a lesion but never allows adequate study
of the depths of the lesion and often results in an incomplete
lateral excision as well. The shave biopsy is perfect for small
protuberant or papillomatous lesions but otherwise causes
more trouble than the time savings it provides.
Curettage biopsy. Superficial lesions like actinic ker-
atoses and seborrheic keratoses are often curetted. The
resulting fragments can be diagnosed, but in the event the
actinic keratosis is a squamous cell carcinoma, it is impos-
sible to comment on the extension of the tumor to the depth
and the adequacy of excision.
Special sites. Biopsies on the scalp should be done par-
allel to the direction of the hair follicles and deep enough to
sample the hairs in the subcutaneous fat. Many prefer to
obtain two deep punch biopsies for alopecia; one is pro-
cessed transversely (horizontal sections) and the other in the
traditional fashion (vertical sections). Biopsies from the
lower aspects of the legs always feature thickened vessels
and stasis changes in adults, while those from the elbow
have pressure and rubbing changes.
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W. Kempf et al., Dermatopathology,
https://doi.org/10.1007/978-3-030-82820-2_2
2
2.2 Fixation
Skin biopsies are routinely fixed in a buffered 10% formalin
solution (about 4% formaldehyde in water) for at least
6–12 h, being sure that the ratio of fixative to biopsy volume
exceeds 20:1. Specimens for immunofluorescent examina-
tion should be flash-frozen or transported in Michel solution.
Specimens for electron microscopic examination require
fixation in paraformaldehyde and glutaraldehyde in a
cacodylate buffer.
2.3 Embedding and Sectioning
Excision specimens usually require special handling. The
traditional method of bread-loafing the specimen―that is,
multiple slices perpendicular to the long axis of an ellipse – is
the most widely accepted method for determining the ade-
quacy of the excision and in our opinion the best approach
for smaller tumors. A variety of other methods are available
for micrographic control of the tumor margins. These tech-
niques, whether it is the Mohs method or the Tübinger Torte
in Europe, result in an almost complete three-dimensional
control of the excision margins, allowing possible maximum
preservation of tissue while best insuring complete excision.
The operating physician generally decides if micro-
graphic control is necessary or not. Ideally consultation with
the dermatopathologist should occur prior to the specimen
appearing in the laboratory if there are special issues. Some
indications for this more time-consuming process include:
• Tumors with unclear clinical borders, locally-destructive
behavior or potential to metastasize (sclerotic basal cell
carcinoma, Merkel cell carcinoma)
• Recurrent tumors, especially in the head and neck region
• Tumors with perineural growth patterns.
5
 Histopathological Techniques
3

stains. Thus these two comment pigments which both appear

3.1 Staining
yellow–brown on H&E stain can be accurately separated
with special stains. Exogenous dyes such as tattoos often
The tissues are embedded in paraffin, cut into 3–6 micron sec-
retain their intrinsic color in histological sections.
tions, placed on glass microscopic slides and stained. The
Gram stain is the usual method for identifying bacteria,
standard stain in dermatopathology is hematoxylin and eosin (H
while mycobacteria are best seen with the Ziehl–Neelsen
& E stain) which stains the nuclei blue and the cytoplasm pink.
stain and Mycobacterium leprae with the Fite-Faraco stain.
A variety of special stains serve to better visualize a wide
A more sensitive alternative approach is to use the anti-M.
variety of cellular and extracellular structures. The most
bovis BCG antibody which stains a wide range of microbes
common additional stain is the periodic acid-Schiff (PAS
(fungi, bacteria). The Giemsa stain is preferred for leish-
stain) which colors sugars and polysaccharides violet. It is
mania. Fungi can also be better visualized with silver stains
used to identify fungal elements, better visualize the base-
such as the Grocott stain.
ment membrane, and identify deposits of glycogen as in
Some prefer the Giemsa stain for studying nuclear detail,
some sweat gland or epithelial proliferations.
especially in the diagnosis of lymphomas. Mast cells are
Acid glycosamines in mucin are best seen with the alcian
usually identified with toluidine blue or Giemsa stains, while
blue stain. Congo red is used to identify amyloid, which also
the chloroacetate esterase (Leder) stain marks both neu-
has a green color when the specimen is polarized; in addi-
trophils and mast cells. Early myeloid cells are best seen
tion, the Pagoda stain imparts an orange color. Elastic fibers
with the myeloperoxidase stain. Extravasates of erythrocytes
are stained black with a variety of stains, usually acid orcein
stain brilliant orange with the Goldner stain, while the col-
or van Gieson; the latter also stains collagen pink and
lagen fibers are marked green.
muscles yellow. Areas of calcification are stained by the von
Lipids can be stained in frozen sections with Sudan
Kossa stain which colors calcium salts black.
orange. Routine processing removes the lipids but may
Melanin appears black in the Masson-Fontana stain.
leave behind distinctive empty spaces.
Hemosiderin colors blue with the iron (or Prussian blue)

Stain Structures identified Color

Acid orcein Elastic fibers Black

Alcian blue Acid glycosaminoglycans Blue
Chloroacetate esterase (Leder) Neutrophils, mast cells (myeloid cells) Red
Congo red Amyloid Red; green in polarized light
Fite-Faraco Mycobacterium leprae Red
Giemsa Nuclei Blue
Eosinophil granules Red
Mast cell granules Purple
Leishmania Blue
(continued)

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022 7

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8 3 Histopathological Techniques

Stain Structures identified Color

Gram Gram-positive bacteria Blue

Gram-negative bacteria Red
Goldner trichrome Erythrocytes Orange
Collagen, mucus Green
Grocott silver Fungi Black
Iron (Prussian blue) Hemosiderin Blue
Masson-Fontana Melanin Black
Myeloperoxidase Immature myeloid cells Orange
Pagoda Amyloid Orange
Periodic acid-Schiff (PAS) Glycogen Red
Fungi Red
Fibrin Red
Sudan Lipids (on frozen section) Orange
Toluidine blue Mast cell granules Blue
Van Gieson Collagen Red
Elastic fibers Black
Muscle fibers Yellow
Von Kossa Calcium salts Black
Warthin-Starry Spirochetes Black
Fungi Black
Ziehl–Neelsen Acid-fast bacteria Red

3.2 Immunohistochemical Stains 3.3 Immunofluorescence Studies

Immunohistochemical stains are essential for modern and
accurate dermatopathologic diagnosis. They are most
important in diagnosing tumors and identifying specific
organisms. Most of the relevant antibodies today can be
employed on formalin-fixed, paraffin-embedded tissue.
Almost all antibodies stain more than a single cell type. Thus
a panel of antibodies should always be employed, also to
provide some internal control, and the final diagnosis should
balance the clinical history, histological diagnosis and
immunohistochemical panel.
Immunohistochemical stains incorporate either mono-
clonal or polyclonal antibodies. Some antigens are relatively
inaccessible after routine processing, so that antigen retrieval
with enzymatic digestion or heating may be required prior to
applying the antibodies to the tissue. The antigen–antibody
complex can then be identified with different detection
systems producing various colors.
A sampling of the important antibodies and their antigens
as used in most dermatopathology practices is given below.
The information is incomplete but many other paper and
electronic references are available.
3.3.1 Direct Immunofluorescence
Direct immunofluorescence examination (DIF) serves to
identify immunoglobulins, complement factors or fibrinogen
in the patient’s tissues. A biopsy is taken, then either
flash-frozen or transported in Michel medium, and then
analyzed.
Fluorescence-labeled antibodies are applied to sections
and allowed to incubate. Then using a special microscope,
the sites of attachment of the labeled antibodies in the skin
can be identified. Typically, antibodies against IgG, IgM,
IgA, C3 and fibrin are used. The most important indications
are the autoimmune bullous dermatoses, which were first
classified in a reproducible manner after the introduction of
DIF. In addition, collagen-vascular disorders (lupus erythe-
matosus and dermatomyositis) and immune complex vas-
culitides also have characteristic findings.
The site of the biopsy is important; generally, perilesional
skin adjacent to a fresh blister is preferred for bullous dis-
eases. Biopsies from a blister may have non-specific deposits
or because of degradation of immunoglobulins can be
3.3 Immunofluorescence Studies 9

false-negative. In analyzing patients with lupus erythe-
matosus, biopsies can be taken from lesional skin as well as
non-sun-exposed skin (usually buttocks); the lupus band test
is no longer widely used because of increased sensitivity and
specificity of serologic tests for diagnosing the disorder. For
vasculitides, DIF may be essential to differentiate immune
complex vasculitides (especially Henoch-Schönlein purpura
with IgA deposits) from pauci-immune (usually
ANCA-positive) disorders; the latter have a much more
severe course.
3.3.2 Indirect Immunofluorescence
Indirect immunofluorescence (IIF) uses the patient’s serum
which is applied to a substrate such as monkey esophagus,
rat bladder, human skin or HEp-2 cells. Antibodies in the
serum attach to tissue antigens. After rinsing, a second
labeling anti-immunoglobulin antibody is applied, identify-
ing the sites of attachment of antibodies from the patient.
The response can be titrated and for several disorders the
titers correlate with the clinical course and can sometimes
predict flares. Anti-nuclear antibodies (ANA) are detected in
the same way using substrate such as HEp-2 cells. Circu-
lating antibodies can also be identified by ELISA and
immunoblot techniques.
3.3.3 Salt-Split Skin
When skin is incubated in 1 M NaCl solution, separation
occurs in the lamina lucida. When indirect immunofluores-
cence is then performed using the patient’s serum, sera from
bullous pemphigoid patients preferentially stain the roof of
blister while those from epidermolysis bullosa acquisita
patients label the floor of the blister. Often the two diseases
are identical clinically, histologically and on routine
immunofluorescence studies. Sera from patients with
mucous membrane pemphigoid sometimes show reactivity
with the roof and floor (laminin332-positive pemphigoid).

