Dental Library
RL
81
-A52
1953
no. I
1954
0
SYLLABUS
OF
DERMAL PATHOLOGY
INSTITUTE
ARMED
ORCES
founded
05
ARMY MEDICAL
Inflammatory Dermatoses
Course No. I
OF
1949
PACHOLOGY
UNIVERSITY OF MICHIGAN LIBRARIES
SYLLABUS
OF
DERMAL PATHOLOGY
Inflammatory Dermatoses
Syllabus of Dermal Pathology
American Academy of Dermatology and Syphilology
Course No. 1
Inflammatory
Dermatoses
Rewritten and Revised by
HAMILTON MONTGOMERY, M.D., M.S.
Chairman of the Committee on Pathology
American Academy of Dermatology and Syphilology
and
ELSON B. HELWIG, M.D.
Chief of Dermal Pathology
Armed Forces Institute of Pathology
Second Edition
1954
Armed Forces Institute of Pathology, Washington, D. C.
Copyright 1954 by the American Registry of Pathology
65-15857
5.1-57
PREFACE
This course on inflammatory dermatoses is one of four sponsored
by the American Academy of Dermatology and Syphilology which have
been planned to cover the subject of dermal pathology. The four courses
need not be taken in any particular order. The granulomas, miscellane-
ous dermatoses and nevi and neoplasms are covered in the other three
courses. The slides purposely are not labeled with the diagnosis, but
only with their numbers, so that the set may be used in the form of
a quiz.
These sets of 50 slides each and the related syllabuses have been
prepared through the kind offices of the Armed Forces Institute of
Pathology and the American Registry of Pathology. Brigadier General
Elbert DeCoursey, Director of the Armed Forces Institute of Pathology,
and Dr. Hugh Grady, Scientific Director of the American Registry of
Pathology, have given valuable assistance in their formation. The slides
have been prepared chiefly from material obtained from the sections of
dermatopathology of the Mayo Clinic and the Armed Forces Institute of
Pathology. Acknowledgment is made in the text where the material has
been provided by other contributors. Dr. Hamilton Montgomery, as
Chairman of this course on inflammatory dermatoses, has assumed re-
sponsibility for the text of this syllabus, including the description of
the slides.
Where the set of slides is to be used in the course at the annual
meeting of the American Academy of Dermatology and Syphilology, it
has been sent out approximately 4 weeks in advance so that the students
may study the slides before attending the course at the Academy.
These slides cannot be duplicated or replaced. Please handle
them carefully and do not use them in a projector, for the light causes
rapid fading of the stained sections. Be sure to bring the set of slides
and this syllabus with you to the meeting of the Academy.
i
Slide No.
1
6
7
8
9
10
10
11
12
13
14
15
16
17 and 18
19
2 3 4 4 5
∞ ∞ ∞ + 10 In ∞
20
21
2223
23 and 24
25
Page No.
26
27
28 and 29
30
31
32
33
34
35
36
37
2
2
3
4
5
5
8
9
10
10
11
11
12
13
14
14
15
16
19
20
20
21
222222
23
25
26
27
28
30
31
31
33333 13
34
35
INDEX
Diagnosis
Contact Dermatitis (Dermatitis Venenata)
Acute Burn (Steam)
Exfoliative Dermatitis (? Atopic Dermatitis)
Neurodermatitis
Neurodermatitis (? Prurigo Nodularis)
Urticaria Pigmentosa
Psoriasis (Early)
Psoriasis (Negro)
Psoriasis (Pustular)
Pityriasis Rubra Pilaris
Pityriasis Rosea
Parapsoriasis (En Plaque)
Tinea Versicolor
Pellagra
Lichen Planus (Early Papule)
Lichen Planus (Pigmented)
Lichen Planus Hypertrophicus
Lichen Nitidus
Chronic Discoid Lupus Erythematosus
Acute Disseminate Lupus Erythematosus
Dermatomyositis
Morphea
Acrosclerosis
Lichen Sclerosus Et Atrophicus
Acrodermatitis Chronica Atrophicans
Variola
Varicella
Herpes Zoster
Kaposi's Varicelliform Eruption
Pemphigus Vulgaris
Pemphigus Vegetans
Benign Pemphigus of Hailey and Hailey
Dermatitis Herpetiformis
Erythema Multiforme
Fixed Drug Eruption (Bismuth)
Arsenical Dermatitis (Exfoliative Dermatitis)
ii
Slide No.
38
39
8 == * * # # 44
85888 = = = ♡ ⇓⇓ 49
40
41
42
43
44
44
45
45
46
46
47
47
48
48
695995
49
Page No.
35
50
36
37
38
38
39
40
41
43
43
44
44
45
46
46
47
48
48
Diagnosis
Erysipelas and Cellulitis
Ecthyma Plus Furuncle
Ecthyma
Sycosis Vulgaris
Panniculitis
Hidradenitis Suppurativa
Pyoderma Faciale
Pyoderma Gangrenosum
Acne Conglobata
Acne Keloid (Dermatitis Papillaris Capillitii)
Rosacea (Acne Rosacea)
Rhinophyma
Chronic Radiodermatitis
Radio-Epidermitis
Nodular Vasculitis
Erythema Nodosum
Thrombophlebitis
Periarteritis Nodosa
iii
INTRODUCTION
Whereas classification of neoplasms can be made on a morphologic
basis, this becomes more difficult in regard to the group of inflammatory
dermatoses, as many of these dermatoses do not present specific histo-
logic pictures. They also show variations in their pathologic response
from acute to chronic types of reactions. Nor can an etiologic classifica-
tion be employed, as the cause of many dermatoses remains unknown.
Therefore, we have deviated somewhat from the grouping employed by
Weidman in a previous course on this same subject and also from the
grouping employed in the Atlas of Dermal Pathology. The slides in this
set have been arranged so that conditions with close pathologic similari-
ties are grouped together in order to attract attention to minute details
and variations which, at times, permit definite diagnosis to be made.
The slides are also grouped when possible on an etiologic basis. Thus,
dermatoses due to viruses (verrucae are taken up in course 4) are
grouped together, as are dermatoses of pyogenic origin. Certain condi-
tions included in the 100-slide set, such as urticaria and impetigo, could
not be included in this set for lack of suitable material. Special stains,
for the most part, have not been employed because of lack of perma-
nence. Inasmuch as this is labeled course 1, primary pathologic reac-
tions will be emphasized in the descriptions of the slides. Thus, certain
slides will be designated for the study of the phenomena of parakera-
tosis, acanthosis, different types of bullae, acute reactions, chronic reac-
tions and so forth. Some of the pathologic descriptions of the disease
processes are taken almost verbatim from the eighth edition of Ormsby
and Montgomery, Diseases of the Skin.
It is especially important in the group of inflammatory dermatoses
to select a site for biopsy of a typical well-developed lesion that has not
been subjected to trauma or irritation from previous treatment. If, on
the other hand, one is attempting to demonstrate a specific etiologic
organism, biopsy, as a rule, should be made from an early lesion. Some
of the inflammatory dermatoses, such as urticaria pigmentosa, lichen
nitidus, lichen sclerosus et atrophicus, acrodermatitis chronica atrophi-
cans and pemphigus vegetans, present pathologic changes that are
almost always diagnostic. Some dermatoses-psoriasis and lichen planus,
for instance-have histopathologic changes that are characteristic but
can, at times, be simulated by other dermatoses. Distinction between
some of the pyodermas, on the other hand, cannot be made on histo-
pathologic grounds alone. If, for example, three different conditions are
being considered clinically, it may be possible pathologically to rule out,
1
for example, condition 1 and say the evidence is in favor of condition 3
over condition 2. The site for biopsy should be chosen by an experienced
dermatologist and not by his younger assistant or student; otherwise, the
percentage value of dermatopathologic diagnosis decreases accordingly.
At times, more than one specimen for biopsy is necessary for diagnosis
together with correlation of the clinical and various laboratory findings
and sometimes repeated observations over a period of time. (Also see
Arch. Dermat. & Syph. 38:329, 1938, and Caro, M. C.: Arch. Dermat. &
Syph. 67:18, 1953.)
Accession 207664
Courtesy Dr. Roy L. Kile
CONTACT DERMATITIS (DERMATITIS VENENATA)
A man had an erythematosquamous eruption on the back for
several months and gave a history of recurrent attacks of dermatitis.
He was thought to have a contact dermatitis, possibly of occupational
origin, as he was a painter. Examination of the blood revealed leukocy-
tosis, but there was no evidence of lymphoblastoma.
Slide 1
The section is consistent with a contact dermatitis. It is an espe-
cially good one for the study of spongiosis. There is also spotted para-
keratosis and irregular acanthosis (compare with regular acanthosis in the
psoriasis slides). Spongiosis is clearly seen to be the result of the inter-
cellular edema. In the section in some of the sets, there may be a small
vesicle. An occasional leukocyte can be seen migrating through the epi-
dermis. There is edema of the cutis with dilatation of lymph vessels
and capillaries and lymph spaces. The infiltrate is very slight in amount,
is chiefly perivascular and is composed of lymphocytes and a few poly-
morphonuclear leukocytes. In contact dermatitis, the epidermal changes
predominate and the infiltrate in the cutis is usually less than in atopic
dermatitis. (Compare with slides No. 3 and 4.) The histologic changes
seen in “eczema," whether contact, atopic or neurodermatitis, are not in
themselves diagnostic.
Accession 211985
Slide 2
ACUTE BURN (STEAM)
A man, aged 54 years; received extensive third degree burns as
the result of a boiler explosion and died 9 hours later. The specimen
was taken from an unstated site at postmortem examination.
2
to
The section presents marked necrosis of the epidermis with sepa-
ration of the epidermis from the cutis. Note the eosinophilic staining
of all the tissues and the loss of cellular detail in the epidermis and in
part of the cutis. There is dilatation of the capillaries which are engorged
and filled with erythrocytes. Throughout the tissue extravasation of
erythrocytes and a few distorted polymorphonuclear leukocytes are seen.
Hemorrhage has occurred about sebaceous glands and also in regions
beneath the skin. If this had been an electrical burn, the nuclei in the
epidermal cells would be elongated, pyknotic and pointing in the direc-
tion of the current. This slide on burn is placed here rather than with
slide No. 47 on actinodermatitis because this is an acute burn from con-
tact and a severe sunburn would not appear a great deal different.
Notice that the edema throughout the cutis is similar to that seen in
contact dermatitis.
Accession 207665
EXFOLIATIVE DERMATITIS
(? ATOPIC DERMATITIS)
Slide 3
A woman, aged 54 years, was seen because of exfoliative derma-
titis of 6 months' duration. There was no familial history. Because of
the short onset, lymphoblastoma was suspected. However, it could not
be proved. There was no history of any allergic factors.
The section, taken from the back, reveals features consistent with
generalized neurodermatitis or atopic eczema. Characteristic features
are a uniform and regular acanthosis and papillomatosis with broaden-
ing of the base of the rete ridges. This regular type of acanthosis simu-
lates that seen in psoriasis, but in this section there is too much inter-
cellular edema and spongiosis to suggest psoriasis. A mild perivascular
infiltrate composed chiefly of lymphocytes is limited to the upper portion
of the cutis. The section is otherwise quite similar to slide No. 1, contact
dermatitis, or slide No. 4, localized neurodermatitis. It is important to
remember that even in exfoliative dermatitis the histologic picture usually
corresponds to the dermatosis which resulted in the exfoliative dermatitis,
whether psoriasis, lichen planus, lymphoblastoma, or some other con-
dition.
3
NEURODERMATITIS
The term "neurodermatitis" used to be limited to localized licheni-
fied plaques, also known as lichen simplex chronicus. However, many
of these cases merge into nummular eczemas and atopic dermatitis or
atopic eczema. The latter two have also been referred to as “generalized
neurodermatitis." Histopathologic distinction in this group is often diffi-
cult, if not impossible. The same applies to the histopathologic changes
in prurigo mitis or prurigo nodularis versus localized neurodermatitis.
Histopathologic as well as clinical combinations of contact and atopic or
generalized neurodermatitis frequently occur. In contact dermatitis, the
epidermal changes predominate, whereas in generalized neurodermatitis,
the epidermal changes at times may be minimal. The section on slide
No. 3 should be compared with the two sections mounted on slide No. 4,
dealing with neurodermatitis and prurigo, and also with slide No. 1.
Seborrheic dermatitis differs in that there usually is a crust simulating
infectious eczematoid dermatitis. Infectious eczematoid dermatitis may
simulate the picture of neurodermatitis of different types, but there
usually are collections of cocci on the surface. These latter two condi-
tions are not included in the present set.
Accession 207674
NEURODERMATITIS
A man, aged 53 years, had an extensive lichenification of the left
leg and left popliteal area of 5 years' duration. The lesions developed
after abrasion of the skin over the tibia, which healed but then became
pruritic. The patient had been drawing compensation because of the
dermatitis. Clinically, the case is best classified as a localized neuro-
dermatitis.
Slide 4
This section (lower one on the slide) is chosen because it depicts
very clearly the phenomena of intercellular edema with resultant spongi-
osis and spotted parakeratosis and hyperkeratosis. A mild degree of
acanthosis, dilatation of the capillaries and a perivascular infiltrate com-
posed of leukocytes and lymphocytes were present in the upper part of
the cutis. The marked degree of spongiosis rules out psoriasis even
though there is some papillomatosis. The histologic changes in various
types of neurodermatitis (eczema) are not diagnostic.
!
4
Accession 207681
NEURODERMATITIS
Accession 186702
(? PRURIGO NODULARIS)
A woman, aged 62 years, had localized areas of neurodermatitis
about the ankles and legs which had been present for 25 or 30 years.