Disease Pattern Antigens

Autoimmune bullous diseases

• Pemphigus foliaceus IgG, C3—intercellular deposits in epidermis Desmoglein 1
• Pemphigus vulgaris IgG, C3—intercellular deposits in epidermis, mucosa Desmogleins 3 and 1, less often desmoglein 4 or
non-desmosomal antigens
• Bullous pemphigoid C3, IgG—linear deposits at DEJ; in early stages, IgM BP 180, BP 230
• Mucous membrane IgG, C3—linear deposits at DEJ; occasionally IgA BP 180, laminin 332 (formerly laminin 5 or epiligrin),
pemphigoic a6ß4 integrin
• Pemphigoid C3, IgG—linear deposits at DEJ BP 180 (BP 230)
gestationis
• Epidermolysis bullosa IgG, C3—linear deposits at DEJ, occasionally IgA Collagen type VII
acquisita
• Dermatitis IgA—granular deposits in papillary tips; rarely C3 Epidermal transglutaminase
herpetiformis
• Linear IgA disease IgA and C3—linear at DEJ BP 180 (BP 230)
Vasculitis
• Leukocytoclastic IgM, IgG, C3, fibrinogen around venules primarily in Unclear
vasculitis superficial dermis
• Henoch-Schönlein IgA in same pattern Unclear
purpura
Lupus erythematosus
• Chronic discoid LE IgG, IgM, IgA, C3—linear or granular deposits at DEJ in lesional skin; no deposits in unaffected, non-sun-exposed
skin
• Subacute cutaneous IgG, IgM, IgA, C3—linear or granular deposits at DEJ in lesional skin; no deposits in unaffected, non-sun-exposed
LE skin
• Systemic LE IgG, IgM, IgA, C3—linear or granular deposits at DEJ in lesional skin and unaffected, non-sun-exposed skin (lupus
band test)
Keratinocyte nuclei fluoresce in normal, non-sun-exposed skin (in vivo ANA)
DEJ = dermal–epidermal junction.
10
3.4 Molecular Biological Procedures
Molecular biological methods are used in dermatopathology
primarily in tumor diagnosis and for identifying microbes.
The most common investigations include in situ hybridiza-
tion, fluorescence in situ hybridization and polymerase chain
reaction. Most studies can be performed on formalin-fixed,
paraffin-embedded tissue. All three techniques depend on the
binding of specific oligonucleotides (probes) to comple-
mentary DNA or RNA target sequences.
3.4.1 In Situ Hybridization (ISH)
• Principle: Specific oligonucleotide probes bind to com-
plementary RNA or DNA sequences in tissue (hy-
bridization). Then they are visualized using enzymatic
color reactions.
• Advantages: Labeling of target sequence in tissue,
allowing one to identify which cells are involved.
• Disadvantages: Less sensitive than PCR because there is
no amplification of target sequences.
• Indications:
– Identification of microorganisms, especially viruses
(for example, HPV using type-specific or common
sequences).
– Demonstration of clonality in B-cell lymphomas by
determining mRNA expression of immunoglobulin
kappa and lambda light chains.
3.4.2 Fluorescence in Situ Hybridization (FISH)
• Principle: Same as ISH, but the probes are
fluorescence-labeled allowing the hybrid sequences to be
visualized with fluorescence microscopy.
3 Histopathological Techniques
• Advantages: Labeling of target sequence in tissue,
allowing one to identify which cells are involved.
• Disadvantages: Harder to interpret than ISH because
fluorescent signals may not be visualized in all planes of
sectioning.
• Indications :
– Identification of chromosomal aberrations in soft tis-
sue tumors (for example, dermatofibrosarcoma
protuberans)
3.4.3 Polymerase Chain Reaction (PCR)
• Principle: After extraction of DNA from the tissue,
specific oligonucleotide primers are added and attached to
target sequences. The hybrid product is sequentially
multiplied using cyclic temperature-dependent enzymatic
amplification over a period of hours. The amplification
product is identified using gel electrophoresis.
• Advantages: Very sensitive because target sequences are
amplified, so that trace amounts of DNA or RNA can be
identified.
• Disadvantages: The DNA or RNA sequences cannot be
localized in tissue. Because of the extreme sensitivity,
false-positive results are a major concern.
• Indications:
– Identification of microorganisms: Viruses (human
papilloma virus, herpes viruses), bacteria (Borrelia
burgdorferi, atypical mycobacteria) and parasites
(leishmania).
– Identification of monoclonality of T-cell receptor gamma
genes in T-cell lymphomas and of immunoglobulin
heavy chain genes in B-cell lymphomas.
– Identification of mutations in oncogenes or tumor
suppressor genes in tumors and in structural proteins
in ichthyoses.
 Dermatopathologic Glossary
Acanthosis: Thickening of the spinous layer. One can dis-
tinguish between broad-based acanthosis as in chronic der-
matitis and psoriasiform acanthosis with elongated rete
ridges as in psoriasis.
Acantholysis: Separation of keratinocytes because of
disruption of desmosomes (intercellular bridges) leading to
intraepidermal blisters (for example herpes infections,
pemphigus vulgaris).
Ballooning degeneration: Destruction of cells because
of increased intracellular fluid in response to cell injury
(often seen with herpes virus infections).
Basement membrane: Thin amorphous zone upon
which the epidermal rests and through which it is bound to
dermis; exact molecular structures are known but not visible
on routine microscopy.
Cornoid lamella: Column of parakeratosis overlying
defect in spinous and granular layer; defining feature of
porokeratosis.
Dyskeratosis: Apoptosis with premature keratinization of
individual keratinocytes with condensation of cytoplasmic
and nuclear proteins (Darier disease) or after sun damage
(sunburn cells).
Epidermal or epithelial giant cells: Multinucleated
keratinocytes seen in herpes virus infections, often identified
in blisters with Tzanck smear.
Epithelioid cell: Cell rich in cytoplasm with vesicular
nucleus; in inflammatory infiltrates usually a macrophage.
Erosion: Superficial epithelial defect in which the basal
layer is not destroyed.
Flame figure: Degenerated collagen fibers surrounded by
eosinophils and their products.
Giant cells: Macrophages with multiple nuclei as a result
of ingestion and fusion, seen in foreign body and inflam-
matory granulomatous processes (sarcoidosis, xanthogranu-
loma). Main types are foreign body (nuclei scattered),
Langhans (nuclei arranged as horseshoe) and Touton
(wreath of nuclei surrounding lipids).
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022
W. Kempf et al., Dermatopathology,
https://doi.org/10.1007/978-3-030-82820-2_4
4
Hemorrhage: Extravasates of erythrocytes either within
epidermis or dermis, usually traumatic or associated with
vasculitis.
Histiocyte: Tissue macrophage; term avoided in this
book because of confusion with Langerhans cell histiocy-
tosis which is a disease of dendritic Langerhans cells, not
tissue macrophages.
Hypergranulosis: Thickened granular layer, especially
common in inflammatory disorders (lichen planus) and in
human papilloma virus infections.
Hyperkeratosis: Thickening of the cornified layer, either
with retained nuclei (hyperparakeratosis) or without
(orthohyperkeratosis).
Inclusions, cytoplasmic: Collections of proteins or other
material in the cytoplasm, often seen with viral infections
(molluscum bodies).
Inclusions, nuclear: Collections of cellular proteins
within the nucleus.
Incontinence of pigment: Deposition of melanin in
upper dermis after inflammation or other damage to dermal–
epidermal junction; it may remain free in tissue or be taken
up by macrophages.
Interface dermatitis: Vacuolar changes in the cells of
the basal layer often with apoptotic cells and a lymphocytic
infiltrate at the dermal–epidermal junction (typical in lichen
planus and lupus erythematosus).
Kogoj pustule: Collection of neutrophils in spinous layer
in psoriasis.
Leukocytoclasia: Nuclear dust (karyorrhexis) from neu-
trophils, most often seen in leukocytoclastic vasculitis or
infections.
Lichenoid infiltrate: Band-like infiltrate of lymphocytes
at dermal–epidermal junction, usually associated with
interface dermatitis; prototype is lichen planus.
Macrophage: Bone-marrow derived cell active in
phagocytosis; when tissue-bound, also known as histiocyte.
Source of epithelioid and giant cells.
11
12
Metachromasia: Situation where a given stain imparts a
variety of colors to different structures.
Microabscess: Small collection of neutrophils in corni-
fied layer in psoriasis (Munro microabscess); also used
incorrectly for collections of atypical lymphocytes in epi-
dermis in mycosis fungoides (Pautrier microabscess).
Papillary abscess: Accumulation of neutrophils in pap-
illary tip, as seen primarily in dermatitis herpetiformis.
Papillomatosis: Enlargement of the dermal papillae
leading to finger-like projections of epidermis and papillary
dermis (also called church spires), most common in verrucae.
Pautrier microabscess: Intraepidermal collections of
atypical lymphocytes (and Langerhans cells). Misnomer, since
it is not an abscess (accumulation of neutrophils and necrosis).
Perivascular infiltrate: Collection of lymphocytes and
macrophages around vessel; most common finding in many
inflammatory dermatoses.
Pustule: Intraepidermal collection of neutrophils or
eosinophils.
4 Dermatopathologic Glossary
Satellite cell necrosis: Necrotic keratinocytes in associ-
ation with cytotoxic T cells.
Spongiosis: Separation of spinous layer because of
increased fluid in epidermis secondary to inflammation.
Excessive spongiosis can lead to intraepidermal vesicles.
Ulcer: Tissue defect extending into the dermis or
subcutis.
Vacuolar degeneration: Cell damage by the formation
of intercellular vacuoles, most common in cells of basal
layer with inflammation at dermal–epidermal junction, usu-
ally followed by cell death.
Vasculitis: Damage to a blood vessel with swelling of
endothelial cells and penetration of wall by inflammatory
cells; most common variant is leukocytoclastic vasculitis
with accumulations of neutrophils with nuclear dust and
leakage of erythrocytes, but little vessel occlusion. Lym-
phocytic vasculitis features dense accumulations of lym-
phocytes, little exocytosis or nuclear dust, but often thrombi
and vessel occlusion.
 Part II
Inflammatory and Infectious Dermatoses
 Epidermis: Spongiosis, Acanthosis
and Hyperparakeratosis 5

5.1 Dermatitis

Definition Allergic or toxic-irritant reaction with various clinical and histological stages and patterns; eczema is a synonym
Clinic • Acute and subacute dermatitis: Inflamed erythematous skin with vesicles and crusts
Variants • Chronic dermatitis: Erythematous scaly lesions, sometimes lichenified Variants
• Atopic dermatitis, contact dermatitis, seborrheic dermatitis, nummular dermatitis

Histopathology

Acute and subacute dermatitis

• Slight parakeratosis with tiny exudate inclusions
• Spongiosis with intraepidermal vesicles
• Exocytosis of lymphocytes and occasional neutrophils
• Perivascular lymphocytic infiltrate, sometimes with eosinophils, in upper dermis
Variant
• Seborrheic dermatitis: Subacute pattern with parakeratotic keratinization around the hair follicle openings

Differential diagnoses

• Tinea
Neutrophils and fungal elements seen in cornified layer
• Scabies
Acute or subacute pattern. Infiltrate rich in eosinophils. Diagnosis confirmed by finding mite, eggs or feces in epidermis
• Pityriasis rosea
Subacute pattern with spongiosis and focal parakeratosis. Superficial perivascular infiltrate without neutrophils. Widened dermal papillae,
erythrocyte exocytosis
• PLEVA
Focal vacuolar change at junction, spongiosis, exocytosis of lymphocytes, apoptotic keratinocytes. Above these areas focal hyperparakeratosis
with inclusions of fibrinous exudate and neutrophils. Wedge-shaped dermal lymphocytic infiltrate with CD8+ cells. Erythrocyte extravasation

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022 15

W. Kempf et al., Dermatopathology,
https://doi.org/10.1007/978-3-030-82820-2_5
16 5 Epidermis: Spongiosis, Acanthosis and Hyperparakeratosis

Histopathology

Chronic dermatitis
• Hyperparakeratosis
• Broad-based acanthosis with markedly thickened rete ridges
• Little spongiosis
• Superficial lymphocytic perivascular infiltrate with possible occasional eosinophils
• Excoriations in pruritic forms

Differential diagnoses

• Psoriasis vulgaris
Psoriasiform acanthosis, intra- and subcorneal collections of neutrophils, broad hyperparakeratosis, minimal or no spongiosis
• Mycosis fungoides (early stage)
Psoriasiform or broad-based acanthosis, little or no spongiosis but epidermotropism of lymphocytes, many of which are atypical

Comment

Distinguishing between chronic dermatitis and psoriasis may be impossible microscopically, especially for palmoplantar, irritated or treated
lesions
Tinea and dermatitis are so similar histologically that a PAS stain should always be performed to exclude the presence of fungal elements
5.1 Dermatitis 17

parakeratosis

acanthotic
epidermis

lymphocytic
perivascular
infiltrate

parakeratosis with
serum crusts

spongiosis with
lymphocytes
18 5 Epidermis: Spongiosis, Acanthosis and Hyperparakeratosis

5.2 Prurigo

Definition Reaction pattern secondary to chronic exogenous irritation through scratching and rubbing. Multiple causes (arthropod assault,
infestation, metabolic disease, artifact)
Clinic Flat nodule with central excoriation or crust, found on areas which can be manipulated, such as forearms. Marked pruritus. Often
lichenification of adjacent skin
Variants Prurigo nodularis with larger nodules

Histopathology

• Hyperparakeratosis with inclusion of fibrinous-hemorrhagic exudate

• Crescendo-like acanthosis, sometimes with pseudo-carcinomatous hyperplasia of epidermis with thickened granular layer, little or no
spongiosis
• Scattered apoptotic keratinocytes, intraepidermal erythrocytes
• Circumscribed epidermal defect (erosion, ulceration) possible
• Fibrotic vertically-arranged collagen bundles in the elongated dermal papillae
• Moderate lymphocytic perivascular infiltrate with occasional eosinophils

Differential diagnoses

• Scabies
Chronic lesions have prurigo changes but still a persistent infiltrate usually with eosinophils. Definitive diagnosis by identifying mite, eggs or
feces
• Reactive perforating collagenosis
Sharply-bordered flat ulceration, collagen at base is damaged with basophilic collagen remnants in crust
• Psoriasis
Hyperparakeratosis with accumulations of neutrophils, psoriasiform acanthosis with elongated rete ridges and dermal papillae
• Verrucous lichen planus
Lichen
Interface dermatitis with vacuolar change especially at tips of rete ridges. Wedgeshaped hypergranulosis. Acanthosis
• Verrucous carcinoma
Pushing or invasive broad strands of well-differentiated squamous epithelium with moderate atypia
5.2 Prurigo 19

Prurigo nodularis
crescendo-like
epidermal hyperplasia

thickened
granular layer

discrete spongiosis

hyperparakeratosis

lymphocyte infiltrate
with admixed
macrophages

fibrosis

Scabies
excoriation

inflammatory
infiltrate

mite

infiltrate with neutrophils

20 5 Epidermis: Spongiosis, Acanthosis and Hyperparakeratosis

5.3 Psoriasis

Definition Inflammatory dermatosis with genetic predisposition, characteristic morphology (scales or pustules on erythematous base), sites of
predilection and a chronic-recurrent course
Clinic Circumscribed erythematous patches and plaques with silvery scales, favoring knees, elbows, gluteal cleft and scalp. Pustular
variant most common on palms and soles

Histopathology

• Hyperparakeratosis
• Collections of neutrophils in tiny unicellular pustules (Kogoj pustule) and larger confluent abscesses (Munro microabscess); in both spinous and
cornified layers
• Focal loss of granular layer, pale-staining epidermis with suprapapillary thinning (thinned epidermis) over elongated dermal papillae
• Uniform acanthosis with elongated rete ridges (psoriasiform acanthosis)
• Ectatic capillaries in the elongated dermal papillae
• Superficial lymphocytic perivascular infiltrate with admixture of occasional neutrophils
Variants
• Pustular psoriasis (Sect. 5.4): Exocytosis of numerous neutrophils forming larger microabscesses or pustules in the upper epidermis, along with
spongiosis
• Guttate psoriasis: Acute form with mild spongiosis, exocytosis of neutrophils with microabscesses and overlying parakeratotic caps

Differential diagnoses

• Dermatitis
Subacute and chronic dermatitis with broad-based acanthosis, with widened rete ridges, spongiosis, and retained granular layer
• Tinea
Exocytosis of neutrophils with presence of fungal elements in cornified layer with PAS stain
• Pityriasis rubra pilaris
Horizontal and vertical pattern of changing ortho- and parakeratosis (chessboard pattern). Discrete acanthosis, sparse lymphocytic infiltrate
• Drug eruptions
Sometimes psoriasiform, for example with ^-blockers and lithium. Eosinophils may be present

Comment

It may be impossible to separate psoriasis from subacute and chronic dermatitis, especially if the lesions have been irritated or treated. Always do
PAS stain to exclude tinea
5.3 Psoriasis 21

hyperparakeratosis

acanthosis with
elongated rete ridges

neutrophils in stratum spinosum

neutrophils

absent stratum
granulosum

dilated
elongated
capillaries
22 5 Epidermis: Spongiosis, Acanthosis and Hyperparakeratosis

5.4 Pustular Psoriasis

Definition Pustular variant of psoriasis

Clinic Pustules on erythematous base; most commonly found on palms and soles

Histopathology

• Moderate hyperparakeratosis
• Exocytosis and primarily subcorneal collections of neutrophils in spinous layer
• Focal loss of granular layer with pale-staining epidermis
• Broad-based acanthosis and modest spongiosis in areas of exocytosis
• Superficial lymphocytic perivascular infiltration with admixture of neutrophils

Differential diagnoses

• Subcorneal pustulosis
Subcorneal collection of neutrophils (see comment)
• Impetiginized dermatitis
Broad-based acanthosis, spongiosis. Inclusions of exudate and neutrophils in cornified layer
• Pustular tinea
Broad-based acanthosis, spongiosis. Inclusions of exudate and neutrophils in cornified layer. Identification of fungi (PAS)
• Impetigo
Subcorneal acantholysis with exudate and numerous neutrophils in cornified layer. Clefting with acantholysis mostly beneath cornified layer,
producing subcorneal blisters
• Pustular drug eruption
Focal discrete spongiosis with subcorneal pustules, occasionally including eosinophils. Usually histologically identical to pustular psoriasis

Comment

Pustular psoriasis, impetigo and subcorneal pustulosis are often impossible to separate histologically. Subcorneal pustulosis may be a presenting
feature of IgA pemphigus. When pustules are present, always do a PAS stain to exclude a pustular tinea
5.4 Pustular Psoriasis 23

parakeratosis

psoriasiform
acanthosis

spongiform pustule

neutrophils
24 5 Epidermis: Spongiosis, Acanthosis and Hyperparakeratosis

5.5 Pityriasis Rosea

Definition Inflammatory dermatosis of unknown, but perhaps viral, etiology

Clinic Initial lesion is scaly erythematous plaque (target lesion); it is followed by numerous smaller oval slightly scaly patches along the
skin lines (Christmas tree pattern). Spontaneous resolution over weeks to months

Histopathology

• Focal hyperkeratosis
• Slight acanthosis with widened rete ridges
• Discrete spongiosis with exocytosis of lymphocytes and occasionally a parakeratotic cap
• Lymphocytic infiltrates with occasional eosinophils in upper dermis, especially in widened dermal papillae
• Extravasation of erythrocytes and occasional intraepidermal erythrocytes

Differential diagnoses

• Subacute dermatitis
Acanthosis, spongiosis, exocytosis of lymphocytes. Superficial lymphocytic perivascular infiltrate, often with eosinophils
• Erythema annulare centrifugum
Minimal epidermal changes and superficial lymphocytic perivascular infiltrate, identical to pityriasis rosea. Clinical information is needed to
separate the two entities

Comment

Acute to subacute dermatitis, pityriasis rosea and erythema annulare centrifugum share many features. The clinical pictures are usually quite
different. The main histological clues are more epidermal changes in dermatitis and a dense infiltrate with less prominent epidermal change in
erythema annulare centrifugum
5.5 Pityriasis Rosea 25

focal parakeratosis modest acanthosis

slight lymphocytic perivascular

infiltrate with exocytosis
of erythrocytes

discrete spongiosis

lymphocytes

erythrocytes outside
of vessel
26 5 Epidermis: Spongiosis, Acanthosis and Hyperparakeratosis

5.6 Cutaneous Fungal Infections

Definition Cutaneous or mucocutaneous infections caused by dermatophytes, yeasts or molds

Clinic Annular, erythematous lesions with peripheral scale; sometimes pustular especially in children. In intertriginous areas, maceration
and erythema; in hair-bearing areas, pustular and folliculitic lesions. Mucosal involvement with yeasts usually with white
easily-removed plaques or atrophic erythematous patches