The section (top one on the slide) shows a histologic picture con-
sistent with prurigo nodularis. Gans, Civatte and others have emphasized
that all transitions from urticaria to lichen urticatus to prurigo nodularis
may be seen and that the histologic picture of prurigo nodularis is indis-
tinguishable from that of localized neurodermatitis. The section reveals
hyperkeratosis, a localized region of parakeratosis, marked acanthosis
and papillomatosis with elongated papillary bodies. Intradermal vesicle
formation has taken place in several regions and there are small areas of
spongiosis. The superficial vessels are considerably dilated but an in-
flammatory reaction in the form of an infiltrate is minimal in amount.
Slide 4
Slide 5
URTICARIA PIGMENTOSA
A baby girl who had had melanotic lesions scattered over the
entire body since birth was seen at the age of 5 months. Some lesions
were raised 2 to 5 mm.; others were level with the contour of the skin.
A clinical diagnosis of urticaria pigmentosa was made.
This section is presented primarily to show mast cells. There are
various hypotheses regarding the origin of mast cells. Unna first be-
lieved that mast cells were migrating wandering cells but later decided
that they developed from connective tissue cells which had taken up
mast-cell granules. (See MacLeod and Muende, Practical Handbook of
the Pathology of the Skin, Ed. 2, New York, P. B. Hoeber, Inc., 1940,
pages 132 and 153, for discussion and excellent illustrations.) In tissue,
mast cells simulate connective-tissue cells or fixed histiocytes. MacLeod
and Muende described spindle-cell and cuboidal-cell types. The mast
cells assume irregular shapes and may show dendrite-like processes.
They are recognized by coarse basophilic granules in the cytoplasm
which stain purplish with polychrome stains, such as polychrome methy-
lene blue, Pappenheim and Giemsa; hence, the use of Giemsa stain for
this section.
That this section was taken from a nodular and congenital form of
urticaria pigmentosa is evident from the dense mass in the midcutis,
composed almost entirely of mast cells. Mast cells usually are distributed
5
more diffusely and less densely in the tissue and are not as numerous,
especially in cases of urticaria pigmentosa developing later in life. If
one studies the section, all various shapes and sizes of mast cells can be
seen. The stellate and dendritic forms are best defined at the periphery
about dilated blood vessels and near the epidermis, where there is less
distortion of the cells than occurs in the center of the mass. The mast-
cell granules may be found in the lymphatics and extra-cellularly in the
connective tissue. There usually is a clear zone between the mast cells
in the cutis and the epidermis, but in this section it seems as if granules
are even to be found in the epidermis. There is evidence of increased
melanin pigmentation in the basal layer of the epidermis, presumably in
melanocytes. The melanin appears as greenish granules, apparently
forming caps over the tops of the basal cells, but also is to be found in
melanophages in the cutis. With experience, it is possible to recognize
large, irregularly shaped histiocytes or connective-tissue cells as mast
cells with ordinary hematoxylin and eosin stain even though it does not
demonstrate the granules.
According to MacLeod and Muende, mast cells are present in
normal cutis and subcutaneous tissue, although, if more than one mast
cell per microscopic field is seen, a pathologic condition is indicated.
Mast cells occur in several inflammatory conditions. They are often
prominent in syphilitic lesions and, according to MacLeod and Muende,
in tuberculosis and erythema multiforme, where they may be increased
in the neighborhood of the blood vessels. Recent studies indicate that
the mast cells contain heparin and also mucin and mucopolysaccharides.
Heparin is water-soluble, hence, when urticaria pigmentosa is suspected
the tissue should be put in absolute alcohol or 2 per cent solution of sub-
acetate lead, rather than in formalin. Mast cells take a positive stain
with Hotchkiss-McManus or other mucopolysaccharide stains, and also
give a positive stain for mucin with mucicarmine.
PSORIASIS
The histopathologic picture of psoriasis is usually diagnostic if a
well-developed papule or plaque that has not been subjected to treat-
ment is selected for biopsy. There is lack of agreement among derma-
tologists as to whether the first changes in psoriasis occur in the epider-
mis or in the cutis. In a study with Burks (Arch. Dermat. & Syph.
diy
6
48:479 (Nov.) 1943), it seemed to us that the earliest changes consist
of slight parakeratosis-with or without formation of abscesses-acan-
thosis and early papillomatosis. The rete ridges push down into the
cutis and at the same time there is proliferation of the papillary bodies.
Migration of the leukocytes through the epidermis to form micro-ab-
scesses is seen in the earliest lesions and before regular acanthosis and
papillomatosis with clubbing of the tips of the rete ridges have become
evident. Micro-abscesses seen in psoriasis are filled with serum and de-
generating leukocytes in contrast to the lymphocytic and monocytic con-
tents of micro-abscesses seen in mycosis fungoides. It is not necessary,
however, to demonstrate micro-abscesses in order to make the diagnos's
of psoriasis. In old indolent plaques they may be relatively few and only
to be demonstrated if multiple sections are made. Psoriasis is charac-
terized by the combination of uniform parakeratosis, the diminution or
absence of the stratum granulosum, occasional regular mitotic figures
in basal and prickle-cell layers and uniform and regular papillomatosis
together with dilatation and tortuosity of the loops of the capillary
vessels. In chronic, indolent types, one may see alternate layers of para-
keratosis and hyperkeratosis, which are simply indicative of the qui-
escence of the process and then the flare-up of the disease respectively.
Frequently, there are only a few layers of parakeratotic cells above the
tip of a papillary body, which accounts for the ease with which so-called
bleeding points can be produced by gentle scraping of the skin. The
acanthosis results from actual thickening of the prickle-cell layer plus
intracellular edema and compression of the nuclei. There is little evi-
dence of spongiosis unless secondary eczematization has occurred, often
as the result of treatment. The infiltrate in the cutis is usually slight
and composed chiefly of lymphocytes and mononuclear cells, although in
the early and acute phases, polymorphonuclear leukocytes may predomi-
nate. Eosinophils are rarely found. In the early stages, the capillaries
show swelling and proliferation of the endothelium, but in the fully
developed papule or in the later stages, they appear tortuous, dilated and
often filled with erythrocytes, and the endothelial cells may be flattened
and compressed. The capillaries appear to be rigid and there is sugges-
tion of hyaline changes in the collagenous tissues of the walls of the
vessel. When psoriasis involutes, parakeratosis is replaced by moderate
hyperkeratosis. Acanthosis and papillomatosis are diminished and the
infiltrate and edema disappear. Pustular psoriasis occurring on the
palms and soles, whether or not accompanied by psoriatic lesions else-
where on the body, usually has macroscopic rather than microscopic
abscesses, which often occupy large portions of the prickle-cell layer but
7
may also extend to the stratum corneum. Parakeratosis is usually associ-
ated with the macro-abscesses, but neither it nor papillomatosis is as
prominent elsewhere in the section as in ordinary psoriasis. There is
likely to be some spongiosis.
The histopathologic changes seen in psoriasis may be closely
simulated by localized and generalized neurodermatitis, including atopic
dermatitis, and, at times, by seborrheic dermatitis and psoriasiform
syphiloderm. In neurodermatitis, parakeratosis may be just as prominent
as in psoriasis, and the papillary bodies may extend to within a few cell
layers of the surface so that bleeding points can be readily produced.
In neurodermatitis, however, tortuosity and apparent rigidity of the
capillary loops are not evident. There may be some edema and apparent
thickening of the smaller arterioles and venules, and normal mitoses in
the epidermis are few. There are, however, borderline cases, both clini-
cally and histopathologically, that require further observation before one
can arrive at the correct diagnosis. Seborrheic dermatitis usually ex-
hibits more spongiosis and cocci may be demonstrable in the epidermis.
Cocci are never demonstrable in psoriasis-a fact which serves to dis-
tinguish pustular psoriasis from acrodermatitis continue or dermatitis
repens and infectious eczematoid dermatitis, in all of which cocci are
found in the stratum corneum. Recalcitrant pustular eruption or so-
called pustular bacterids show a greater degree of spongiosis. The same
is true of dyshidrosis. Distinction of these two conditions from pustular
psoriasis, when the latter is limited to the palms and soles, as emphasized
by Andrews (Diseases of the Skin, Ed. 3, Philadelphia, W. B. Saunders
Company, 1946, p. 259), may be extremely difficult and often calls for
a period of observation. Finally, we recently saw a case of ichthyosi-
form erythroderma in which the histopathologic changes duplicated
those seen in a well-developed papule of psoriasis, including micro-
abscess formation, and differing only in that there was more serous
exudate in the stratum corneum. The similarities of the histopathologic
changes in ichthyosiform erythroderma to those seen in psoriasis have
been emphasized in the past by Gans and others.
Accession 205535
Slide 6
PSORIASIS (EARLY)
A man, aged 33 years, was seen because of latent syphilis, for
which he had been treated for some time. He had, in addition, large,
scaly plaques on both legs and papulosquamous lesions on the legs,
8
wrists and scalp. Some of the lesions were fissured and revealed a
purulent exudate. The condition had been present for eight months and
the diagnosis of psoriasis had first been made two years previously. He
had been using boric acid wet dressings and 50 per cent thymol iodide
powder. He was hospitalized; a diagnosis of psoriasis was made clin:-
cally and was confirmed by two separate but simultaneous biopsies.
This condition proved rather resistant to treatment. There seemed to be
an element of secondary infection. He returned after several months
with a recurrence of the psoriasis.
The section from the leg shows the histopathologic features of
psoriasis in an early stage plus secondary eczematization, perhaps the
result of overtreatment. It might be difficult to make a diagnosis simply
on the basis of this section because of the intercellular edema and spon-
giosis, such as one sees in contact dermatitis. There are definite para-
keratosis and migration of leukocytes through the epidermis, and in some
of the sections micro-abscess formation is beginning in the upper part
of the prickle-cell layer. Acanthosis is slight and as yet there is little
evidence of papillomatosis or prolongation of the rete ridges with club-
bing of the tips of the rete ridges, as in a well-developed psoriatic plaque.
These latter changes, however, are not seen in the early stages of psori-
asis. They were evident in the other specimen taken at the same time,
apparently from an older lesion.
Accession 205515
Slide 7
PSORIASIS (NEGRO)
The section was taken from the chest of a dark-skinned Negro, 30
years of age. He had had psoriasis with generalized distribution inter-
mittently for a number of years. The case has been described in the
Archives of Dermatology and Syphilology (19:524 (Mar.) 1929). It is
unusual to see psoriasis in a full-blooded Negro.
This section shows all the typical changes of a well-developed
plaque of psoriasis. It is worth studying independently for the uniform
parakeratosis and also for the multiple small micro-abscesses. The mul-
tiple layers of parakertosis and micro-abscesses make the picture in this
slide almost that of rupial psoriasis. All the other characteristic changes
of psoriasis are present. The increased pigment is explained by the fact
that the section is from the skin of a Negro. Usually, there is a decrease
in the amount of melanin pigment during the acute stage of the process.
In this section, the infiltrate in the cutis is minimal. The dilatation and
9
the apparent rigidity of the capillaries are not as prominent as in some
cases of psoriasis.
Accession 205528
PSORIASIS (PUSTULAR)
A man, aged 68, had a pustular eruption on the palms of both
hands in 1930, at which time a diagnosis of dyshidrotic eczema (dyshi-
drosis) was made. There was also some hyperhidrosis of the soles of
the feet. When seen nine years later, the lesions on the palms were more
suggestive of a recalcitrant pustular eruption or pustular psoriasis, and
the histopathologic changes were those of pustular psoriasis. Unfortu-
nately, the patient has since been lost sight of, and the response to
treatment is not known.
The section clearly shows all the features of pustular psoriasis.
There are no cocci. There is practically no spongiosis, and parakeratosis
is limited to the region of macro-abscess formation, as is common in
pustular psoriasis.
Accession 211029
Slide 8
Slide 9
PITYRIASIS RUBRA PILARIS
A man, aged 32, was seen because of an erythematosquamous
eruption which had developed on the palms and face six weeks pre-
viously and which had gradually spread to involve the skin of the entire
body. A clinical diagnosis of psoriasis was made, but after further ob-
servation, together with the histopathologic findings, the diagnosis was
changed to pityriasis rubra pilaris.
The section shows most of the features of pityriasis rubra pilaris:
hyperkeratosis in relation to plugging of the hair follicle and spotted
parakeratosis occurring chiefly above the tip of the papillary bodies but
also forming a collarette about the orifice of the hair follicle. The regu-
lar acanthosis and papillomatosis in this section are more like those seen
in psoriasis than the more irregular distribution in most cases of pityriasis
rubra pilaris. The intracellular edema of individual cells may, in part,
be an artefact. One usually sees a litttle more infiltrate in the upper part
of the cutis than is present in this section, and a slight liquefaction de-
generation of the basal-cell layer, especially in relation to the walls of
the hair follicles, which is not present in this section. The follicular
hyperkeratosis and plugging fit the concept that this disease is a vitamin
10
A deficiency disease, and the intracellular edema or shriveling of the
nucleus of the epidermal cells would also conform to this concept. It is
not unusual for pityriasis rubra pilaris to simulate the clinical appear-
ance of psoriasis, especially in generalized cases or cases in which the
skin is extensively involved.
PITYRIASIS ROSEA AND PARAPSORIASIS
Sections of these two conditions are mounted together because of
their similarity to one another and because neither condition is diag-
nestic histopathologically.
Accession 207686
Slide 10
PITYRIASIS ROSEA
A man, aged 34 years, was seen because of a primary syphiloderm
and was placed under antisyphilitic treatment. With the second course
of treatment, a papulosquamous eruption developed. This eruption was
thought by some dermatologists to be a secondary syphiloderm and by
others to be pityriasis rosea. The Wasserman reaction was a weak 2
plus. Biopsy performed after the second injection of arsphenamine in the
second course of treatment failed to reveal evidence of syphilis and
showed features consistent with pityriasis rosea.
This section (left side) is not entirely characteristic since the
basal cells in the epidermis are pyknotic and shriveled. There is some
shrinkage of the connective tissue, probably the result of fixation, for it
is not likely to be due to injection of arsphenamine. The lesion is charac-
terized by spotted parakeratosis, a very slight degree of acanthosis, and
localized regions of edema and spongiosis. In one or two regions in the
sections of most of the sets, there is a small micro-abscess in the upper
part of the prickle-cell layer. There is some dilatation of the superficial
vessels in the upper part of the cutis with a perivascular infiltrate com-
posed chiefly of polymorphonuclear leukocytes and lymphocytes. Note
the similarities of this section to that of parapsoriasis, which is on the
right side.
Accession 205527
PARAPSORIASIS (EN PLAQUE)
A man, 22 years of age, had a dull red spot of five weeks' duration
on the right thigh. Lesions involving the entire body soon developed.
11
Clinical diagnosis rested between early mycosis fungoides and para-
psoriasis. Biopsy from the right arm revealed histologic changes com-
patible with parapsoriasis en plaque.
The histopathologic changes in parapsoriasis are not distinctive
nor can a sharp distinction as to type of parapsoriasis always be made
on a histologic basis alone. This section (right side) is fairly representa-
tive of parapsoriasis en plaque and shows a spotted parakeratosis which
is not always present. There is some edema of the epidermis and again
regions of slight spongiosis and early micro-abscess formation in the
section in most of the sets. The small micro-abscess formation is more
usually seen in the guttate variety. Contrary to the statement of Mc-
Carthy (Arch. Dermat. & Syph. 45:81, 1942), one of us (H.M.) has seen
eczematoid changes in parapsoriasis en plaque. The section also shows
edematous changes in the superficial vessels and a very mild degree of
perivascular infiltrate composed chiefly of lymphocytes. Parapsoriasis en
plaque practically never develops into mycosis fungoides. Most lesions
in which this change has been reported have been early premycotic
lesions of mycosis fungoides simulating parapsoriatic lesions but reveal-
ing histologic evidence of early mycosis fungoides, including pyknosis,
karyorrhexis and clumping of cells to form pseudo-giant cells. None of
these latter phenomena are present in this section. (Also see Arch.
Dermat. & Syph. 46:673, 1942 [Lit.].)
Accession 207284
Slide 11
TINEA VERSICOLOR
A man, aged 40 years, was seen in March 1948, because of typical
tinea versicolor of the trunk of unknown duration.
The section shows slight hyperkeratosis and a little spotted para-
keratosis. There is no appreciable degree of acanthosis, however, as
compared with the preceding papulosquamous dermatoses. Practically
no infiltrate can be seen in the cutis, although there is some dilatation of
the superficial blood vessels in the upper part of the cutis. If the in-
tensity of the light is reduced a bit, Microsporon furfur is readily seen
in the stratum corneum, the fungi appearing as short filaments and
clusters of budding cells. It was possible to obtain such a preparation
only by omitting the usual scrubbing of the site before biopsy; otherwise,
the superficial, loosely laminated stratum corneum would have been
rubbed off. Biopsy is not a satisfactory method to use in the search for
fungi in superficial mycoses; it is much simpler and easier and a much
12
larger field can be covered by obtaining superficial scrapings with a
curet or by decapping a vesicle and studying the material for fungi in
potassium hydroxide preparations or cultures or both. Superficial fungi
are usually difficult to demonstrate histopathologically, although in
fungous diseases of the hair follicles they may be seen at the hair
shaft. These remarks do not apply to the deep-seated mycoses.
Accession 205529
Slide 12
PELLAGRA
A woman, aged 35 years, gave a history of gastric distress, sore
tongue and mental disorders of unknown duration. The clinical diag-
nosis was pellagra.
The section from the wrist shows a relative and absolute hyper-
keratosis and the section in some of the sets will reveal a spotted para-
keratosis. There are a moderate degree of acanthosis, some vacuoliza-
tion of both basal and prickle cells, a little pyknosis and karyorrhexis.
These changes are also to be seen in vitamin-A-deficiency states and other
vitamin-deficiency states. There is some dilatation of capillaries and
smaller vessels in the upper part of the cutis with a very slight perivascu-
lar infiltrate, chiefly lymphocytic in type. There seems to be some
atrophy of hair follicles and no sebaceous glands can be seen in the sec-
tion in most of the sets, although, as the specimen was taken from the
wrist, one would not expect to find sebaceous glands if it were near the
palm. Eddy and Dalldorf (The Avitaminoses, Ed. 3, Baltimore, The
Williams & Wilkins Company, 1944, 438 pp.) emphasized edematous
changes in the cutis and deterioration of the superficial collagenous
fibers, as well as liquefaction degeneration of the basal-cell layer and in-
crease of melanin pigment and, at times, inflammatory and degenerative
changes in the nerves. None of these latter changes are seen in this
section. In vitamin A deficiency, atrophy of sebaceous glands and hair
follicles is associated with atrophic changes in the epidermis. The histo-
pathologic picture of pellagra, therefore, is not diagnostic, nor is the
histopathologic picture diagnostic for any of the vitamin-deficiency states.
LICHEN PLANUS
The histopathologic changes in lichen planus are characteristic
and diagnostic, providing various other conditions which may produce
13
lichen-planus-like lesions can be ruled out. The fundamental changes
consist of relative and absolute hyperkeratosis, increase of the stratum
granulosum, acanthosis, liquefaction degeneration of the basal-cell layer
and an infiltrate limited rather sharply to the upper part of the cutis.
The reason for this limitation is that the lesion is perivascular and in-
volves the superficial horizontal network of blood vessels. Not in all
cases of lichen planus, however, is the infiltrate sharply limited to the
upper part of the cutis. This is true especially of the hypertrophic forms
of lichen planus and all conditions which may be imitating lichen planus.
At first, the infiltrate is composed of polymorphonuclear leukocytes, later,
of lymphocytes and various types of histiocytes, as well as plasma cells
and occasional mast cells. In older lesions and involuting lesions, many
melanophages laden with melanin pigment may be found in the cutis.
This is also true of the atrophic stage of lichen planus, in which stage
the epidermis becomes markedly thinned. Parakeratosis is practically
never seen, even in the bullous forms of lichen planus, unless the lesion
has undergone vigorous treatment. Elastic tissue in lichen planus is not
destroyed but simply pushed aside by the infiltrate.
Changes in the blood vessels in lichen planus are minimal as con-
trasted to lichenoid syphiloderm. Lichen-planus-like eruptions occur
after administration of drugs, such as arsenicals, atabrine (New Guinea
lichen planus) and bismuth (see slide No. 36). Hypertrophic forms of
lichen planus are to be distinguished from lichen pilaris seu spinulosus.
We have seen lichenoid lesions in chronic disseminate lupus erythema-
tosus which histologically also duplicated the picture seen in lichen
planus. Lichenoid eruptions also occur in various types of lymphoblas-
toma but, histologically, the character of the infiltrate serves to dis-
tinguish them from lichen planus.
Accession 205517
!
Slide 13
LICHEN PLANUS (EARLY PAPULE)
The section was taken from the thigh of a white woman, aged 59
years, who had generalized lichen planus including involvement of
palms and soles.
The section shows all the features described for lichen planus.
The section in some of the sets is cut a little on the bias so that it gives
the appearance of the infiltrate not being sharply limited to the upper
part of the cutis. There is marked increase of the granular layer. The
liquefaction degeneration of the basal-cell layer is not as prominent, as
will be seen in the subsequent sections.
14
Accession 205516
LICHEN PLANUS (PIGMENTED)
The section was taken from the back of a Negro woman, aged 29
years, who had a generalized eruption of 1 month's duration. The scalp,
face, palms and soles were not involved. Lesions varied from pinhead-
sized papules to infiltrated, coin-sized and larger plaques. Pruritus was
severe. Clinically, there was an extreme degree of pigmentation, the
lesions appearing as though coated with stove polish.
This section is more representative of lichen planus than the pre-
vious one, since it shows all the characteristic features of lichen planus
that have been enumerated. The liquefaction degeneration presumably
is the result of lymphedema and is an outstanding feature not only in
lichen planus, but also in lupus erythematosus and, to a lesser extent, in
pityriasis rubra and several other conditions, including mycosis fungoides.
This slide is excellent for the study of liquefaction degeneration as well
as for the study of pigment. Melanin pigment is found in the basal cell
layer and in dendritic cells (melanocytes) in the epidermis, and melano-
phages in the cutis are laden with pigment. Of course, this section is
from a Negro woman; yet I have seen as marked deposits of pigment in
lesions of lichen planus in the white race.
Accession 205530
Slide 14
Slide 15
LICHEN PLANUS HYPERTROPHICUS
A woman, aged 50 years, had verrucous lesions of some months'
duration on the legs. The lesions were suggestive of bromoderma and
tuberculosis verrucosa cutis.
The section shows marked keratotic plugging in relation to sweat
ducts and hair follicles and keratotic plugging independent of either.
There is marked acanthosis as well as liquefaction degeneration of the
basal-cell layer, limited largely to the epidermis at the base of the kera-
totic plugs. This type of involvement at the base of the hair follicles is
seen particularly in lichen pilaris seu spinulosus and lichen-planus-like
eruptions due to drugs, especially atabrine dermatitis. (Also compare
this section with fixed drug eruption from bismuth, slide No. 36.) There
is more than the usual amount of dilatation of the capillaries and
lymphatics. Homogenization and fibrosis of the connective tissue are
present. These are not part of the ordinary picture of lichen planus.
15
Accession 205518
LICHEN NITIDUS
A specimen for biopsy was taken from the scapular region of a
white woman, aged 22 years. For 9 months, the patient had had large
areas of papules in the axillae and smaller ones scattered on the chest,
side of arms, upper part of legs and underneath the breast.
This slide is a typical one for lichen nitidus. It shows discrete
papules compressing the epidermis. Each papule is sharply limited to a
papillary body in which it has produced widening. This in itself is a
diagnostic feature. The infiltrate comprising the papule consists of
lymphocytes, epithelioid cells and giant cells. There is no regular ar-
rangement of pattern, however, such as one sees in a true tuberculous
process. The only cutaneous type of tuberculosis that resembles lichen
nitidus is lichen scrofulosus and here the tubercles are centered, as a
rule, around hair follicles and are not limited to a papillary body. Ellis
and Hill (Arch. Dermat. & Syph. 38:569 [Oct.] 1938) mentioned cases
of coexistent lichen nitidus and lichen planus, but we have not had the
opportunity of seeing such a case and, as a rule, the two conditions are
independent of one another. There is no good evidence to substantiate
the older concept that lichen nitidus is of tuberculous origin.
Slide 16
:
LUPUS ERYTHEMATOSUS
The histopathologic changes in lupus erythematosus are diagnostic
in more than 90 per cent of the cases if a specimen is obtained from a
lesion of at least several weeks' duration, which has not been subjected
to irritating or stimulating preparations or to roentgen therapy. In my
experience, this is true not only for the chronic discoid type but also for
the acute disseminate (systemic) type. I have been able to see all
transitions from chronic discoid types to acute disseminate types and
vice versa. Whereas the earliest pathologic changes in lupus erythema-
tosus consist of dilatation of superficial vessels and lymphatics together
with extravasation of leukocytes and later of lymphocytes and monocytes,
especially in the upper part of the cutis, it is the combination of the epi-
dermal changes and the changes in the cutis that permits a definite diag-
nosis. Characteristic pathologic changes in the epidermis consist of rela-
tive and absolute hyperkeratosis, keratotic plugging of hair follicles and
16
sweat ducts and keratotic plugging independent of either, preservation
and often thickening of the granular layer, acanthosis with adjacent
regions of atrophy of the epidermis and liquefaction degeneration of the
basal-cell layer. In the cutis, there are perivascular, chiefly lymphocytic,
infiltrates about the dermal appendages, dilatation of the superficial
capillaries and lymphatics, edematous changes in the connective tissue
and destruction of elastic tissue where the infiltrate occurs. There may
be a varying number of melanophages laden with melanin. Only a
very few cases of chronic discoid, generalized disseminate or subacute
and acute disseminate lupus erythematosus show hyaline or other col-
lagenous change or obliterative changes in the walls of the vessels, in
contrast to the rather frequent so-called wire-loop changes to be found in
the kidneys and fibrinoid changes in the heart and other organs in cases
of disseminate lupus erythematosus. At first glance, there would appear
to be no histopathologic similarity between chronic discoid lupus ery-
thematosus and acute disseminate lupus erythematosus. In the subacute
and acute disseminate type, dilatation of the superficial capillaries and
lymph vessels and edema of the cutis, together with marked atrophy of
the epidermis and liquefaction degeneration of the basal-cell layer, be-
come more prominent and the infiltrate is usually less marked. All the
factors are present in both chronic and disseminate forms but in differ-
ent proportions. Lupus erythematosus, therefore, is a disease illustrative
of a situation in which attention to minutiae permits definite diagnosis
to be made.