Histopathology

Tinea corporis, manuum et pedum

• Epidermis with mild acanthosis, focal spongiosis and parakeratosis
• Exocytosis of neutrophils with small collections in cornified layer
• Fungal hyphae in cornified layer especially at border between ortho- and parakeratosis
• Superficial lymphocytic perivascular infiltrate with occasional neutrophils or eosinophils
Tinea capitis
• Hair follicle is infiltrated by inflammatory cells, edematous, acanthotic and focally destroyed, producing abscess
• Perifollicular dense mixed infiltrate with neutrophils, eosinophils and plasma cells
• Fungal hyphae in or around the hair shaft and occasionally in the interfollicular cornified layer

Additional studies

Hyphae and spores can be stained with PAS or Grocott stains. Fungi can also be identified immunohistochemically with an anti-M. bovis
(BCG) antibody

Differential diagnoses

• Acute and subacute dermatitis

Acanthosis, spongiosis, exocytosis of lymphocytes and neutrophils. Superficial lymphocytic perivascular infiltrate sometimes with eosinophils
• Psoriasis
Psoriasiform acanthosis of rete ridges. Collections of neutrophils in areas with hyperparakeratosis
• Impetigo
Subcorneal acantholysis and clefts containing neutrophils
• Folliculitis Follicular inflammation with bacteria identified with Gram or Giemsa staining

Comment

Dermatophyte infections can mimic many inflammatory dermatoses; thus PAS or Grocott staining of all dermatitic or psoriatic lesions is wise.
Sometimes the spores and hyphae are seen on H&E but usually the PAS or Grocott stains are required. In tinea versicolor, there is little
inflammation and a cornified layer full of hyphae and spores
Pityrosporon are often found in hair follicles but usually not clinically relevant (exception is massive follicular damage with many organisms and
inflammation). In contrast fungal hyphae in follicles are always pathogenic
5.6 Cutaneous Fungal Infections 27

Tinea
parakeratosis

acanthotic
epidermis

fungal elements
in stratum corneum
(right side PAS stain)

Candidiasis
parakeratosis

acanthotic
mucosal epithelium

yeast elements
(right side PAS stain)
28 5 Epidermis: Spongiosis, Acanthosis and Hyperparakeratosis

5.7 Human Papilloma Virus-Associated Acanthopapillomas: Verruca Vulgaris

and Condyloma Acuminatum

Definition Benign epithelial tumors caused by human papilloma virus (HPV)

Clinic • Verruca vulgaris: hyperkeratotic papules with dark inclusions (inclusions of hemorrhagic exudate in hyperparakeratotic cornified
layer). Typical sites include hands, palms and soles
Variants • Verruca plana: polygonal flat papules without marked hyperkeratosis
• Condyloma acuminatum: hyperpigmented or skin-colored papule without hyperkeratosis in anogenital area

Histopathology

Verruca vulgaris
• Focal acanthosis and papillomatosis with confluence of elongated rete ridges
• Hyperparakeratosis with focal parakeratosis and hemorrhage over the papillary tips
• Koilocytes with clear cytoplasm, condensed nuclei in granular layer
• Ectatic capillaries in papillae
• Variable lymphocytic infiltrate
Condyloma acuminatum
• Broad-based acanthosis, papillomatosis, no hyperkeratosis
• Focal parakeratosis
• Few koilocytes, sparse infiltrate

Differential diagnoses

• Seborrheic keratosis
Broad-based localized acanthosis, intraepithelial horn cysts. No confluence of elongated rete ridges
• Palmoplantar keratoderma
Hyperkeratosis, thickened or otherwise altered (for example in epidermolytic hyperkeratosis) granular layer
• Epidermal nevus
Many histological variants; some with only papillomatosis and hyperkeratosis, thus very similar to seborrheic keratosis but latter usually has horn
pseudocysts; others with persistent inflammation and parakeratosis (ILVEN = inflammatory linear verrucous epidermal nevus); yet others show
epidermolytic hyperkeratosis with abnormal granular layer
• Bowenoid papulosis
Many histological variants; some with only papillomatosis and hyperkeratosis, thus very similar to seborrheic keratosis but latter usually has horn
pseudocysts; others with persistent inflammation and parakeratosis (ILVEN = inflammatory linear verrucous epidermal nevus); yet others show
epidermolytic hyperkeratosis with abnormal granular layer

Comment

In anogenital area seborrheic keratosis and condyloma acuminatum can be histologically identical. The age of patient helps most. HPV antigens
or DNA can be identified with immunohistochemical staining or PCR
5.7 Human Papilloma Virus-Associated Acanthopapillomas: … 29

Verruca vulgaris
columns of
hyperparakeratosis

orthohyperkeratosis

filiform hyper-
plastic epidermis

koilocytes

parakeratosis

koilocytes

Condyloma acuminatum

hyperplastic epithelium

vessel-rich stroma

koilocytes
30 5 Epidermis: Spongiosis, Acanthosis and Hyperparakeratosis

5.8 Molluscum Contagiosum

Definition Benign epithelial tumor caused by infection with molluscum contagiosum virus, a DNA virus in the poxvirus group
Clinic Usually multiple grouped, dome-shaped papules with a central dell. Smaller lesions often lack dell. More common in children,
especially those with atopic dermatitis. In adults usually anogenital

Histopathology

• Circumscribed multilobular epithelial proliferation with central keratinization

• Intracytoplasmic inclusions, at the periphery eosinophilic and towards the center of the tumor more basophilic
• Associated mixed or lymphocytic infiltrate
• Occasionally lymphocytes are activated and enlarged
Variant
• Molluscum contagiosum folliculitis: Involvement of follicular epithelia with inclusion bodies and associated mixed infiltrate

Differential diagnoses

The histological changes are pathognomonic. When the inflammation is intense or in folliculitis, the inclusion bodies may initially be masked and
the infiltrate mistaken for a lymphoma until deeper sections unearth the classic changes
5.8 Molluscum Contagiosum 31

central crater

cystic tumor with

acanthotic epithelium

eosinophilic
inclusion bodies
(molluscum bodies)
32 5 Epidermis: Spongiosis, Acanthosis and Hyperparakeratosis

5.9 Parapoxvirus Infections

Definition Parapoxvirus (family poxviridae) induced skin infection after contact with infected animals, with centrally necrotic and ulcerated
nodules at the contact site, mostly on the hands
Clinic • Solitary or occasionally grouped, partially necrotic and ulcerated nodules with crust formation on the areas which were in contact
with infected animals
Variants • Milker nodule: after contact with infected calves: polygonal flat papules without marked hyperkeratosis
• Orf disease: after contact with sheep, goats; cats; rodents

Histopathology

Milker nodule and Orf disease

• Acanthosis of the epidermis
• Reticular degeneration of the epidermis with intraepidermal vesicles
• Ballooned keratinocytes and intracytoplasmic eosinophilic inclusion bodies in apoptotic keratinocytes
• In some cases dense lymphocytic infiltrate with admixture of enlarged activated lymphocytes as well as eosinophils and plasma cells
Cowpox infections
• Extensive hemorrhagic necrosis
• Necrotic hair follicles (pathognomonic)
• Characteristic intraepithelial basophilic inclusion bodies type A (Guarnieri bodies)
• Dense lymphocytic infiltrates

Additional studies

Detection of virus specific DNA by PCR or detection of Orf virus or parapox viruses by electron microscopy

Differential diagnoses

• Alpha herpes virus infections (herpes simplex virus, varicella zoster virus)
Intraepidermal vesicle, ballooning degeneration of keratinocytes, syncytial keratinocytic giant cells with marginalized chromatin and
homogenized nucleoplasm (steel gray nuclei)
• Cytomegalovirus infection
Intranuclear eosinophilic inclusion bodies in endothelial cells, fibroblasts and histiocytes (so called owl’s eye cells). Detection of the virus by in
situ-hybridization
• Hand-foot-mouth disease
Coxsackievirus-induced disease with characteristic clinical manifestation and distribution of skin lesions. Histology: Necrotic keratinocytes,
partially necrotic epidermis and ballooning degeneration
5.9 Parapoxvirus Infections 33

Cowpox (parapox virus infection)

Deep hemorrhagic inflammatory reaction and necrosis

Neutrophilic inflammation and

necrosis of hair follicle

Guarnieri bodies
 Epidermis Acantholysis
6

6.1 Darier Disease

Definition Common genodermatosis inherited in an autosomal dominant fashion

Clinic Hyperkeratotic, often crusted papules usually on the trunk favoring the seborrheic areas. Chronic course with pruritus, secondary
infections and inability to handle herpes viruses. Oral hyperkeratosis (cobblestones) and nail dystrophies

Histopathology

• Focal hyperparakeratosis
• Focal suprabasal acantholysis
• Dyskeratotic keratinocytes with cytoplasmic clearing (corps ronds) and pyknotic nuclei (grains) in areas of acantholysis
• Superficial lymphocytic perivascular infiltrate

Additional studies

IF studies do not reveal antibodies against epidermal components

Differential diagnoses

• Grover disease (transient acantholytic dermatosis)

Intensely pruritic tiny papules on trunk, usually in men >50 years of age. Focal suprabasal acantholysis with dyskeratosis and hyperkeratosis.
Occasionally fibrinous exudate in cornified layer
• Hailey-Hailey disease
Suprabasal acantholysis involving all epidermal layers, dyskeratotic keratinocytes, crusts with secondary bacterial infection. IF examinations
negative
• Pemphigus vulgaris
Extensive suprabasal acantholysis extending into hair follicles; no dyskeratosis. Infiltrate often contains eosinophils. IF: Epidermal intercellular
deposits of IgG and C3 directed against desmogleins, components of the hemidesmosome; circulating antibodies are present
• Warty dyskeratoma
Solitary benign epithelial tumor with epidermal invagination, suprabasal acantholysis and dyskeratotic cells; often involves hair follicle

Comment

Grover disease may exactly mimic Darier disease, Hailey-Hailey disease or pemphigus vulgaris. The clinical picture usually provides the answer

© The Author(s), under exclusive license to Springer Nature Switzerland AG 2022 35