-
In lupus erythematosus of any type, elastic fibers in the beginning
are frayed and splintered and later are destroyed where the infiltrate
occurs. Atrophic changes occur in the sebaceous glands and hair folli-
cles. Liquefaction degeneration of the basal-cell layer resulting from
edema and lymphostasis may result in intra-epidermal formation of
bullae. Even in the bullous types, the stratum corneum tends to remain
intact without evidence of parakeratosis. There is definite increase of
reticulum fibers, suggesting involvement of the reticuloendothelial sys-
tem. In the stage of involution, there is atrophy with residual pigmen-
tation of the epidermis.
Several authors in the past have emphasized that basophilic
degeneration of the elastic tissue is important in the diagnosis of lupus
erythematosus. It is true that merging of collagen and elastic fibers to
form collacin is seen in the majority of cases of chronic discoid lupus
erythematosus and occasionally in disseminate forms when a specimen
for biopsy is taken from the face or portions of the body exposed to light.
This merging of collagen and elastic tissue to form homogeneous, bluish-
17
staining masses of collacin is not, however, diagnostic of lupus erythema-
tosus but is seen to just as prominent a degree in senile skin and actino-
dermatitis. Collacin is not present in specimens from regions not ex-
posed to the light. Because of the inflammatory changes about the hair
follicle, a foreign-body giant-cell reaction is sometimes set up, but defi-
nite tubercles or any tuberculous structure is of rare occurrence and
undoubtedly simply represents a coincidental finding.
We are opposed to the apparently growing concept initiated by
the Mount Sinai group of physicians in New York that lupus erythema-
tosus is primarily a collagenous disease and that it belongs with derma-
tomyositis, various forms of scleroderma and possibly with periarteritis
nodosa. Even Klemperer acknowledges that the conditions just men-
tioned should be kept distinct from one another until we know more
about their etiology. Lupus erythematosus alone in its systemic forms
possesses a so-called L. E. cell in blood plasma and bone marrow. The
lack of fibrinoid, hyaline and collagenous changes in the walls of the
vessels in the skin (with the exception of a few cases) would speak
against the concept that lupus erythematosus is primarily a collagenous
disease. The skin is one of the organs richest in connective tissue. Dila-
tation of the vessels and edema of the connective tissue are seen in a
great many other dermatoses. Hematoxylin-stained bodies, which
Klemperer would compare with the L. E. cell in blood plasma and
demonstrable in systemic lupus erythematosus and various organs in the
body, are seen only exceptionally in the skin. (For further discussion
of this subject, see Ormsby and Montgomery, Diseases of the Skin,
eighth edition, 1954; also McCreight and Montgomery: Cutaneous
Changes in Lupus Erythematosus: Histopathologic Aspects, With Special
Reference to Vascular Changes. Arch. Dermat. & Syph. 61:1, 1950;
Montgomery and McCreight: Disseminate Lupus Erythematosus. Arch.
Dermat. & Syph. 60:356, 1949; Klemperer: Pathology of Systemic Lupus
Erythematosus. In: McManus, J. F. A.: Progess in Fundamental Medi-
cine. Philadelphia, Lea & Febiger, 1952, p. 51, and L. E. Cell Queries
and Minor Notes, The Lupus Erythematosus Test. J.A.M.A. 151:1460,
1953 (Hargraves). The student should compare the three slides of lupus
erythematosus with dermatomyositis and with the slides on morphea and
acrosclerosis. Morphea and acrosclerosis can be regarded as collagenous
diseases and more specifically can slide No. 25, dealing with acroderma-
titis chronica atrophicans, in which there are destruction of collagen and
loss of almost the entire cutis, because of this.
18
Accession 206336
CHRONIC DISCOID LUPUS ERYTHEMATOSUS
Slide 17 and 18
A man, aged 35 years, was seen in 1919 with typical lesions of
discoid lupus erythematosus limited to the face. He had various types
of treatment over a period of years. When he was last seen in 1947,
the lupus erythematosus was well under control.
The upper section on slide No. 17, stained with hematoxylin and
eosin, reveals all the typical features of lupus erythematosus that have
been enumerated. In addition, there is dilatation of the sweat glands,
the result of plugging of the sweat ducts. Note the merging of the
collagen and elastic tissue to form purplish-staining homogenous masses
in the upper part of the cutis. Besides dilatation of the capillaries, there
is edema of the walls of some of the capillaries but no true proliferative
changes.
The upper section on slide No. 18, staine for elastic tissue, shows
more clearly the merging of collagen and elastic fibers, as well as dis-
tinct swollen basophilic elastic fibers. Elastic tissue is absent where the
infiltrate is at all dense.
+
Accession 206335
A woman, aged 31 years, was seen with a typical chronic lupus
erythematosus of the face.
The lower section on slide No. 17, stained with hematoxylin and
eosin, shows the typical changes enumerated for lupus erythematosus.
The epidermis is thinner than in the section just above it, but the epi-
dermis remains intact in spite of the overlying crust containing debris
and leukocytes. The infiltrate in the cutis is denser, there is one region
of ulceration, but even here there is no evidence of parakeratosis, even
in the two regions where the epidermis is thinned down to only two or
three layers of cells. There is considerable destruction of the dermal
appendages.
In the lower section on slide No. 18, stained for elastic tissue, note
that there is no evidence of senile skin or merging of collagen and elastic
fibers to form collacin; hence, this feature is not necessary for the diag-
nosis of lupus erythematosus. Otherwise, the changes in the elastic
tissue in the two cases are comparable to one another.
19
Accession 206334
Slide 19
ACUTE DISSEMINATE (SYSTEMIC) LUPUS ERYTHEMATOSUS
A man, aged 19 years, was seen because of a superficial type of
lupus erythematosus with evidence of dissemination. He gave a history
of a transitory eruption on the face 3 years prior to examination. He
received two courses of roentgen treatment to the gland-bearing areas
but all the systemic symptoms of disseminate lupus erythematosus de-
veloped and he died on January 15, 1925.
This section reveals features of both chronic discoid lupus ery-
thematosus and acute disseminate lupus erythematosus. There are a few
regions where the epidermis is thickened, but, for the most part, the epi-
dermis is thinned and atrophic and in some places consists of only two
layers of cells. Even here, however, there is no evidence of parakera-
tosis, except in the section in a few of the sets where there is a small
region of parakeratosis in relation to collection of leukocytes on the sur-
face and another region in relation to an area of acanthosis which is
certainly atypical. In many cases of acute disseminate lupus erythema-
tosus, the infiltrate is not as prominent as in this section, and the dilata-
tion of the capillaries and lymphatics and the edema throughout the
cutis are more prominent. There is no evidence of collagenous or fibri-
noid change in the walls of the dilated capillaries, lymphatics or the
deeper and larger vessels. We did not put in a Masson-stained section
because it shows nothing that cannot be seen in the section stained with
hematoxylin and eosin in this case. Compare this section with the two
sections on discoid lupus erythematosus and note absence of merging of
collagen and elastic tissue in this section as compared with one of the
cases of discoid lupus erythematosus.
Accession 207668
Slide 20
DERMATOMYOSITIS
A woman, aged 42 years, complained of a pruritic eruption on the
forearms and face of five months' duration. Physical examination re-
vealed marked weakness of the major muscles of the trunk. Diagnosis
was made of early dermatomyositis.
The section includes both skin and muscle. There is some edema
in the papillary bodies and throughout the cutis. A mild perivascular
infiltrate is seen deep in the cutis and also about the sweat glands. No
changes such as one sees in lupus erythematosus are to be found in the
20
epidermis. The section is a good one in which to study cutaneous nerve
bundles both in the cutis and deep in the subcutaneous tissue. The
muscle bundles show parenchymatous involvement in places being in-
vaded by a dense infiltrate of lymphocytes. Many of the muscle bundles
are pale staining and others have lost their cross striations. On careful
search, granular, vacuolar and hyaline degenerative changes can be found
in muscle bundles and homogenization in other bundles. It is these
multiple changes, together with absence of obliterative changes in the
interseptal vessels, that enable one to make the diagnosis of dermato-
myositis. In contrast, the muscle changes seen in scleroderma have a
more uniform pattern with homogenization and hyalinization, which,
however, are secondary to obliterative changes in the interseptal vessels.
It is unfortunate that confusion regarding the distinction between derma-
tomyositis, scleroderma and disseminate lupus erythematosus still exists
in the literature. (For further description of dermatomyositis, see
O'Leary, P. A. and Waisman, Morris: Arch. Dermat. & Syph. 41:1001,
1940.)
Accession 205525
Slides 21 and 22
MORPHEA
A woman, aged 54 years, was found to have a typical lesion of
morphea (circumscribed scleroderma) 4 to 8 cm. in diameter to the left
of the left nipple. This lesion had been present for about 8 months.
The section (larger one) is not diagnostic. It shows some flatten-
ing of the epidermis and loss of rete ridges, which latter, however, are
not prominent in this region. There is increase in density and thickness
of the cutis, and in some areas marked homogenization of the collagen
fibers. There is a perivascular infiltrate about both superficial and
deeper vessels together with obliterative changes in many of the vessels.
It is this infiltrate, which occurs especially at the periphery of the lesion,
that gives the lilac color to the border of the patch of morphea. If this
section were stained with elastic-tissue stain, fragmentation of the fibers
and possibly some attempt at new formation of the elastic fibers would
be seen. Morphea does not differ from scleroderma or acrosclerosis ex-
cept that there is more inflammatory reaction in the cutis. All forms of
scleroderma can be accepted as belonging with true collagenous diseases.
They have nothing in common with the cutaneous histopathologic picture
of lupus erythematosus.
21
Accession 207667
ACROSCLEROSIS
A man, aged 44 years, was seen because of progressive weakness
and recent inability to walk more than a few steps. He had first noticed
redness and later stiffness of the extensor surfaces of the forearms 2 years
previously. Subsequently, tightness of the fingertips developed. Exami-
nation revealed ironing out of the lines of expression of the face, although
there was little evidence of sclerosis. Clinical diagnosis was acrosclerosis
(O'Leary, P. A. and Waisman, Morris: Arch. Dermat. & Syph. 47:382,
1943).
The smaller section on slide No. 21 differs from the larger section,
dealing with morphea, in that there is practically no inflammatory re-
action. Again, there is flattening of the rete ridges and sclerosis of the
connective tissue and also atrophy of the dermal appendages except the
sweat glands. There is some thickening of the blood vessels, but this is
not as prominent as one usually finds. This section is a good one in
which to study cutaneous nerve bundles.
The section on slide No. 22 is from the same block on acrosclerosis.
The section reveals fragmentation of the elastic fibers and also depicts
more clearly the thickening of the blood vessels in the deeper portions
of the cutis and subcutaneous tissue. Gans has expressed the belief that
there may be new formation of the elastic fibers in scleroderma of various
types. In this section, however, the elastic fibers seem to be absent in
some regions and apparently there is no true regeneration of fibers.
Accession 207666
Slides 23 and 24
LICHEN SCLEROSUS ET ATROPHICUS
A woman, aged 64 years, was seen because of itching, burning
and soreness in the region of the vulva which had begun 30 years earlier
and, at times, had been associated with small vesicles. She had received
considerable roentgen therapy. Clinical diagnosis was made of lichen
sclerosus et atrophicus. The lesions were limited to the vulva and the
perianal region.
The section from the vulva shows most of the features that are
characteristic and diagnostic of lichen sclerosus et atrophicus. There is
marked hyperkeratosis with keratotic plugging of the orifices of the der-
mal appendages and keratotic plugging independent of them. Acan-
thosis is limited, for the most part, to regions involved in the keratotic
plugging. Elsewhere the epidermis is thinned and the rete ridges are
22
obliterated by pressure atrophy from edema in the cutis. There is one
small region where ulceration of the epidermis has occurred, but this is
probably the result of a so-called scratch papule. There is marked edema
in the upper part of the cutis with dilatation of lymphatics, capillaries and
lymph spaces and rarefaction and homogenization of connective tissue.
Beneath this there is a mild perivascular infiltrate, chiefly lymphocytic in
character. Note that there are no obliterative changes in the blood ves-
sels, a fact which serves to distinguish lichen sclerosus from kraurosis
and balanitis xerotica obliterans.
In the section on slide No. 24, taken from the same block and
stained for elastic tissue, the elastic fibers have been separated from the
epidermis by the region of edema. The elastic fibers, however, are still
preserved, and in the section in some of the sets, one can still see their
arrangement outlining the pattern of the papillary body.
It is apparent that lichen sclerosus et atrophicus is a condition en-
tirely different from lichen planus (Montgomery, Hamilton, and Hill,
W. R.: Arch. Dermat. & Syph. 42:755, 1940). There is a little mcre
acanthosis in the section than one usually sees in lichen sclerosus et
atrophicus, but then it is known that leukoplakia may occur simultane-
ously with lichen sclerosus on the vulva and also with pruritus vulvae
with lichenification. This woman had much more intense pruritus than
usually occurs in lichen sclerosus et atrophicus. Hence, there are two
alternative explanations for the increased acanthosis in this section. In
kraurosis, one does not see the marked keratotic plugging that is shown
here and there is thickening of the walls of the blood vessels in kraurosis.
Accession 205531
Slide 25
ACRODERMATITIS CHRONICA ATROPHICANS
A man, aged 57 years, had involvement of the skin, first of the left
hand, then of the forearms and later of the legs, which had begun 17
years previously. The clinical diagnosis was acrodermatitis chronica
atrophicans.
Biopsy of a lesion from the left elbow reveals all the typical fea-
tures of well-developed acrodermatitis chronica atrophicans. These histo-
pathologic changes, the combination of which is diagnostic, consist of
relative and absolute hyperkeratosis, keratotic plugging, preservation of
the granular layer, flattening and also marked atrophy of the prickle-cell
layer, and loss of rete ridges and papillary bodies with resultant flattening
of the epidermis into a thin, wavy line. There is a narrow border or
23
“grenz” zone of relatively normal connective tissue between the epidermis
and the infiltrate in the cutis. In most places in this section this narrow
zone is very thin. In other cases, the border zone is much wider and
more distinct. The infiltrate appears as a narrow or wide band beneath
the border zone. There is destruction of the connective and elastic tissue
in this region with atrophy of the dermal appendages except the sweat
glands. The section in this set also shows edema in the lower part of
the cutis. It is this combination of hyperkeratosis, flattening of the epi-
dermis, border zone between the epidermis and infiltrate in the cutis and
atrophy of the cutis and subcutaneous tissue that creates the diagnostic
picture. Usually, one cannot see both epidermis and sweat glands in the
same field under the microscope with low power objective, but this is
almost always possible in cases of acrodermatitis chronica atrophicans
because of the atrophy of the cutis. Lack of agreement in the literature
regarding the significant histopathologic changes, one of us (H.M.) be-
lieves, results because in the early acute phase there is often an inflam-
matory and edematous stage in which there is an inflammatory reaction
of the cutis but without alteration of the epidermis, and in this stage the
rete ridges are still preserved. Why edema may persist histologically for
many years after the onset of the disease and why a dense infiltrate may
persist remain to be explained. Early in the course of the disease, the
connective tissue is destroyed, as are the sebaceous glands and hair folli-
cles. Destructive changes in the elastic tissue, contrary to some authors,
do not occur until later. Changes in the blood vessels are usually mini-
mal, although at times there is considerable thickening. (For fuller
description of the histopathologic changes in this condition and in regard
to the changes in the ulnar bands and subcutaneous nodules, see Arch.
Dermat. & Syph. 51:32, 1945.)
One of us (H.M.) believes that acrodermatitis chronica atrophi-
cans can be regarded as a true collagenous disease in which collagenous
tissue is destroyed by the infiltrate in the cutis. The exact mechanism of
this destruction of collagenous tissue requires further explanation. There
is some hyaline and fibrinoid change in the connective tissue before it
disappears, but usually the disappearance is abrupt. Note that in acro-
dermatitis chronica atrophicans there very rarely is liquefaction degen-
eration of the basal-cell layer, which is a diagnostic feature of lupus ery-
thematosus, and that in lupus erythematosus one never sees marked
atrophy and disappearance of the cutis and much of the subcutaneous
tissue such as that which allows the blood vessels to appear like vari-
cosities in acrodermatitis chronica atrophicans. Please compare this
24
slide also with slides on morphea and acrosclerosis in which there is
hypertrophy rather than atrophy of collagenous tissue.
Accession 214441
Slide 26
VARIOLA
A man, aged 20 years, was admitted to a hospital because of gen-
eral malaise and weakness of 2 years' duration. Clinical diagnosis was
made of smallpox with hemorrhagic and pemphigoid tendencies. Two
days later, extensive hemorrhages developed in the conjunctiva of both
eyes and, 3 days after this, hemorrhagic vesicles in the skin became um-
bilicated. The patient's condition became progressively worse and he
died 7 days after admission.
The section in some of the sets may be from a different but a
similar case. The vesicle or bulla in variola is the result of intracellular
edema. Reticular degeneration or colliquative vesiculation the result of
intracellular edema or ballooning degeneration, occurs with formation of
large reticulated spaces or vesicles. Ballooning degeneration is seen best
in the lower portions and center of the vesicle. According to Unna, cavity
formation begins in the upper portion of the prickle-cell layer, even in
the papular stage, by reticulating colliquation of the edematous epithelial
cells. The process gradually advances so that compressed layers of cells
form trabeculae and septa lie between and above the small cavities. Even
the prickle-cell layer of the hair follicle may be involved in ballooning
colliquation. Balloon cells are smaller than those seen in varicella, being
only two to three times the size of a normal cell. They contain two to
four nuclei. Swelling of nucleoli also takes place and they become acido-
philic and remain in the nucleus or emerge to the cell plasma. These
are referred to as Guarnieri bodies. Epithelial giant cells, common in
varicella, are rarely seen in variola. The process extends more slowly in
the lower portion of the vesicle about the hair follicle where balloon cells
are more frequent. Marked degenerative changes later occur in these
cells, and there may be flattened cellular cords and fibrinoid changes.
Umbilication is explained by the more active reticulating colliquation
going on at the periphery, whereas the slower ballooning degeneration
continues at the center. Thus, the margin enlarges more rapidly than
the center, producing a depression. It has also been explained on the
basis that the lesion centers around the hair follicle or sweat pore which
holds the center of the vesicle down, but umbilicated lesions occur where
there is no hair. There is an infiltrate in the cutis first composed of leu-
25
kocytes, later of lymphocytes and plasma cells. There may be secondary
infection with cocci of various types, and this is seen in the section in
some of the sets. The section in most of the sets will show practically
all the changes that have just been described. For further description,
see Michelson and Ikeda: Microscopic Changes in Variola. Arch. Der-
mat. & Syph. 15:139, 1927.
Accession 190467
Slide 27
VARICELLA
A colored man, aged 24 years, had an eruption of 3 days' duration
consisting of papules, vesicles and pustules and ulcers scattered over the
body. The clinical diagnosis was varicella.
The section shows marked increase of melanin pigment to be
seen in the basal layer of the epidernis and in melanophages in the cutis,
as well as throughout the vesicle. The section shows a vesicle extending
down into the upper part of the cutis. The vesicle is filled with serum
and fibrin, erythrocytes and degenerating forms of leukocytes and lym-
phocytes. There is hyalinization of many of the nuclei. Gans empha-
sized that small changes of acid or alkaline reaction result in difference in
staining of inclusion bodies which are present in this section. He ques-
toned whether these inclusion bodies represent virus or degeneration
products of the nuclei. The section also shows intracellular edema which
results in so-called balloon cells or ballooning degeneration. These cells
fuse to form vesicles resulting in so-called reticular degeneration and
colliquative vesiculation. This is a modified form of acantholysis, com-
parable but not identical to true acantholysis seen in various types of
pemphigus. The type of vesiculation seen in varicella, variola, varicell:-
form eruption and herpes zoster, which is intracellular in character,
should be distinguished from the intercellular vesicles seen in eczema and
the so-called pressure bullae seen in dermatitis herpetiformis and ery-
thema multiforme, in which the cells are simply pressed aside by edema
and extravasation of the fluid into the epidermis.
To a great extent, variola and varicella, as well as herpes zoster
and other viral diseases, present the same type of vesicle or bulla as that
seen in true forms of pemphigus, including the phenomenon of acantho-
lysis. Ballooning degeneration is essentially a variant of what is now
referred to as "acantholysis." (See pemphigus.)
26
Accession 205534
HERPES ZOSTER
The patient was a man, aged 26 years, who had had Hodgkin's
disease for some years. A herpetic eruption without pain developed in
the right inguinal area and lower part of the abdomen and a similar
eruption developed on the face and extremities. The lesions had been
present for two weeks. Clinical diagnosis of generalized herpes zoster
was made.
Slide 28
This section reveals features of herpes zoster, and there is no
evidence of Hodgkin's disease. There is a large bulla, the result of intra-
cellular edema, with all types of cells in various stages of necrosis within
it; also collections of serum and fibrin. The section shows marked intra-
cellular edema of the epidermal cells, so-called ballooning degeneration.
This phenomenon is also seen in the sections on variola, varicella and
Kaposi's varicelliform eruption. The roof of the vesicle in herpes zoster
is usually the stratum corneum or the granular layer and the floor is the
degenerated cells of the basal-cell layer or even the papillary layer of
the cutis. Vesicles may be intercellular and unilocular or intracellular
and multilocular, the result of Unna's “reticular colliquation." Note that
the various degenerative cells in the vesicle are all eosinophilic staining
and stain poorly. In the section in some of the sets, eosinophilic bodies
known as the “zoster bodies of Lipschütz” may be found within balloon
cells. The cutis shows edematous changes and also perivascular infil-
trate of polymorphonuclear leukocytes and lymphocytes. At times, a few
plasma cells are present. In severe cases, necrosis results in destruction
of the papillae and, therefore, in subsequent scar formation.
Accession 651152
Slide 29
HERPES ZOSTER
A man, aged 59, was seen in September, 1952, because of a residual
dermatitis from poison ivy, which had begun 10 days previously. Six
days later two small bullae developed on the left upper arm and another
appeared on the hip. Subsequently, a generalized vesicular bullous
eruption developed, which was diagnosed as generalized herpes zoster.
This cleared up in some two weeks. He then underwent left subtotal
hemilaminectomy of the third lumbar vertebra. There was a suspicion
of lymphoblastoma, possibly Hodgkin's disease. The patient died at
home in January, 1954. The postmortem examination revealed Hodgkin's
disease. The herpes zoster in this patient, therefore, may have been pre-
27
cipitated by the attack of poison ivy or it may have represented the early
dissemination of Hodgkin's disease.
The section shows an intra-epidermal bulla and the various types
of degenerating cells that are described in the previous section of herpes
zoster and also many cells that have undergone partial-to-complete acan-
tholysis, thus in many respects simulating the histologic picture of true
pemphigus.
Accession 205514
Courtesy Dr. Francis W. Lynch
KAPOSI'S VARICELLIFORM ERUPTION
Slide 30
A woman, aged 54 years, had a herpetic eruption for 3½ months,
which was diagnosed clinically as Kaposi's varicelliform eruption. The
case was reported by Lynch and associates (Arch. Dermat. & Syph. 51:
129, 1945; also see additional report on Kaposi's Varicelliform Eruption,
by Lynch, F. W. and Steves, R. J., Arch. Dermat. & Syph. 55:327, 1947).
A specimen for biopsy was taken from a lesion on the cheek near the
hairline. The lesion was of 2 days' duration.
Concurring with Lynch's description, the section shows a unilocu-
lar vesicle resulting from epithelial degeneration and separation of the
epidermis from the cutis. There is evidence of ballooning degeneration
and nuclear degeneration, but this is not as marked as in the sections on
variola and varicella. In the section in some of the sets, inclusion bodies
can be demonstrated. There is a dense infiltrate, especially at the base
of the vesicle, and the infiltrate extends deeply into the cutis. Some of
the edema and the infiltrate, which in places is composed chiefly of
lymphocytes rather than leukocytes, may, as Lynch has suggested, be
due to an underlying eczema rather than to acute herpetic eruption. At
the base of the vesicle, there is an unusual amount of distortion of the
cells of the infiltrate, which are no longer identified as either leukocytes
or lymphocytes but appear as shriveled, elongated, stringy cells. This
phenomenon often occurs when the infiltrate is very dense. Ebert dem-
onstrated nuclear inclusions in a case of Kaposi's varicelliform eruption;
thus, vaccinia is ruled out on histologic grounds. Nuclear inclusions are
seen in herpes simplex, herpes zoster and varicella.
PEMPHIGUS
True forms of pemphigus include pemphigus vulgaris, pemphigus
28
vegetans, pemphigus foliaceus and pemphigus erythematodes. They are
all characterized by the presence of intra-epidermal acantholytic bullae.
By "acantholysis" is meant a prickle cell that has lost its prickles and
intercellular bridges and has undergone degenerative or lytic changes;
in other words, a cell that is inactive and dying. The acantholytic cell
becomes enlarged and spherical, and its periphery is intensely basophilic,
forming a halo at its edge. The nucleus is also spherical and enlarged,
and the nucleoli are prominent. Such changes give rise to the so-called
Tzanck cell, which is diagnostic of pemphigus and can be demonstrated
in smears obtained from natural or artificial bullae in pemphigus. The
Tzanck cell is better demonstrated in fresh preparations than in tissue
fixed in formalin and embedded in paraffin, although many of the acan-
tholytic cells closely simulate Tzanck cells and, as a matter of fact, are
Tzanck cells. The acantholytic cell is essentially a cell that has under-
gone lysis, just as the balloon cell in virus diseases has undergone lysis.
Hence, one etiologic concept of pemphigus is that it is a viral disease.
The balloon cell in viral diseases, however, contains inclusion bodies.
Pemphigus vulgaris is characterized by an intra-epidermal acan-
tholytic bulla. The floor of the bulla usually is formed by the basal layer
and the roof by the upper layers of the stratum mucosum. The margins
of the bulla are usually angulated and the walls present serrated edges.
Horizontal clefts within the layer of prickle cells are often seen, and
similar changes are to be found in the hair follicle. Quite often the hair
itself is torn off.
The fundamental histologic changes in pemphigus vegetans are
essentially those of pemphigus vulgaris, but in addition there is extensive
proliferation of the epithelium, with the formation of intra-epidermal
abscesses similar to the abscesses seen in blastomycosis. The abscesses.
contain leukocytes and acantholytic cells in variable numbers. In the
majority of cases, there is a great increase in the number of eosinophils,
not only in the abscesses but also in the infiltrate beneath the abscesses.
The histologic changes in pemphigus foliaceus usually reveal that
the bullae begin in the upper layers of the prickle-cell layer and thus are
more superficial than in pemphigus vulgaris. Hyperkeratosis, parakera-
tosis, acanthosis and papillomatosis are present in varying degrees, de-
pending on the age of the lesion.
The histologic changes in pemphigus erythematodes are indis-
tinguishable from those in pemphigus foliaceus.
The study of bullae in pemphigus must be made from early lesions.