W. Kempf et al., Dermatopathology,
https://doi.org/10.1007/978-3-030-82820-2_6
36 6 Epidermis Acantholysis

focal hyperparakeratosis

suprabasal acantholysis

dyskeratotic
keratinocytes

acantholysis

lymphocytic
infiltrate
6.2 Hailey-Hailey Disease 37

6.2 Hailey-Hailey Disease

Definition Genodermatosis with classic predilection sites inherited in an autosomal dominant fashion
Clinic Circumscribed erythematous eroded or crusted patches and plaques usually in the axillae, groin and nape. Chronic-recurrent course
with frequent secondary infections

Histopathology

• Hyperparakeratosis with inclusions of fibrinous exudate, neutrophils and bacteria

• Broad-based transepidermal acantholysis (dilapidated brick wall)
• Scattered dyskeratotic keratinocytes
• Superficial perivascular lymphocytic infiltrate

Additional studies

IF studies do not reveal antibodies against epidermal components

Differential diagnoses

• Darier disease and Grover disease

Focal suprabasal acantholysis; many dyskeratotic keratinocytes (corps ronds and grains) with hyperparakeratosis. IF examinations negative
• Pemohieus vulgaris
Extensive suprabasal acantholysis extending into hair follicles; no dyskeratosis. Infiltrate often contains eosinophils. IF: Epidermal intercellular
deposits of IgG and C3 directed against desmogleins, components of the hemidesmosome; circulating antibodies are present
• Wartv dvskeratoma
Solitary benign epithelial tumor with epidermal invagination, suprabasal acantholysis and dyskeratotic cells; often involves hair follicles

Comment

The histological findings in pemphigus vulgaris can overlap with Hailey-Hailey disease, leading to the confusing name of benign familial
pemphigus. Under the microscope pemphigus vulgaris is more likely to have suprabasal acantholysis while Hailey-Hailey disease shows
full-thickness acantholysis. Pemphigus vulgaris involves adnexal structures. The distinction is best made with direct immunofluorescence studies,
as Hailey-Hailey disease is invariably negative
38 6 Epidermis Acantholysis

parakeratosis

acanthosis
with
acantholysis

acantholysis in all
layers of epidermis

lymphocytic
infiltrate
6.3 Herpes Virus Infections 39

6.3 Herpes Virus Infections

Definition Infection of the skin or mucosa by herpes simplex virus (HSV) type 1 or 2, or by varicella zoster virus (VZV)
Clinic Variants Grouped blisters on erythematous base
• Herpes folliculitis, VZV vasculitis
• Hyperkeratotic ulcerated chronic lesions in immunosuppressed patients

Histopathology

• Acantholysis with intraepidermal vesicles

• Epithelial cells with ballooning degeneration, steel gray nuclei, multinucleate syncytial epithelial giant cells
• Superficial and deep lymphocytic perivascular infiltrate often with neutrophils and plasma cells
• With VZV infection often focal vasculitis with nuclear dust
Variant
• “Herpes incognito” with dense dermal lymphocytic infiltrate and necrotic adnexal structures (usually hair follicles)

Additional studies

Viral antigens or DNA can be identified with immunohistochemical stains, in situ hybridization or polymerase chain reaction (PCR). DIF is
negative

Differential diagnoses

• Pemphigus vulgaris
Extensive suprabasal acantholysis extending into hair follicles; no dyskeratotic cells. Infiltrate often contains eosinophils. No ballooning
degeneration or multinucleate giant cells. IF: Epidermal intercellular deposits of IgG and C3 directed against desmogleins, components of the
hemidesmosome; circulating antibodies are present
• Darier disease and Grover disease
Focal suprabasal acantholysis; many dyskeratotic keratinocytes (corps ronds and grains) with hyperparakeratosis. IF examinations negative
• Orf and milker’s nodule
Pale keratinocytes with ballooning degeneration, no acantholysis or blisters. Tricolor sign—red cornified layer, pale (white) necrotic epidermis,
blue (basophilic) dermal infiltrate (red, white and blue—the three colors of the French flag)

Comments

HSV and VZV infections cannot be separated histologically. VZV does tend to have deeper and denser infiltrates
Another random document with
no related content on Scribd:
this expedition, along with another vessel styled the Greenwich, he
was saluted with the unwelcome sight of two powerful pirate vessels
sailing into the bay, one being of 30, and the other of 34 guns.
Though he was immediately deserted by the Greenwich, the two
pirates bearing down upon him with their black flags, did not daunt
the gallant Macrae. He fought them both for several hours, inflicting
on one some serious breaches between wind and water, and
disabling the boats in which the other endeavoured to board him. At
length, most of his officers and quarter-deck men being killed or
wounded, he made an attempt to run ashore, and did get beyond the
reach of the two pirate vessels. With boats, however, they beset his
vessel with redoubled fury, and in the protracted fighting which
ensued, he suffered severely, though not without inflicting fully as
much injury as he received. Finally, himself 1733.
and the remains of his company succeeded
in escaping to the land, though in the last stage of exhaustion with
wounds and fatigue. Had he, on the contrary, been supported by the
Greenwich, he felt no doubt that he would have taken the two pirate
vessels, and obtained £200,000 for the Company.[723]
The hero of this brilliant affair was a native of the town of
Greenock, originally there a very poor boy, but succoured from
misery by a kind-hearted musician or violer named Macguire, and
sent by him to sea. By the help of some little education he had
received in his native country, his natural talents and energy quickly
raised him in the service of the East India Company, till, as we see,
he had become the commander of one of their goodly trading-
vessels. The conflict of Juanna gave him further elevation in the
esteem of his employers, and, strange to say, the poor barefooted
Greenock laddie, the protégé of the wandering minstrel Macguire,
became at length the governor of Madras! He now returned to
Scotland, in possession of ‘an immense estate,’ which the journals of
the day are careful to inform us, ‘he is said to have made with a fair
character’—a needful distinction, when so many were advancing
themselves as robbers, or little better, or as truckling politicians. One
of Governor Macrae’s first acts was to provide for the erection of a
monumental equestrian statue of King William at Glasgow, having
probably some grateful personal feeling towards that sovereign. It
was said to have cost him £1000 sterling. But the grand act of the
governor’s life, after his return, was his requital of the kindness he
had experienced from the violer Macguire. The story formed one of
the little romances of familiar conversation in Scotland during the
last century. Macguire’s son, with the name of Macrae, succeeded to
the governor’s estate of Holmains, in Dumfriesshire,[724] which he
handed down to his son.[725] The three daughters, highly educated,
and handsomely dowered, were married to men of figure, the eldest
to the Earl of Glencairn (she was the mother of Burns’s well-known
patron); the second to Lord Alva, a judge in the Court of Session; the
third to Charles Dalrymple of Orangefield, near Ayr. Three years
after his return from the East Indies, Governor Macrae paid a visit to
Edinburgh, and was received with public as 1733.
well as private marks of distinction, on
account of his many personal merits.
An amusing celebration of the return of the East India governor
took place at Tain, in the north of Scotland. John Macrae, a near
kinsman of the great man, being settled there in business, resolved to
shew his respect for the first exalted person of his hitherto humble
clan. Accompanied by the magistrates of the burgh and the principal
burgesses, he went to the Cross, and there superintended the
drinking of a hogshead of wine, to the healths of the King, Queen,
Prince of Wales, and the Royal Family, and those of ‘Governor
Macrae and all his fast friends.’ ‘From thence,’ we are told, ‘the
company repaired to the chief taverns in town, where they repeated
the aforesaid healths, and spent the evening with music and
entertainments suitable to the occasion.’[726]
 The tendency which has already been Dec. 6.
alluded to, of a small portion of the Scottish
clergy to linger in an antique orthodoxy and strenuousness of
discipline, while the mass was going on in a progressive laxity and
subserviency to secular authorities, was still continuing. The chief
persons concerned in the Marrow Controversy of 1718[727] and
subsequent years, had recently made themselves conspicuous by
standing up in opposition to church measures for giving effect to
patronage in the settlement of ministers, and particularly to the
settlement of an unpopular presentee at Kinross; and the General
Assembly, held this year in May, came to the resolution of rebuking
these recusant brethren. The brethren, however, were too confident
in the rectitude of their course to submit to censure, and the
commission of the church in November punished their contumacy by
suspending from their ministerial functions, Ebenezer Erskine of
Stirling, William Wilson of Perth, Alexander Moncrieff of Abernethy,
and James Fisher of Kinclaven.
The suspended brethren, being all of them men held in the highest
local reverence, received much support among their flocks, as well as
among the more earnest clergy. Resolving not to abandon the
principles they had taken up, it became necessary that they should
associate in the common cause. They accordingly met at this date in
a cottage at Gairney Bridge near Kinross, and constituted themselves
into a provisional presbytery, though 1733.
without professing to shake off their
connection with the Established Church. It is thought that the taking
of a mild course with them at the next General Assembly would have
saved them from an entire separation. But it was not to be. The
church judicatories went on in their adopted line of high-handed
secularism, and the matter ended, in 1740, with the deposition of the
four original brethren, together with four more who took part with
them. Thus, unexpectedly to the church, was formed a schism in her
body, leading to the foundation of a separate communion, by which a
fourth of her adherents, and those on the whole the most religious
people, were lost.
An immense deal of devotional zeal, mingled with the usual alloys
of illiberality and intolerance, was evoked through the medium of
‘the Secession,’ The people built a set of homely meeting-houses for
the deposed ministers, and gave them such stipends as they could
afford. In four years, the new body appeared as composed of twenty-
six clergy, in three presbyteries. It was the first of several occasions
of the kind, on which, it may be said without disrespect, both the
strength and the weakness of the Scottish character have been
displayed. A single anecdote, of the truth of which there is no reason
to doubt, will illustrate the spirit of this first schism. There was a
family of industrious people at Brownhills, near St Andrews, who
adhered to the Secession. The nearest church was that of Mr
Moncrieff at Abernethy, twenty miles distant. All this distance did
the family walk every Sunday, in order to attend worship, walking of
course an equal distance in returning. All that were in health
invariably went. They had to set out at twelve o’clock of the Saturday
night, and it was their practice to make all the needful preparations
of dress and provisioning without looking out to see what kind of
weather was prevailing. When all were ready, the door was opened,
and the whole party walked out into the night, and proceeded on
their way, heedless of whatever might fall or blow.