The bullae can be produced artificially by the application of cantharides
for 3 to 6 hours to the apparently normal skin of patients that have pem-
29
phigus. There is no standard available for the strength of cantharides,
the British National Formulary being the most reliable. The phenome-
non of acantholysis will then be revealed in specimens for biopsy taken
immediately or shortly after the 3 hours of cantharides application. It is
not possible, however, by this method to distinguish between the differ-
ent types of pemphigus. If cantharides is left on 24 or more hours, then
secondary pressure or tension bullae develop. It is becoming increas-
ingly evident that bullae presenting acantholysis are diagnostic of pem-
phigus, excluding the viral diseases. It is true that acantholytic cells may
be seen in other conditions, including neoplasms, but the histopathologic
picture is readily distinguished on the basis of concomitant findings.
Butcher's pemphigus (pemphigus acutus), pemphigus neonatorum and
pemphigus conjunctiva (essential shrinkage or shriveling of the con-
junctiva) do not show acantholysis, but exhibit the phenomenon of pres-
sure or tension bullae such as are seen in dermatitis herpetiformis and
erythema multiforme. Again, however, if biopsy is performed on an
older bulla in these latter conditions, degenerative changes may be present
which resemble acantholytic cells and, conversely, old bullae in true
forms of pemphigus may show secondary tension or pressure phenomena.
The bullae in benign pemphigus of Hailey and Hailey show partial acan-
tholysis with separation of the cells but retention of their prickles or
intercellular bridges. The presence of mitotic and amitotic cell divi-
s'on is evidence that these cells are still viaible, whereas the acantho-
lytic cell in true pemphigus is a dead cell. The subject of bullous derma-
toses, including the literature, is taken up in recent articles by Brennan
and Montgomery, by Brennan, and in an extensive review by Lever.
The concept of acantholysis has resulted from the work of many authors
especially in France, Belgium, England and North and South America.
Auspitz from Vienna first described acantholysis in 1881, but its d'ag-
nostic significance was not revived until 1936, by Darier and Civatte, and
later in 1943, by Civatte.
REFERENCES:
Brennan, J. G., and Montgomery, Hamilton, J. Invest. Dermat. 21:349-361,
1953. Brennan, J. G., A.M.A. Arch. Dermat. & Syph. 68:481-495, 1953. Lever, W.
F., Medicine, 32:1-123, 1953.
Accession 651153
Slide 31
PEMPHIGUS VULGARIS
A man, aged 44, was first seen in October, 1953, because of blister
eruption, which had begun 3 years previously. The bullae were con-
30
fined chiefly to the trunk, although there were some on the arms, face
and mucous membranes of the mouth. It was first thought that he had
pemphigus erythematodes but the diagnosis was later changed to pem-
phigus vulgaris. The section reveals an intra-epidermal bulla with char-
acteristic acantholysis.
Accession 651154
Accession 651155
PEMPHIGUS VEGETANS
(The sets will contain one of these cases)
A man, aged 42, a service-station operator, was seen in January,
1954, because of an eruption that had been present for about 6 months.
He had first noticed pruritis and blisters of both axillae. These had been
treated as contact dermatitis. Later he received cortisone. A month
before he was seen, lesions developed in the eye periorbitally, and later
lesions appeared on the chest and back. The mucous membranes of the
mouth had not been involved. The lesions in the axillae were not of the
nature of the pemphigus vegetans, but those elsewhere were those of
pemphigus vulgaris. Without a history, the lesion seen in this slide
would be indistinguishable from the natural blister of pemphigus vul-
garis. Biopsy of the lesions from the axillae failed to reveal the histo-
logic picture of pemphigus vegetans, but rather presented a typical pic-
ture of pemphigus vulgaris with an intra-epidermal bulla containing
many acantholytic cells. Biopsy of a 3-hour cantharides blister from the
skin of the thigh also revealed a similar histologic picture.
A man, aged 70, was seen in October, 1950, because of a general-
ized bullous eruption of 3 months' duration. The clinical diagnosis favored
pemphigus vulgaris. There was a 50 per cent improvement during the
26 days of hospitalization. The histopathologic picture, however, is more
that of pemphigus vegetans with acanthosis and pronounced eosinophilia
in the bulla which, however, reveals acantholytic cells.
Accession 209339
Slide 32
BENIGN PEMPHIGUS OF HAILEY AND HAILEY
Slide 33
A woman, aged 47 years, had an eczematoid eruption on the sides
and toward the back of the neck clinically suggestive of benign pem-
31
phigus of Hailey and Hailey. The lesions had been present intermittently
for several years and continuously for the past 3 years.
Accession 206340
A man, aged 62 years, was seen because of an erythematous,
vesicular and bullous eruption about the neck. There was definite vesicu-
lation and crusting. The patient stated that the lesion had cleared up
after ultra violet therapy and that a brother had a similar condition.
Clinical diagnosis was that of benign pemphigus of Hailey and Hailey.
Some sets will have sections from the first case and others from
the second, but the pathologic description is essentially the same for both.
It is well to remember that this condition has various names, including
"familial benign chronic pemphigus," "recurrent herpetiform dermatitis.
repens" (Ayres and Anderson), "bullous Darier's disease" (Pels and
Goodman) and "dyskeratosis bullosa hereditaria" (Becker and Ober-
mayer). A familial history cannot be obtained in every case. The multi-
plicity of names results from divergent opinion regarding the histologic
changes, and there are several dermatologists who still believe that the
condition is a bullous form of Darier's disease. The relationship between
chronic benign familial pemphigus and vesicular Darier's disease, to-
gether with the literature, is set forth in papers presented by Finnerud
and Szymanski (Finnerud, C. W. and Szymanski, F. J., Arch. Dermat. &
Syph. 61:737-749, 1950) and Ellis (Ellis, F. A., Arch. Dermat. & Syph.
61:715-736, 1950) and discussions thereof. We are of the school that
believes familial benign pemphigus of Hailey and Hailey is distinct from
Darier's disease. In familial benign pemphigus there is partial acan-
tholysis, but the cells for the most part retain their prickles and inter-
cellular bridges, and as stated previously show evidence of viability as
manifested by mitotic and amitotic cell division. No Tzanck cells are
present. A few cells simulating the benign dyskeratotic cells of Darier's
disease in the form of grains may be encountered, but corps ronds are
rarely, if ever, seen. Keratotic plugging with corps ronds and grains
such as is seen in Darier's disease is absent; instead, there may be a crust
composed of serum and leukocytes. The formation of elongated rete
ridges, suggestive of pseudoepitheliomatous hyperplasia, is more promi-
nent in Darier's disease, including its bullous forms, than in benign
pemphigus. The sections in this set from the 2 cases present a typical
appearance of benign pemphigus of Hailey and Hailey, a judgment which
was substantiated in each case by the subsequent course of the disease.
32
Accession 206329
DERMATITIS HERPETIFORMIS
A man, aged 65 years, was seen because of generalized dermatitis
with residual pigmentation. A diagnosis of dermatitis herpetiformis had
been made elsewhere, in December, 1938. Clinical examination revealed
changes of dermatitis herpetiformis plus arsenical pigmentation and ar-
senical keratoses of the palms. The differential blood count showed 53
per cent eosinophils.
The section from the forearm reveals changes usually found in
dermatitis herpetiformis. There are pressure bullae resulting from edema
and in this section occurring chiefly in the prickle-cell layer. The vesicles
are filled with serum and eosinophils together with polymorphonuclear
leukocytes. There is edema in the cutis with dilatation of superficial
vessels and also an infiltrate predominantly eosinophilic in type. Often-
times vesicles and bullae in dermatitis herpetiformis occur at the epider-
mal-cutis junction and the bullae may be quite large. Both sections are
good for the study of tissue eosinophils, which are essentially mononuclear
cells, presumably histiocytes, and the multilobulated blood eosinophils
The section in the set reveals more acanthosis and papillomatosis than
one usually sees in dermatitis herpetiformis and, therefore, simulates
somewhat slide No. 32 on pemphigus vegetans. Possibly some of this
acanthosis resulted from a previous episode of exfoliative dermatitis plus
the stimulating effect of the arsenic medication. This is a good section
in which to study melanophages in the cutis which are laden with pig-
ment. Increased melanin pigment is seen as the residue or terminal
manifestation of dermatitis herpetiformis independent of any arsenic.
medication. Dermatitis herpetiformis does not always show eosinophilia
either in the tissue or in the blood, and whereas the histopathologic
changes may be suggestive, they usually are not diagnostic and may
closely simulate those seen in erythema multiforme. The bullae in der-
matitis herpetiformis are pressure or tension bullae and usually occur at
the epidermal or dermal junction, although at times they may be intra-
epidermal in origin.
Accession 206341
Slide 34
Slide 35
ERYTHEMA MULTIFORME
A man, aged 61 years, was found to have Hodgkin's disease, the
diagnosis being confirmed by biopsy of an epitrochlear lymph node.
Starting a year and a half prior to examination, dermatitis developed after
33
he had taken liver extract.
At the time of examination, there was a
polymorphous eruption with large, multicolored, gyrate plaques on the
trunk which tended to be confluent. The clinical appearance suggested
phenolphthalein eruption or erythema multiforme. No history or evi-
dence of drug eruption could be obtained.
The section from the right arm reveals most of the changes that
one usually associates with erythema multiforme, and in this case on the
basis of the history one must label this as a toxic type of erythema multi-
forme rather than an idiopathic type or one secondary to medication.
The histopathologic changes of erythema muliforme are not diagnostic.
There is more edema in the cutis than is seen in urticaria, including
edema of the walls of the vessels. The section reveals an infiltrate in the
upper part of the cutis which is chiefly polymorphonuclear in character
but also contains some lymphocytes and many melanophages laden with
pigment. There is liquefaction degeneration of the basal-cell layer, some
atrophy of the prickle-cell layer and migration of leukocytes and erythro-
cytes through the epidermis to form serosanguineous crusts. Although
there are hyperkeratosis and suggestive keratotic plugging in two regions,
the presence of parakeratosis and abscess formation would rule out a dis-
seminate lupus erythematosus. The tendency toward eosinophilic stain-
ing of the epidermal cells together with eosinophilic and hyaline-like de-
generative changes in some of these cells is a feature frequently seen in
various types of erythema multiforme. These pink-staining, hyaline,
degenerating cells are not to be mistaken for tissue or blood eosinophils,
although this patient had 25 per cent of eosinophils in the blood. There
is no evidence to be found of any lymphoblastoma, including Hodgkin's
disease, but it must be remembered that most cutaneous lesions associated
with Hodgkin's disease are nonspecific and toxic in character. Bullous
forms of erythema multiforme may be indistinguishable from dermatitis
herpetiformis and, again, are characterized by tension or pressure bullae
occuring just beneath the epidermis.
Accession 205519
Slide 36
FIXED DRUG ERUPTION (BISMUTH)
The section was taken from a Negro woman, aged 45, who had a
generalized pigmented and eczematoid eruption of 6 weeks' duration
with a history of intramuscular administration of bismuth. The clinical
diagnosis was bismuth eruption, but in many respects the eruption re-
sembled lichen planus. In the first specimen for biopsy, lichen planus
34
was suggested because of liquefaction degeneration of the basal-cell
layer.
The section shows essentially the picture of lichen planus and
should be compared with the slides on lichen planus. There is marked
hyperkeratosis, increase of the granular layer, acanthosis, liquefaction
degeneration of the basal-cell layer and an infiltrate limited to the upper
part of the cutis. There are many melanocytes laden with pigment and
also melanophages in the cutis laden with melanin pigment. In the
section in some of the sets, there is keratotic plugging of a hair follicle
with liquefaction degeneration at the base of the hair follicle. This
marked degree of pigmentation can be seen equally well in a person of
the white race who has a drug eruption. This slide would be equally
good for atabrine dermatitis or lichenoid eruption after adminstration of
arsphenamine.
Accession 205521
ARSENICAL DERMATITIS (EXFOLIATIVE DERMATITIS)
The necropsy specimen was taken from a Negro woman, aged 35
years.
Exfoliative dermatitis had developed after injections of neo-
arsphenamine, and the woman had died after an unexplained high fever.
The section is suggestive but not diagnostic. The pyknosis and
karyorrhexis and palisade arrangement of the basal cells of the epidermis
are features seen especially in arsenic pigmentation. This section shows
this phenomenon in several regions in the epidermis, but the changes are
not as marked as in arsenic pigmentation. Otherwise, the section simply
shows a chronic nonspecific dermatitis. There are alternate regions of
hyperkeratosis and parakeratosis and some regions of micro-abscess for-
mation. There is a moderate degree of acanthosis. Pigment may be
found in melanocytes in the epidermis and in melanophages in the cutis.
There is an infiltrate in the upper part of the cutis composed of leuko-
cytes, lymphocytes, plasma cells and monocytes of different types.
Accession 211984
Slide 37
Slide 38
ERYSIPELAS AND CELLULITIS
The patient was a woman, aged 51 years, who had lymphatic leu-
kemia. Erysipelas developed in the inguinal region. The erysipelas was
of only a few days' duration at the time of death. The specimen was
taken at necropsy.
35
The section shows thinning and atrophy of the epidermis. The
rete ridges are flattened, as the result of acute edema in the upper part
of the cutis. There is a region of necrosis and a region where the epider-
mis is absent. There are marked dilatation and engorgement of the capil-
laries, which are filled with erythrocytes and lymphocytes rather than leu-
kocytes. The packing of the capillaries with lymphocytes might be ex-
plained on the basis that this condition was of several day's duration, but
closer inspection will show an occasional immature lymphocyte; there-
fore, the lymphocytosis in the capillaries here is explained on the basis of
the lymphatic leukemia. There is less migration of the polymorpho-
nuclear leukocytes into the cutis than one usually sees in erysipelas. Ir
several regions in the deeper part of the cutis there is definite abscess
formation composed of masses of polymorphonuclear leukocytes and
necrotic debris. A few cocci may be seen in this region, as well as
regions of fat-replacement atrophy in the subcutaneous tissue where
again a leukocytic infiltrate predominates. There are no immature
lymphocyes in these abscesses, so that one cannot attribute the erysipelas
to lymphatic leukemia.
Accession 206342
Slide 39
ECTHYMA PLUS FURUNCLE
A man, aged 39 years, was seen because of pruritis of 6 months'
duration. He thought that the lesions had started as chigger bites. He
had multiple, infiltrated, bluish nodules and pustules, chiefly on the ankles
and lower part of the arms. Clinical diagnosis was indeterminate-ques-
tion of insect bites. Hemocytologic studies were negative for any of the
lymphoblastomas.
The section is chosen because it shows ecthyma plus beginning
furuncle. There is superficial crusting and ulceration of the epidermis in
close relation to a hair follicle and in a region of acanthosis. This crust
contains bluish-staining masses which under higher magnification are
seen to be masses of cocci. There is an infiltrate of polymorphonuclear
leukocytes and other cells which extends down around the hair follicle
and involves the base of the follicle. There are also some eosinophils
scattered throughout the cutis. This process, therefore, is different from
acne, in which the infection begins within the hair follicle and sebaceous
gland and comedo. In impetigo, the vesicle and the crust usually occur
directly under the stratum corneum and the stratum granulosum usually
remains intact. Impetigo can change into an ecthyma, which simply rep-
36
resents a deeper process with destruction of the epidermis. Deep-seated
impetigo of Bockhart involves the ostium of the hair follicle and extends
down about the hair follicle, causing definite folliculitis. Sycosis vulgaris
means deeper and more extensive involvement of the follicle. According
to Unna, most furuncles begin within an impetiginous lesion due to inocu-
lation of the pilosebaceous follicle with cocci, usually Staphylococcus
aureus. Eventually, an abscess is produced about the follicle which
undergoes necrosis. The cocci may be carried along lymph vessels to
form abscesses around neighboring follicles. After the wall of the hair
follicle is ruptured, the hair may act as a foreign body and set up a
foreign-body giant-cell reaction. The deeper the inflammation is in the
cutis, the more difficult it is for pus to escape. Therefore, there may be
closure of the hair follicle and the pus breaks through the epidermis at
other points. If these are connected with each other and with other hair
follicles, we then have a carbuncle. There is nothing distinctive in the
histologic picture of these pyogenic infections primarily or fundamentally
involving the hair follicles, whether it be acne varioliformis, forms of
sycosis or dermatitis papillaris capillitii, and so forth. Biopsy in these
conditions is usually only of negative value in helping to rule out specific
chronic granulomas such as various forms of tuberculosis and deep-seated
mycoses.
Accession 206325
Slide 40
ECTHYMA
The patient was a man, aged 26 years. A crusted ulcerative lesion
of the ankle and later one of the thigh developed. These were of several
months' duration. The clinical diagnosis was ecthyma.
This section should be compared with the preceding one on ecthy-
ma and furuncle and with the following ones on sycosis vulgaris and
pyodermas.
The section shows two large regions of crusting filled with degen-
erating polymorphonuclear leukocytes and serum, the larger crust at the
right also containing dense masses of cocci. Just beneath the latter, there
is a region of ulceration of the epidermis, containing many polymorpho-
nuclear leukocytes. There is a fairly pronounced acanthosis and in some
places almost a pseudo-epitheliomatous hyperplasia. Unlike the preced-
ing slide, No. 39, there is no infiltrate about the hair follicles, and if it
were not for the ulceration of the epidermis, this slide could be labeled
impetigo rather than ecthyma. There is a sparse perivascular infiltrate
37
in the upper part of the cutis composed of lymphocytes and polymorpho-
nuclear leukocytes.
Accession 207670
SYCOSIS VULGARIS
A man, aged 52 years, was examined because of pustular lesions of
9 years' duration on both cheeks. The clinical diagnosis was sycosis
vulgaris. Search for fungi gave negative results.
This section is not diagnostic and reveals essentially a perifollicular
but also a perivascular infiltrate in the upper part of the cutis, composed
chiefly of lymphocytes and mononuclear cells. It is a picture of a chronic
indolent dermatitis with an infiltrate extending deep into the cutis. In
the acute phases of sycosis vulgaris, one often sees penetration of the
walls of the hair follicle by wandering leukocytes and a staphylococcus
abscess extending downward in the follicle. A foreign-body reaction also
may be set up. MacLeod and Muende (Pathology of the Skin, Ed. 2,
New York, P. B. Hoeber, Inc., 1940, p. 234) explained the indolent char-
acter of the folliculitis on the basis that sebaceous glands connected with
the hair follicles of the beard are smaller than those of the lanugo hairs,
and that cocci passing down the follicles into these glands do not produce
such active changes or such marked abscess formation as they do in the
large sebaceous glands of lanugo hairs.
Accession 205520
Slide 41
Slide 42
PANNICULITIS
A man, aged 40 years, had a widely distributed eruption of sub-
cutaneous nodules associated with fever. The case was regarded clini-
cally as well as histologically as one of relapsing febrile nodular nonsup-
purative panniculitis (Weber-Christian disease), also termed “nodular
nonsuppurative panniculitis." The case eventually proved to be one of
Hodgkin's disease (reported by Reimann, H. A., Havens, W. P., and
Herbut, P. A.: Arch. Int. Med. 70:434 [Sept.] 1942). You are urged to
read this article as it illustrates the difficulties of arriving at a correct
diagnosis. Thus, it would appear that Hodgkin's disease can simulate
panniculitis clinically and histologically. The section has been retained
in the sets because it is representative of panniculitis in general.
In relapsing febrile nodular nonsuppurative panniculitis (see
Bailey, R. J.: J.A.M.A. 109:1419, 1937), there usually is little inflam-
38
matory reaction in the cutis in contrast to what is seen in this section.
In the subcutaneous tissue, one sees an infiltrate of lymphocytes, plasma
cells and polymorphonuclear leukocytes with relatively little increase of
connective tissue or evidence of fibrosis, such as is seen in thrombophle-
bitis, erythema induratum and other forms of granulomas involving the
subcutaneous tissues. The infiltrate replaces the fat, so-called fat-replace-
ment atrophy. At times, foreign-body giant cells may be present, but
they are not seen in this section. The fat-replacement atrophy is well
shown in this section as well as the various types of cells of the infiltrate.
There are some thickening and edema of the walls of the blood vessels.
Eosinophilia or a region of necrosis, such as is usually associated with
Hodgkin's disease is absent. On careful examination with a high-
power objective or oil-immersion objective, however, one will find a
number of large cells with hyperchromatic nuclei occupying most of the
cell and having relatively little cytoplasm-in other words, cells that are
suggestive if not compatible with Reed-Sternberg cells of Hodgkin's
disease. In the section in some of the sets you may be able to find large
cells containing two or three nuclei which have the morphologic features,
for the most part, of Reed-Sternberg giant cells. With Dr. Kierland
(Proc. Staff Meet., Mayo Clin. 16:124 [Feb. 19] 1941), one of us (H.M.)
has emphasized that mononucleated Reed-Sternberg cells are often
atypical in appearance when seen in the skin, in contrast to their more
characteristic appearance when found in a lymph node. This block
apparently was from the first biopsy from this patient. Later specimens
from cutaneous lesions apparently were more suggestive of the diagnosis,
although the diagnosis in this case was established only at necropsy. A
positive diagnosis of Hodgkin's disease on the basis of this section would
not be warranted, although it might be suspected. This section and case,
therefore, illustrate the necessity of most careful scrutiny even of what
on first glance appears to be a benign inflammatory process.
Accession 207683
Slide 43
HIDRADENITIS SUPPURATIVA
A man, aged 38 years, had lesions which had started in the right
axilla 4 years previously. These became fluctuant abscesses. Clinical
diagnosis was that of hidradenitis suppurativa of Verneuil.
It is impossible in one section to show the whole course of this
disease, for histologic description of which the reader is referred to
Brunsting, L. A.: Arch. Dermat. & Syph. 39:108, 1939. It would appear
39
that the earliest infiltrate is seen in the subcutis within the lumen of
the apocrine gland and in adjacent periglandular connective tissue. It is
believed that the infection starts in the hair follicle but does not produce
a reaction until the gland is reached (Tachau). The disease is spread
by means of the lymph channels and lymph spaces, which may contain
leukocytes and cocci. There apparently is not a primary rupture of the
glandular epithelium. The infection spreads throughout the subcutane-
ous tissues, and the eccrine glands are involved from without. Later,
there is a perivascular infiltrate of plasma cells and lymphocytes.
The section that you have shows a chronic stage of the process
in which there is a dense infiltrate about an inspissated hair follicle (the
hair is no longer present) but also a dense infiltrate throughout the cutis
composed chiefly of lymphocytes and plasma cells, although there are
some polymorphonuclear leukocytes, and, in the section in some of the
sets, abscess formation with polymorphonuclear leukocytes. Both eccrine
and apocrine glands are involved, and there is a considerable number
of foreign-body giant cells. Some of these foreign-body giant cells, how-
ever, on closer scrutiny would appear to be remnants of apocrine glands.
In the section in some of the sets, cocci may be found in the ostium of
the hair follicle and also deep in the subcutaneous tissue. There is fibrous
replacement of the fat and also replacement of fat by an infiltrate.
When one appreciates how deep and suppurative a process hidra-
denitis is, it is readily understood why it is resistant to superficial treat-
ment including superficial incision rather than deep filtered roentgen
therapy or radical surgical excision. Brunsting (personal communi-
cation) has emphasized the frequent association of hidradenitis with der-
matitis papillaris capillitii and acne conglobata.
Accession 207685
D
PYODERMA
Slide 44
PYODERMA FACIALE
A man, aged 21 years, was seen because of deep-seated pyoderma
faciale, which had many draining sinuses and bridges of epithelium over
the sinuses. The condition had been present for several years. The
patient also had hidradenitis suppurativa of the axillae.
This section is not diagnostic. It shows irregular epithelial hyper-
40
plasia even to the point of pseudo-epitheliomatous hyperplasia. Mitotic
figures, however, are regular and orderly in arrangement and no
true malignant cells are present. There is abscess formation filled with
polymorphonuclear leukocytes, lymphocytes and plasma cells, as well as
some fibrosis. Whereas there is some keratotic plugging in the section in
some of the sets, there is no true comedo formation, a fact which serves to
distinguish this condition from acne. The smallest section on this slide
either is part of an abscess from the pyoderma faciale or belongs with
pyoderma gangrenosum. It is impossible to be sure which is the case
except that the smallest section shows predominantly a plasma-cell infil-
trate, a fact that suggests that the lesion belongs with pyoderma gan-
grenosum.
Accession 207684
Judd
Slide 44
PYODERMA GANGRENOSUM
A man, aged 48 years, was seen because of large undermining
ulcerative pyodermic areas on the face and abdomen. A clinical diag-
nosis of pyoderma gangrenosum was made.
The section represents a chronic phase of pyoderma gangrenosum.
It shows undermining of the epidermis by a dense infiltrate composed
chiefly of plasma cells. In the section in some of the sets, there are also
irregular proliferation of the epidermis and invasion of the epidermis by
the cells of the infiltrate. In the original slide, masses of cocci were to
be found in relation to a region of ulceration and also deep in the cutis.
These are not present in the section in this set. In the acute phase, one
is more likely to find collections of polymorphonuclear leukocytes and
extravasation of erythrocytes in serum. The undermining of the epithe-
lium at the margin of the process is characteristic of this disorder and
can best be appeciated clinically rather than histologically. Pyoderma
gangrenosum is usually but not always associated with ulcerative colitis.
Greenbaum (Arch. Dermat. & Syph. 43:775, 1941) applied the
term “phagadena geometrica” to both pyoderma gangrenosum and
chronic undermining burrowing ulcers. Meleney's cases, chiefly post-
operative, were regarded by him as nongangrenous in contrast to acute
hemolytic streptococcic gangrene of the skin or chronic progressive post-
operative gangrene of the synergistic type. Brunsting (personal com-
munication) emphasized that all gradations between dry and moist types
of gangrene occur and that in pyoderma gangrenosum there is a lowered
resistance to infection from various organisms and that except for prog-
G
41
nosis it is similar in many respects to other chronic pyodermas such as
pyoderma faciale, acne conglobata, hidradenitis suppurativa and dis-
secting cellulitis of the scalp; in fact, any or all of these conditions may
be present at the same time in the same individual.
ACNE
The early lesion of acne is that of the comedo, but Lynch in an
excellent study found no clues as to the cause of the comedo (Arch.
Dermat. & Syph. 42:593, 1940). There is a perifolliculitis with a central
plug of sebum and a hyperkeratotic scale. In the beginning, no rupture
of the follicle or evidence of bacterial invasion of the follicular walls
or of the glands or connective tissue is apparent. The persistence of
the comedo results in atrophy and fragmentation of the glandular ap-
pendages; the fragments become surrounded by an infiltrate of lym-
phocytes, plasma cells and even giant cells. It is in the later stages
that abscesses filled with polymorphonuclear leukocytes develop. The
bacteria in the ostia of the follicles do not invade the wall of the follicle.