Our Scottish ancestors had a peculiar way 1734. Jan.

of dealing with cases of ill-usage of women
by their husbands. The cruel man was put by his neighbours across a
tree or beam, and carried through the village so enthroned, while
some one from time to time proclaimed his offence, the whole being
designed as a means of deterring other men from being cruel to their
spouses.
We have a series of documents at this date, illustrating the regular
procedure in cases of Riding the Stang [properly, sting—meaning a
beam]. John Fraser, of the burgh of regality 1734.
of Huntly, had gone to John Gordon, bailie
for the Duke of Gordon, complaining that some of his neighbours
had threatened him with the riding of the stang, on the ground of
alleged ill-usage of his wife. The first document is a complaint from
Ann Johnston, wife of Fraser, and some other women, setting forth
the reality of this bad usage: the man was so cruel to his poor spouse,
that her neighbours were forced occasionally to rise from their beds
at midnight, in order to rescue her from his barbarous hands. They
justified the threat against him, as meant to deter him from
continuing his atrocious conduct, and went on to crave of the bailie
that he would grant them a toleration of the stang, as ordinarily
practised in the kingdom, ‘being, we know, no act of parliament to
the contrary.’ If his lordship could suggest any more prudent
method, they said they would be glad to hear of it ‘for preventing
more fatal consequences.’ ‘Otherwise, upon the least disobligement
given, we must expect to fall victims to our husbands’ displeasure,
from which libera nos, Domine.’ Signed by Ann Johnston, and ten
other women, besides two who give only initials.
Fraser offered to prove that he used his wife civilly, and was
allowed till next day to do so. On that next day, however, four men
set upon him, and carried him upon a tree through the town, thus
performing the ceremony without authority. On Fraser’s complaint,
they were fined in twenty pounds Scots, and decerned for twelve
pounds of assythment to the complainer.[728]

The execution of the revenue laws gave 1735. Sep.

occasion for much bad blood. In June 1734,
a boat having on board several persons, including at least one of
gentlemanlike position in society, being off the shore of Nairn with
‘unentrable goods,’ the custom-house officers, enforced by a small
party from the Hon. Colonel Hamilton’s regiment, went out to
examine it. In a scuffle which ensued, Hugh Fraser younger of
Balnain was killed, and two of the soldiers, named Long and
Macadam, were tried for murder by the Court of Admiralty in
Edinburgh, and condemned to be hanged on the 19th of November
within flood-mark at Leith.
An appeal was made for the prisoners to the Court of Justiciary,
which, on the 11th of November, granted a 1735.
suspension of the Judge-admiral’s sentence
till the 1st of December, that the case might before that day be more
fully heard. Next day, the Judge-admiral, Mr Graham, caused to be
delivered to the magistrates sitting in council a ‘Dead Warrant,’
requiring and commanding them to see his sentence put in execution
on the proper day. The magistrates, however, obeyed the Court of
Justiciary. Meanwhile, four of those who had been in the boat, and
who had given evidence against the two soldiers on their trial, were
brought by the custom-house authorities before the Judge-admiral,
charged with invading and deforcing the officers, and were acquitted.
On the 5th December, the Court of Justiciary found that the
Judge-admiral, in the trial of Long and Macadam, had ‘committed
iniquity,’ and therefore they suspended the sentence indefinitely. On
a petition three weeks after, the men were liberated, after giving
caution to the extent of 300 merks, to answer on any criminal charge
that might be exhibited against them before the Court of Justiciary.
[729]

Dancing assemblies, which we have seen Nov. 18.

introduced at Edinburgh in 1723, begin
within the ensuing dozen years to be heard of in some of the other
principal towns. There was, for example, an assembly at Dundee at
this date, and an Edinburgh newspaper soon after presented a copy
of verses upon the ladies who had appeared at it, celebrating their
charms in excessively bad poetry, but in a high strain of compliment:
‘Heavens! what a splendid scene is here,
How bright those female seraphs shine!’ &c.

From the indications afforded by half-blank names, we may surmise

that damsels styled Bower, Duncan, Reid, Ramsay, Dempster, and
Bow—all of them names amongst the gentlefolks of the district—
figured conspicuously at this meeting—
‘Besides a much more numerous dazzling throng,
Whose names, if known, should grace my artless song.’

The poet, too, appears to have paid 2s. 6d. for the insertion of his
lines in the Caledonian Mercury.
From this time onward, an annual ball, given by ‘the Right
Honourable Company of Hunters’ in the Palace of Holyroodhouse, is
regularly chronicled. At one which took place on the 8th January
1736—the Hon. Master Charles Leslie being 1735.
‘king,’ and the Hon. Lady Helen Hope being
‘queen’—‘the company in general made a very grand appearance, an
elegant entertainment and the richest wines were served up, and the
whole was carried on and concluded with all decency and good order
imaginable.’ A ball given by the same fraternity in the same place, on
the ensuing 21st of December, was even more splendid. There were
two rooms for dancing, and two for tea, illuminated with many
hundreds of wax-candles. ‘In the Grand Hall [the Gallery?], a table
was covered with three hundred dishes en ambiqu, at which sate a
hundred and fifty ladies at a time ... illuminated with four hundred
wax-candles. The plan laid out by the council of the company was
exactly followed out with the greatest order and decency, and
concluded without the least air of disturbance.’
On the 27th January 1737, ‘the young gentlemen-burghers’ of
Aberdeen gave ‘a grand ball to the ladies, the most splendid and
numerous ever seen there;’ all conducted ‘without the least confusion
or disorder.’ The anxiety to shew that there was no glaring
impropriety in the conduct of the company on these occasions, is
significant, and very amusing.[730]

The reader of this work has received—I fear not very thankfully—
sundry glimpses of the frightful state of the streets of Edinburgh in
previous centuries; and he must have readily understood that the
condition of the capital in this respect represented that of other
populous towns, all being alike deficient in any recognised means of
removing offensive refuse. There was, it must be admitted,
something peculiar in the state of Edinburgh in sanitary respects, in
consequence of the extreme narrowness of its many closes and
wynds, and the height of its houses. How it was endured, no modern
man can divine; but it certainly is true that, at the time when men
dressed themselves in silks and laces, and took as much time for
their toilets as a fine lady, they had to pass in all their bravery
amongst piles of dung, on the very High Street of Edinburgh, and
could not make an evening call upon Dorinda or Celia in one of the
alleys, without the risk of an ablution from above sufficient to
destroy the most elegant outfit, and put the wearers out of conceit
with themselves for a fortnight.
The struggles of the municipal authorities at sundry times to get
the streets put into decent order against a 1735.
royal ceremonial entry, have been adverted
to in our earlier volumes. It would appear that things had at last
come to a sort of crisis in 1686, so that the Estates then saw fit to
pass an act[731] to force the magistrates to clean the city, that it might
be endurable for the personages concerned in the legislature and
government, ordaining for this purpose a ‘stent’ of a thousand
pounds sterling a year for three years on the rental of property. A
vast stratum of refuse, through which people had made lanes
towards their shop-doors and close-heads, was then taken away—
much of it transported by the sage provost, Sir James Dick, to his
lands at Prestonfield, then newly enclosed, and the first that were so
—which consequently became distinguished for fertility[732]—and the
city was never again allowed to fall into such disorder. There was
still, however, no regular system of cleaning, beyond what the street
sewers supplied; and the ancient practice of throwing ashes, foul
water, &c., over the windows at night, graced only with the warning-
cry of Gardez l’eau, was kept up in full vigour by the poorer and
more reckless part of the population.
An Edinburgh merchant and magistrate, named Sir Alexander
Brand, who has been already under our attention as a manufacturer
of gilt leather hangings, at one time presented an overture to the
Estates for the cleaning of the city. The modesty of the opening
sentence will strike the reader: ‘Seeing the nobility and gentry of
Scotland are, when they are abroad, esteemed by all nations to be the
finest and most accomplished people in Europe, yet it’s to be
regretted that it’s always casten up to them by strangers, who admire
them for their singular qualifications, that they are born in a nation
that has the nastiest cities in the world, especially the metropolitan.’
He offered to clean the city daily, and give five hundred a year for the
refuse.[733] But his views do not seem to have been carried into effect.
After 1730, when, as we have seen, great changes were beginning
to take place in Scotland, increased attention was paid to external
decency and cleanliness. The Edinburgh magistrates were anxious to
put down the system of cleaning by ejectment. We learn, for
example, from a newspaper, that a servant-girl having thrown foul
water from a fourth story in Skinners’ Close, ‘which much abused a
lady passing by, was brought before the bailies, and obliged to enact
herself never to be guilty of the like 1735.
practices in future. ’Tis hoped,’ adds our
chronicler, ‘that this will be a caution to all servants to avoid this
wicked practice.’
 There lived at this time in Edinburgh a respectable middle-aged
man, named Robert Mein, the representative of the family which had
kept the post-office for three generations between the time of the
civil war and the reign of George I., and who boasted that the pious
lady usually called Jenny Geddes, but actually Barbara Hamilton,
who threw the stool in St Giles’s in 1637, was his great-grandmother.
Mein, being a man of liberal ideas, and a great lover of his native city,
desired to see it rescued from the reproach under which it had long
lain as the most fetid of European capitals, and he accordingly drew
up a paper, shewing how the streets might be kept comparatively
clean by a very simple arrangement. His suggestion was, that there
should be provided for each house, at the expense of the landlord, a
vessel sufficient to contain the refuse of a day, and that scavengers,
feed by a small subscription among the tenants, should discharge
these every night. Persons paying what was then a very common
rent, ten pounds, would have to contribute only five shillings a year;
those paying fifteen pounds, 7s. 6d., and so on in proportion. The
projector appears to have first explained his plan to sundry
gentlemen of consideration—as, for example, Mr William Adam,
architect, and Mr Colin Maclaurin, professor of mathematics, who
gave him their approbation of it in writing—the latter adding: ‘I
subscribe for my own house in Smith’s Land, Niddry’s Wynd, fourth
story, provided the neighbours agree to the same.’ Other subscribers
of consequence were obtained, as ‘Jean Gartshore, for my house in
Morocco’s Close, which is £15 rent,’ and ‘the Countess of
Haddington, for the lodging she possessed in Bank Close,
Lawnmarket, valued rent £20.’ Many persons agreed to pay a half-
penny or a penny weekly; some as much as a half-penny per pound
of rent per month. One lady, however, came out boldly as a recusant
—‘Mrs Black refuses to agree, and acknowledges she throws
over.’[734]
Mr Mein’s plan was adopted, and acted upon to some extent by the
magistrates; and the terrible memory of the ‘Dirty Luggies,’ which
were kept in the stairs, or in the passages within doors, as a
necessary part of the arrangement, was fresh in the minds of old
people whom I knew in early life. The city was in 1740 divided into
twenty-nine districts, each having a couple 1735.
of scavengers supported at its own expense,
who were bound to keep it clean; while the refuse was sold to persons
who engaged to cart it away at three half-pence per cart-load.[735]