Lynch was unable to support Sutton's contention (South. M. J. 34:1071,
1941) that acne is due to an imbalance between the intake of lipids and
their metabolization and that histologically there is a foreign body re-
action to lipids in the form of pustular lipoidosis. Lynch found that the
fats were present in sebaceous gland cells rather than in histiocytes. A
papule or pustule develops as an inflammatory reaction about remnants
of atrophied sebaceous glands but this probably is the sequel to stasis
and pressure caused by the comedo. McCarthy (Histopathology of Skin
Diseases, St. Louis, The C. V. Mosby Company, 1931, p. 176) regarded
acne vulgaris essentially as an endofolliculitis and perifolliculitis of the
lanugo hair follicles. The wall of the hair follicle is thinned through
pressure by the comedo. A perifollicular abscess develops and is fol-
lowed by granulation of the cavity and by the formation of scar tissue.
In a study of severe forms of acne, including pyoderma faciale and
various types of folliculitis, one of the committee (Montgomery) has
found that a foreign body giant cell reaction or tuberculoid reaction
occurs only occasionally and then only where there has been a complete
rupture or partial disintegration of the hair follicle. A tuberculoid reac-
tion or the presence of epithelioid cells, contrary to prevailing opinion, is
not a common occurrence. Schwartz and Peck (New York State J. Med.
42
43:1711, 1943) described variations of histologic features between acne
vulgaris and different types of occupational acne, such as those attribu-
table to cutting oils, petrolatum, waxes, coal tar, chlornaphthalenes, chlor-
benzols, et cetera. In the main, cystic formation is more prominent and
the cysts tend to be filled with keratinous rather than sebaceous material.
There is an increase in melanin in the epidermis in the tar acnes.
none of the occupational acnes are bacteria demonstrable.
In
The histologic changes in acne are not specific, and similar changes
are seen in many types of folliculitis and also in seborrheic states such as
seborrhea peripillare and seborrheic dermatitis.
Accession 207677
ACNE CONGLOBATA
A man, aged 59 years, was seen because of a crusted lesion on the
outer aspect of the right thigh in which several comedones were to
be seen. Although the location of the lesion and the age of the patient
are unusual for acne conglobata, nevertheless the clinical changes as well
as the histiologic ones are quite consistent with this diagnosis and should
be accepted as such for teaching purposes.
Slide 45
The section (top one on slide) in most of the sets shows a large
double comedo containing numerous cocci, and the chronic inflammatory
reaction in the cutis is nonspecific in type, varying from collections of
polymorphonuclear leukocytes to a diffuse infiltrate of lymphocytes and
cccasional plasma cells. In the section in some of the sets, there is some
pseudo-epitheliomatous hyperplasia. Considerable fibrosis is seen. Se-
baceous glands are absent and the sweat glands have undergone some
atrophic changes. This is an old chronic indolent lesion and is not
diagnostic per se.
Accession 207682
Slide 45
ACNE KELOID
(DERMATITIS PAPILLARIS CAPILLITII)
A man, aged 20 years, was examined because of lesions of 1 year's
duration on the back of the neck. The clinical picture was typical of
dermatitis papillaris capillitii.
The section (lower one on slide) is not diagnostic. There is
fibrosis in the upper part of the cutis with marked dilatation and apparent
rigidity of the capillaries and lymphatics, which are also increased in
43
number. In the section in some of the sets, there is a moderate degree
of pseudo-epitheliomatous hyperplasia. The infiltrate in the cutis varies
in type and amount from lymphocytes and plasma cells to acute abscess
formation with polymorphonuclear leukocytes at the base of the section.
One can understand, therefore, how the abscesses undermine not only
normal epidermis but fibrotic tissue in the upper part of the cutis-hence
the failure in treating these lesions by simple incision; rather, filtered
irradiation or deep surgical excision is indicated. Dermatitis papillaris
capillitii is often associated with pyodermas and hidradenitis suppurativa.
Accesson 207675
ROSACEA (ACNE ROSACEA)
A woman, aged 50 years, had lesions on her face that had been
present for 4 years. Clinical diagnosis rested between rosacea and rosa-
cea-like tuberculid. She responded promptly to treatment with a strong
lotio alba.
Slide 46
The section is not diagnostic but is consistent with the diagnosis
of acne rosacea. There is little change in the epidermis. Dilatation of
the capillaries and lymphatics is seen in the upper part of the cutis along
with an infiltrate composed chiefly of lymphocytes involving the dermal
appendages and especially the sebaceous glands. The latter are invaded
by the infiltrate and are partially destroyed. Compare this section, the
top one, with the larger section on the same slide on rhinophyma. A
specimen for biopsy in rosacea is of value in ruling out rosacea-like tuber-
culid and lupus erythematosus. Rosacea does not have the epidermal
changes seen in lupus erythematosus. The demonstration of a few epi-
thelioid cells, on the other hand, does not establish the diagnosis of
rosacea-like tuberculid. One should see epithelioid tubercles before
making such a diagnosis. Note that there is no hypertrophy of sebaceous
glands in rosacea as contrasted to rhinophyma.
Accession 207676
Slide 46
RHINOPHYMA
A man, aged 30 years, was seen because of redness of the face and
especially of the nose of 10 years' duration. He had moderate enlarge-
ment of the nose. A clinical diagnosis of rhinophyma was made.
The section again is not diagnostic. There is little change in the
epidermis except in relation to the pilosebaceous orifices. Dilatation
44
of the capillaries and lymphatics is seen in the upper part of the cutis,
as well as fibrosis. Numerous comedones and cysts are present. One of
the cysts is secondarily infected and infiltrated with polymorphonuclear
leukocytes and also reveals a foreign-body giant-cell reaction. There is
definite hyperplasia of sebaceous glands, even though they are numerous
on the nose, evidenced by the increase in the supporting epithelial stroma
of the sebaceous glands. In the section in some of the sets, there is a
small cyst that has undergone calcification. One can appreciate why
rhinophyma is rather resistant to treatment when one sees deeply situated
cysts that are secondarily infected as shown in this section.
Accession 207680
ACTINODERMATITIS
Slide 47
CHRONIC RADIODERMATITIS
A man, aged 48 years, was seen because of two nodules on the right
leg which had developed 2 months prior to examination. Further nodules
developed, reaching into the groin. Radium was employed. Biopsy of
a lymph node revealed a round-cell sarcoma. Review of sections of the
skin taken elsewhere revealed malignant squamous-cell epithelioma (car-
cinoma) simulating fibrosarcoma. There was also definite evidence of
actinodermatitis. A specimen from a portion of the skin of the leg which
was amputated revealed evidence of chronic radiodermatitis.
The section shows fairly regular acanthosis of the epidermis and,
at one side, a region of ulceration totally lacking epidermis and appear-
ing as a mass of necrotic eosinophilic-staining tissue with small aggrega-
tions of cocci and abscesses filled with leukocytes, serum and debris.
It is difficult even to recognize any structures, although faint pinkish-
staining walls of blood vessels that are partially obliterated can still be
made out. The cutis beneath the epidermis where it is still intact shows
marked thickening and increase of collagenous tissue without increase of
number of nuclei. There is atrophy of the dermal appendages and ob-
literative changes in the deeper vessels, whereas the superficial capillaries
and lymphatics are markedly dilated. The homogeneous and hyaline
changes in the collagen, loss of dermal appendages, obliterative changes
in the deeper vessels and dilatation of the superficial vessels permit a
definite diagnosis of radiodermatitis in this case. Elastic-tissue stain re-
vealed marked destruction of elastic tissue.
45
Accession 207679
RADIO-EPIDERMITIS
A woman, aged 23 years, was seen because of an eruption on the
legs, which had started 1 year previously as bluish nodules under the
skin and which was diagnosed histologically as lymphoblastoma. Shortly
before the patient was examined, she received a course of filtered irra-
diation. On examination, the patient showed a rather acute erythema-
tous eruption localized to both lower legs with some edema and sugges-
tion of cellulitis.
Slide 47
The section from the leg shows a rather characteristic picture of
acute actinodermatitis, in this case radio-epidermitis, following irradiation
à la Coutard. The changes are essentially similar for both acute x-ray
dermatitis and radium dermatitis following a single dose or following
fractional daily filtered irradiation. The section shows hyperkeratosis
and a little acanthosis. The striking feature is the eosinophilic staining
of the upper layers of the epidermis together with Swiss-cheese-like vacu-
olization of degenerating epidermal cells in the prickle-cell layer. There
is some liquefaction degeneration of the basal-cell layer resulting from
edema, but there also is an apparent attempt at proliferation of the basal-
cell layer which, for the most part, stains bluish with hematoxylin. Edema
is present throughout the cutis and capillaries and lymphatics are dilated.
There is destruction of most of the dermal appendages except for the
sweat glands. The vessels show edematous changes in the walls and
early proliferative changes. We have seen other cases of radio-epider-
mitis or radiodermatitis which have shown marked obliterative changes
in the walls of the vessels; hence, this condition cannot be looked on as
a benign transitory one, but in some cases undoubtedly will lead in sub-
sequent years to more serious sequelae such as malignant changes. (See
MacKee, G. M. and Cipollaro, A. C.: X-rays and Radium in the Treat-
ment of Diseases of the Skin. Ed. 4, Philadelphia, Lea & Febiger, 1946,
pp. 263-295.)
Accession 206332
Slide 48
NODULAR VASCULITIS
A woman, aged 36 years, complained that she had recurrent attacks
of nodules on her legs for 20 years. These appeared as subcutaneous
nodules which eventually broke down and drained slowly. A diagnosis
of erythema induratum was made elsewhere. Two specimens for biopsy
revealed more nearly the picture of nodular vasculitis and failed to show
46
evidence of tuberculosis. The tuberculin reaction, however, was 2 plus in
the first strength. Cultures and inoculation into guinea pigs, however,
failed to reveal any acid-fast organisms. When the patient was last heard
from, 2 years later, she had continued to have recurrent attacks.
The term "nodular vasculitis" has been applied to relatively
chronic, resistant and recurrent nodular lesions of nontuberculous origin
occurring chiefly on the legs below the knee, especially in women past
the age of 30 years (Montgomery, Hamilton, O'Leary, P. A. and Barker,
N. W.: Nodular Vascular Diseases of Legs; Erythema Induratum and
Allied Conditions. J.A.M.A. 128:335 [June 2] 1945).
The larger section shows most of the features of nodular vasculitis,
including obliterative changes in the vessels, fibrosis, fat necrosis and
caseation without definite tubercle formation. In the section in some of
the sets, there is a region of caseation with a few epithelioid cells at the
periphery but no appreciable number of giant cells. It is not unusual
to find collections of foreign-body giant cells which are not present in
this section. The diagnosis of nodular vasculitis is made by exclusion,
and, in some instances, further observation will prove the case to be
tuberculous; namely, erythema induratum. This is understandable when
one appreciates that in 30 per cent of the cases of erythema induratum a
specimen for biopsy fails to reveal the histopathologic picture of tuber-
culosis.
Accession 206673
Slide 48
ERYTHEMA NODOSUM
A woman, aged 47 years, complained of painful nodules on the
legs and elsewhere on the body of 6 weeks' duration. Nodules varied
from the size of a pea to that of an egg and were more extensive in dis-
tribution than in the ordinary case of erythema nodosum, which, how-
ever, was the clinical diagnosis. The tuberculin reaction was negative in
weak dilution. Cultures from the throat revealed green-producing Strep-
tococcus. Sedimentation rate was 77 mm. per hour (Westergren).
The smaller section shows a fairly characteristic picture of ery-
thema nodosum. The histology of erythema nodosum is not diagnostic.
There is fat-replacement atrophy in the subcutaneous tissue. The infil-
trate consists chiefly of polymorphonuclear leukocytes and, to a lesser
extent, lymphocytes and plasma cells. There is some thickening of the
vessels and beginning fibrosis. There is a varying degree of perivascular
infiltration in the upper part of the cutis. Whereas one may occasionally
47
find a few epithelioid cells, there is no evidence of formation of true
tubercles.
Accession 206331
THROMBOPHLEBITIS
A man, aged 41 years, complained of pain in the finger tips and in
the joints and subcutaneous nodules in the legs. A clinical diagnosis of
thrombophlebitis and Buerger's disease was made.
Slide 49
The section shows a proliferative thrombophlebitis and in some of
the sets one may see foreign-body giant-cell reaction. There is also
fibrosis and fat-replacement atrophy. For discussion of different types of
thrombophlebitis, see Allen and Barker in Tice's Practice of Medicine,
Hagerstown, Maryland, W. F. Prior Company, Inc., 1940, vol. 6, pp. 36-52.
Accession 214442
Slide 50
PERIARTERITIS NODOSA
A man, aged 39 years, had a diagnosis of dermatomyositis made
elsewhere. About 3 months before examination, he had a febrile illness
and received sulfadiazine, after which dermatitis and tenderness of the
muscles of the calves and forearms developed. A diagnosis of periarteritis
nodosa of allergic type, as described by Rich and probably resulting from
sulfadiazine, was made on the basis of a biopsy of the skin and muscle.
The section of muscle from the leg reveals a rather characteristic
picture of periarteritis nodosa. There is involvement of both arteries and
veins with infiltration of the media and extensive endothelial proliferation
and a peripheral infiltrate of lymphocytes. There are very few eosinc-
phils, but eosinophilia, either in the blood or tissue, does not always
occur in periarteritis nodosa. The section of the skin showed similar
changes but could not be included in the set as there was insufficient
material. Some of the vessels in the section show a one-sided involvement
rather than involvement of the entire wall, and this is a rather common
occurrence in periarteritis nodosa. Ignore the brownish substance on the
slide, which is some extraneous material. For description of periarteritis
nodosa, see Grant, R. T.: Clin. Sc. 4:245 (Oct.) 1940.
48