Five men, who had suffered from the 1736. Jan. 9.

severity of the excise laws, having formed
the resolution of indemnifying themselves, broke into the house of
Mr James Stark, collector of excise, at Pittenweem, and took away
money to the extent of two hundred pounds, besides certain goods.
They were described as ‘Andrew Wilson, indweller in Pathhead;
George Robertson, stabler without Bristoport [Edinburgh]; William
Hall, indweller in Edinburgh; John Frier, indweller there; and John
Galloway, servant to Peter Galloway, horse-hirer in Kinghorn.’
Within three days, the whole of them were taken and brought to
Edinburgh under a strong guard.
Wilson, Robertson, and Hall were tried on the 2d of March, and
condemned to suffer death on the ensuing 14th of April. Five days
before that appointed for the execution—Hall having meanwhile
been reprieved—Wilson and Robertson made an attempt to escape
from the condemned cell of the Old Tolbooth, but failed in
consequence of Wilson, who was a squat man, sticking in the grated
window. Two days later, the two prisoners being taken, according to
custom, to attend service in the adjacent church, Wilson seized two
of the guard with his hands, and a third with his teeth, so as to enable
Robertson, who knocked down the fourth, to get away. The citizens,
whose sympathies went strongly with the men as victims of the
excise laws, were much excited by these events, and the authorities
were apprehensive that the execution of Wilson would not pass over
without an attempt at rescue. The apprehension was strongly shared
by John Porteous, captain of the town-guard, who consequently
became excited to a degree disqualifying him for so delicate a duty as
that of guarding the execution. When the time came, the poor
smuggler was duly suspended from the gallows in the Grassmarket,
without any disturbance; but when the hangman proceeded to cut
down the body, the populace began to throw stones, and the detested
official was obliged to take refuge among the men of the guard.
Porteous, needlessly infuriated by this demonstration, seized a
musket, and fired among the crowd, commanding his men to do the
same. There was consequently a full 1735.
fusillade, attended by the instant death of six persons, and the
wounding of nine more.
The magistrates being present at the windows of a tavern close by,
it was inexcusable of Porteous to have fired without their orders,
even had there been any proper occasion for so strong a measure. As
it was, he had clearly committed manslaughter on an extensive scale,
and was liable to severe punishment. By the public at large he was
regarded as a ferocious murderer, who could scarcely expiate with
his own life the wrongs he had done to his fellow-citizens.
Accordingly, when subjected to trial for murder on the ensuing 5th of
July, condemnation was almost a matter of course.
The popular antipathy to the excise laws, the general hatred in
which Porteous was held as a harsh official, and a man of profligate
life, and the indignation at his needlessly taking so many innocent
lives, combined to create a general rejoicing over the issue of the
trial. There were some, however, chiefly official persons and their
connections, who were not satisfied as to the fairness of his assize,
and, whether it was fair or not, felt it to be hard to punish what was
at most an excess in the performance of public duty, with death. On a
representation of the case to the queen, who was at the head of a
regency during the absence of her husband in Hanover, a respite of
six weeks was granted, five days before that appointed for the
execution.[736]
The consequent events are so well known, 1736.
that it is unnecessary here to give them in
more than outline. The populace of Edinburgh heard of the respite of
Porteous with savage rage, and before the eve of what was to have
been his last day, a resolution was formed that, if possible, the
original order of the law should be executed. The magistrates heard
of mischief being designed, but disregarded it as only what they
called ‘cadies’ clatters;’ that is, the gossip of street-porters. About
nine in the evening of the 7th September, a small party of men came
into the city at the West Port, beating a drum, and were quickly
followed by a considerable crowd. Proceeding by the Cowgate, they
shut the two gates to the eastward, and planted a guard at each. The
ringleaders then advanced with a large and formidable mob towards
the Tolbooth, in which Porteous lay confined. The magistrates came
out from a tavern, and tried to oppose the progress of the
conspirators, but were beat off with a shower of stones. Other
persons of importance whom they met, were civilly treated, but
turned away from the scene of action. Reaching the door of the
prison, they battered at it for a long time in vain, and at length it was
found necessary to burn it. This being a tedious process, it was
thought by the magistrates that there might 1736.
be time to introduce troops from the
Canongate, and so save the intended victim. Mr Patrick Lindsay,
member for the city, at considerable hazard, made his way over the
city wall, and conferred with General Moyle at his lodging in the
Abbeyhill; but the general hesitated to act without the authority of
the Lord Justice Clerk (Milton), who lived at Brunstain House, five
miles off. Thus time was fatally lost. After about an hour and a half,
the rioters forced their way into the jail, and seized the trembling
Porteous, whom they lost no time in dragging along the street
towards the usual place of execution. As they went down the West
Bow, they broke open a shop, took a supply of rope, and left a guinea
for it on the table. Then coming to the scene of what they regarded as
his crime, they suspended the wretched man over a dyer’s pole, and
having first waited to see that he was dead, quietly dispersed.
The legal authorities made strenuous efforts to identify some of
the rioters, but wholly without success. The subsequent futile
endeavour of the government to punish the corporation of
Edinburgh by statute, belongs to the history of the country.

Considering how important have been the June 24.

proceedings under the act of the ninth
parliament of Queen Mary Anentis Witchcrafts, it seems proper that
we advert to the fact of its being from this day repealed in the
parliament of Great Britain, along with the similar English act of the
first year of King James I. It became from that time incompetent to
institute any suit for ‘witchcraft, sorcery, enchantment, or
conjuration,’ and only a crime to pretend to exercise such arts, liable
to be punished by a year’s imprisonment, with the pillory. There
seems to be little known regarding the movement for abolishing
these laws. We only learn that it was viewed with disapprobation by
the more zealously pious people in Scotland, one of whom, Mr
Erskine of Grange, member for Clackmannanshire, spoke pointedly
against it in the House of Commons. Seeing how clearly the offence is
described in scripture, and how direct is the order for its
punishment, it seemed to these men a symptom of latitudinarianism
that the old statute should be withdrawn. When the body of
dissenters, calling themselves the Associate Synod in 1742, framed
their Testimony against the errors of the established church and of
the times generally, one of the specific things condemned was the
repeal of the acts against witchcraft, which was declared to be
‘contrary to the express letter of the law of 1736.
God, “Thou shalt not suffer a witch to live.”’

Amongst the gay and ingenious, who Nov. 8.

patronised and defended theatricals, Allan
Ramsay stood conspicuous. He entertained a kind of enthusiasm on
the subject, was keenly controversial in behalf of the stage, and
willing to incur some risk in the hope of seeing his ideal of a sound
drama in Scotland realised. We have seen traces of his taking an
immediate and personal interest in the performances carried on for a
few years by the ‘Edinburgh Company of Comedians’ in the Tailors’
Hall. He was now induced to enter upon the design of rearing, in
Edinburgh, a building expressly adapted as a theatre; and we find
him going on with the work in the summer of this year, and
announcing that ‘the New Theatre in Carrubber’s Close’ would be
opened on the 1st of November. The poet at the same time called
upon gentlemen and ladies who were inclined to take annual tickets,
of which there were to be forty at 30s. each, to come forward and
subscribe before a particular day, after which the price would be
raised to two guineas.
Honest Allan knew he would have to encounter the frowns of the
clergy, and be reckoned as a rash speculator by many of his friends;
but he never expected that any legislative enactment would interfere
to crush his hopes. So it was, however. The theatre in Carrubber’s
Close was opened on the 8th of November, and found to be, in the
esteem of all judges, ‘as complete and finished with as good a taste as
any of its size in the three kingdoms.’[737] A prologue was spoken by
Mr Bridges, setting forth the moral powers of the drama, and
attacking its enemies—those who
 ‘From their gloomy thoughts and want of sense,
Think what diverts the mind gives Heaven offence.’

The Muse, it was said, after a long career of glory in ancient times,
had reached the shores of England, where Shakspeare taught her to
soar:
‘At last, transported by your tender care,
She hopes to keep her seat of empire here.
For your protection, then, ye fair and great,
This fabric to her use we consecrate;
On you it will depend to raise her name,
And in Edina fix her lasting fame.’

Alas! all these hopes of a poet were soon 1736.

clouded. Before the Carrubber’s Close
playhouse had seen out its first season, an act was passed (10 Geo. II.
chap. 28) explaining one of Queen Anne regarding rogues and
vagabonds, the whole object in reality being to prevent any persons
from acting plays for hire, without authority or licence by letters-
patent from the king or his Lord Chamberlain.[738] This put a
complete barrier to the poet’s design, threw the new playhouse
useless upon his hands,[739] and had nearly shipwrecked his fortunes.
He addressed a poetical account of his disappointment to the new
Lord President of the Court of Session, Duncan Forbes, a man who
united a taste for elegant literature with the highest Christian graces.
He recites the project of the theatre:
‘Last year, my lord, nae farther gane,
A costly wark was undertane
By me, wha had not the least dread
An act would knock it on the head:
A playhouse new, at vast expense,
To be a large, yet bien defence,
In winter nights, ’gainst wind and weet,
To ward frae cauld the lasses sweet;
While they with bonny smiles attended,
To have their little failings mended.’

He asks if he who has written with the approbation of the entire

country, shall be confounded with rogues and rascals, be twined of
his hopes, and
 ‘Be made a loser, and engage
With troubles in declining age,
While wights to whom my credit stands
For sums, make sour and thrawn demands?’

Shall a good public object be defeated?

‘When ice and snaw o’ercleads the isle,
Wha now will think it worth their while
To leave their gousty country bowers,
For the ance blythesome Edinburgh’s towers,
Where there’s no glee to give delight,
And ward frae spleen the langsome night?’

He pleads with the Session for at least a limited licence.

‘... I humbly pray
Our lads may be allowed to play,
At least till new-house debts be paid off,
The cause that I’m the maist afraid of;
Which lade lies on my single back,
And I maun pay it ilka plack.’

Else let the legislature relieve him of the 1736.

burden of his house,
‘By ordering frae the public fund
A sum to pay for what I’m bound;
Syne, for amends for what I’ve lost,
Edge me into some canny post.’

All this was of course but vain prattle. The piece appeared in the
Gentleman’s Magazine (August 1737), and no doubt awoke some
sympathy; but the poet had to bear single-handed the burden of a
heavy loss, as a reward for his spirited attempt to enliven the beau
monde of Edinburgh.

Amongst other symptoms of a tendency Nov. 28.

to social enjoyments at this time, we cannot
overlook a marked progress of free-masonry throughout the country.
This day, the festival of the tutelar saint of Scotland, the Masters and
Wardens of forty regular lodges met in St Mary’s Chapel, in
Edinburgh, and unanimously elected as their Grand Master, William
Sinclair, of Roslin, Esq., representative of an ancient though reduced
family, which had been in past ages much connected with free-
masonry.
On St John’s Day, 27th December, this act was celebrated by the
freemasons of Inverness, with a procession to the cross in white
gloves and aprons, and with the proper badges, the solemnity being
concluded with ‘a splendid ball to the ladies.’[740]

The Edinburgh officials who had been 1737. June 30.

taken to London for examination regarding
the Porteous Riot, being now at liberty to return, there was a general
wish in the city to give them a cordial reception. The citizens rode out
in a great troop to meet them, and the road for miles was lined with
enthusiastic pedestrians. The Lord Provost, Alexander Wilson, from
modesty, eluded the reception designed for him; but the rest came
through the city, forming a procession of imposing length, while bells
rang and bonfires blazed, and the gates of the Netherbow, which had
been removed since the 7th of September last, were put up again
amidst the shouts of the multitude.
A month later, one Baillie, who had given evidence before the
Lords’ Committee tending to criminate the magistrates, returned in a
vessel from London, and had no sooner set 1737.
his foot on shore than he found himself
beset by a mighty multitude bent on marking their sense of his
conduct. To collect the people, some seized and rang a ship’s bell;
others ran through the streets ringing small bells. ‘Bloody Baillie is
come!’ passed from mouth to mouth. The poor man, finding that
thousands were gathered for his honour, flung himself into the stage-
coach for Edinburgh, and was solely indebted to a fellow-passenger
of the other sex for the safety in which he reached his home.
Captain Lind, of the Town-guard, having given similar evidence,
was discharged by the town-council; but the government
immediately after appointed him ‘lieutenant in Tyrawley’s regiment
of South British Fusiliers at Gibraltar.’[741]
 It was still customary to keep recruits in 1738. Feb. 3.
prison till an opportunity was obtained of
shipping them off for service. A hundred young men, who had been
engaged for the Dutch republic in Scotland, had been for some time
confined in the Canongate Tolbooth, where probably their treatment
was none of the best. Disappointed in several attempts at escape,
they turned at length mutinous, and it was necessary to carry four of
the most dangerous to a dungeon in the lower part of the prison. By
this the rest were so exasperated, ‘that they seized one of their
officers and the turnkey, whom they clapped in close custody, and,
barricading the prison-door, bade defiance to all authority. At the
same time they intimated that, if their four comrades were not
instantly delivered up to them, they would send the officer and
turnkey to where the d—— sent his mother; so that their demand was
of necessity complied with.’
During all the next day (Saturday) they remained in their fortress
without any communication either by persons coming in or by
persons going out. The authorities revolved the idea of a forcible
attempt to reduce them to obedience; but it seemed better to starve
them into a surrender. On the Sunday evening, their provisions being
exhausted, they beat a chamade and hung out a white flag;
whereupon some of their officers and a few officers of General
Whitham’s regiment entered into a capitulation with them; and, a
general amnesty being granted, they delivered up their stronghold.
‘It is said they threatened, in case of non-compliance with their
articles, to fall instantly about eating the turnkey.’[742]
Isabel Walker, under sentence of death at 1738. Aug.
Dumfries for child-murder, obtained a
reprieve through unexpected means. According to a letter dated
Edinburgh, August 10, 1738, ‘This unhappy creature was destitute of
friends, and had none to apply for her but an only sister, a girl of a
fine soul, that overlooked the improbability of success, and helpless
and alone, went to London to address the great; and solicited so well,
that she got for her, first, a reprieve, and now a remission. Such
another instance of onerous friendship can scarce be shewn; it well
deserved the attention of the greatest, who could not but admire the
virtue, and on that account engage in her cause.’[743]
 Helen Walker, who acted this heroic part, was the daughter of a
small farmer in the parish of Irongray. Her sister, who had been
under her care, having concealed her pregnancy, it came to be
offered to Helen as a painful privilege, that she could save the
accused if she could say, on the trial, that she had received any
communication from Isabel regarding her condition. She declared it
to be impossible that she should declare a falsehood even to save a
sister’s life; and condemnation accordingly took place. Helen then
made a journey on foot to London, in the hope of being able to plead
for her sister’s life; and, having almost by accident gained the ear and
interest of the Duke of Argyle, she succeeded in an object which most
persons would have said beforehand was next to unattainable.
Isabel afterwards married her lover, and lived at Whitehaven for
many years. Helen survived till 1791, a poor peasant woman, living
by the sale of eggs and other small articles, or doing country work,
but always distinguished by a quiet self-respect, which prevented any
one from ever talking to her of this singular adventure of her early
days. Many years after she had been laid in Irongray kirkyard, a lady
who had seen and felt an interest in her communicated her story to
Sir Walter Scott, who expanded it into a tale (The Heart of Mid-
Lothian) of which the chief charm lies in the character and actings of
the self-devoted heroine. It was one of the last, and not amongst the
least worthy, acts of the great fictionist to raise a monument over her
grave, with the following inscription:
‘This stone was erected by the Author of Waverley to the memory
of Helen Walker, who died in the year of God 1791. This humble
individual practised in real life the virtues with which fiction has
invested the imaginary character of Jeanie 1738.
Deans; refusing the slightest departure
from veracity, even to save the life of a sister, she nevertheless
shewed her hardiness and fortitude in rescuing her from the severity
of the law, at the expense of personal exertions which the time
rendered as difficult as the motive was laudable. Respect the grave of
poverty when combined with love of truth and dear affection.’

This month was commenced in 1739. Jan.

Edinburgh a monthly miscellany and
chronicle, which long continued to fill a useful place in the world
under the name of the Scots Magazine. It was framed on the model
of the Gentleman’s Magazine, which had commenced in London
eight years before, and the price of each number was the modest one
of sixpence. Being strictly a magazine or store, into which were
collected all the important newspaper matters of the past month, it
could not be considered as a literary effort of much pretension,
though its value to us as a picture of the times referred to is all the
greater. Living persons connected with periodical literature will hear
with a smile that this respectable miscellany was, about 1763 and
1764, conducted by a young man, a corrector of the press in the
printing-office which produced it, and whose entire salary for this
and other duties was sixteen shillings a week.[744]

A hurricane from the west-south-west, Jan. 14.

commencing at one in the morning, and
accompanied by lightning, swept across the south of Scotland, and
seems to have been beyond parallel for destructiveness in the same
district before or since. The blowing down of chimneys, the strewing
of the streets with tiles and slates, were among the lightest of its
performances. It tore sheet-lead from churches and houses, and
made it fly through the air like paper. In the country, houses were
thrown down, trees uprooted by hundreds, and corn-stacks
scattered. A vast number of houses took fire. At least one church,
that of Killearn, was prostrated. Both on the west and east coast,
many ships at sea and in harbour were damaged or destroyed. ‘At
Loch Leven, in Fife, great shoals of perches and pikes were driven a
great way into the fields; so that the country people got horse-loads
of them, and sold them at one penny per hundred.’ The number of
casualties to life and limb seems, after all, to have been small.[745]
James, second Earl of Rosebery, was one 1730.
who carried the vices and follies of his age
to such extravagance as to excite a charitable belief that he was
scarcely an accountable person. In his father’s lifetime, he had been
several times in the Old Tolbooth for small debts. In 1726, after he
had succeeded to the family title, he was again incarcerated there for
not answering the summons of the Court of Justiciary ‘for
deforcement, riot, and spulyie.’ A few years later, his estates are
found in the hands of trustees.
 At this date, he excited the merriment of the thoughtless, and the
sadness of all other persons, by advertising the elopement of a girl
named Polly Rich, who had been engaged for a year as his servant;
describing her as a London girl, or ‘what is called a Cockney,’ about
eighteen, ‘fine-shaped and blue-eyed,’ having all her linen marked
with his cornet and initials. Two guineas reward were offered to
whoever should restore her to her ‘right owner,’ either at John’s
Coffee-house, or ‘the Earl of Roseberry, at Denham’s Land, Bristow,
and no questions will be asked.’[746]

The potato—introduced from its native South American ground by

Raleigh into Ireland, and so extensively cultivated there in the time
of the civil wars, as to be a succour to the poor when all cereal crops
had been destroyed by the soldiery—transplanted thence to England,
but so little cultivated there towards the end of the seventeenth
century, as to be sold in 1694 at sixpence or eightpence a pound[747]—
is first heard of in Scotland in 1701, when the Duchess of Buccleuch’s
household-book mentions a peck of the esculent as brought from
Edinburgh, and costing 2s. 6d.[748] We hear of it in 1733, as used
occasionally at supper in the house of the Earl of Eglintoun, in
Ayrshire.[749] About this time, it was beginning to be cultivated in
gardens, but still with a hesitation about its moral character, for no
reader of Shakspeare requires to be told that some of the more
uncontrollable passions of human nature were supposed to be
favoured by its use.[750]
At the date here noted, a gentleman, 1739.
styled Robert Graham of Tamrawer, factor
on the forfeited estate of Kilsyth, ventured on the heretofore
unknown step of planting a field of potatoes. His experiment was
conducted on a half-acre of ground ‘on the croft of Neilstone, to the
north of the town of Kilsyth.’ It appears that the root was now, and
for a good while after, cultivated only on lazy beds. Many persons—
amongst whom was the Earl of Perth, who joined in the insurrection
of 1745—came from great distances to witness so extraordinary a
novelty, and inquire into the mode of culture.
The field-culture of the potato was introduced about 1746 into the
county of Edinburgh by a man named Henry Prentice, who had made
a little money as a travelling-merchant, and was now engaged in