DERMATOLOGY 0195-5616/99 $8.00 + .

00

STERILE NODULAR DERMATITIS

IN DOGS
Sheila M.F. Torres, DVM, MS, PhD

The forms of canine nodular dermatitis discussed in this article

include sterile nodular panniculitis (SNP), cutaneous sterile pyogranu-
loma/ granuloma syndrome (SPGS), cutaneous histiocytosis, eosinophilic
granuloma, and systemic histiocytosis of the Bernese Mountain Dog.
These disorders have in common their unknown etiopathogenesis and
the clinical presence of nodules or plaques.

STERILE NODULAR PANNICULITIS

Panniculitis refers to inflammation of the subcutaneous fat tissue

(panniculus adiposus). 1-4· 7· 10• 14• 20· 23· 33-35· 38 It can be associated with
multiple causes, including infectious agents, vasculopathies, pancreatic
disorders, neoplastic diseases, and a variety of immunological, nutri-
tional, physicochemical, and drug-related factors. 1-4· 7· 14• 20· 23· 26· 33-35· 38 Most
cases of panniculitis in dogs are idiopathic in origin and have been
referred to as sterile nodular panniculitis, idiopathic nodular panniculitis, or
idiopathic sterile nodular panniculitis. In this review, the condition is re-
ferred to as SNP.
SNP has been reported in association with systemic lupus erythema-
tosus,33· 35· 37 rheumatoid arthritis/ 4 and pancreatic disorders such as
pancreatitis/4 pancreatic carcinoma/ 6 pancreatic nodular hyperplasia/0
and pancreatic necrosis. 23 In man, a deficiency of alpha 1 antitrypsin has
been associated with panniculitis, and it has been suggested that this
enzyme deficiency predisposes people to develop panniculitis in re-

From the Department of Veterinary Comparative Dermatology, College of Veterinary

Medicine, University of Minnesota, St. Paul, Minnesota

VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE

VOLUME 29 • NUMBER 6 • NOVEMBER 1999 1311

1312 TORRES

sponse to trauma and other stimuli.8• 24• 25• 39 A recent study of nine
canine cases could not demonstrate the association between nodular
panniculitis and serum alpha1 antitrypsin deficiency, however. 14 A deter-
mination of the etiology can be challenging, because SNP may result
from one of several causes, each of which may present with similar
clinical and histopathological findings. A rigorous search for underlying
causes should be undertaken in all cases of sterile panniculitis before
considering the condition to be idiopathic.

Clinical Signs

Clinically, SNP is characterized by the formation of single or multi-

ple subcutaneous nodules varying in size from 1 to several centimeters
in diameter (Fig. 1). Initially, the nodules are firm, but later they liquefy
and become soft.I-3• 10• 26• 29• 33• 35• 38 Some nodules regress without rupturing,
whereas others fistulate and discharge an oily clear to yellow-brown
material.l· 3• 7• 10• 33• 35• 38 Older ulcerated lesions are infected secondarily
and are associated with a purulent exudate.38 Ruptured nodules may
subsequently result in scarring, which can be pronounced in some
cases.3 • 10• 26• 33• 35• 38 Nodules are typically localized on the neck, trunk, and
proximal extremities. In the majority of cases, they are nonpruritic and
do not elicit pain on palpation.33• 35• 38 Pyrexia, lethargy, and anorexia are
common presenting signs in dogs with multiple lesions. These signs
usually occur simultaneously with or just prior to the onset of nodule
formation. 3• 7• 38 Dogs with SNP associated with systemic lupus erythema-
tosus, pancreatic disorders, or rheumatoid arthritis may present with

Figure 1. Sterile nodular panniculitis in a 4-year-old Shetland Sheepdog. Multiple subcuta-

neous nodules are present on the trunk. Some nodules ruptured and drained an oily,
yellow-brown material.
 STERILE NODULAR DERMATITIS IN DOGS 1313

constitutional signs related to these primary disorders (e.g., emesis,

polyuria, polydipsia, tender abdomen, reluctance to move, arthralgia,
joint effusion).14, 2o, 35, 38
No gender or age predilection has been reported in dogs with SNP
and multiple nodules; however, these cases occur most frequently in
Dachshunds and Poodles. No gender, age, or breed predilection is evi-
dent in dogs with single lesions. 35• 38

Diagnosis

The clinical differential diagnosis for SNP should include mycobac-

terial infections, bacterial folliculitis and furunculosis, cutaneous neo-
plasms, cutaneous cysts, mycotic infections, drug eruption, and foreign
body reactions.
A systematic diagnostic approach is needed to help identify a pre-
cise etiological factor associated with SNP. The initial diagnostic investi-
gation must include a complete history and physical examination, im-
pression smears or fine needle aspirates of the cutaneous nodules,
bacterial and fungal cultures of the skin lesions, biopsy of cutaneous
nodules, serum amylase or lipase evaluations, and evaluation of the
serum alpha1 antitrypsin concentration. 1· 10· 14· 33• 35• 38 Other ancillary tests
may include a hemogram, chemistry profile, urinalysis, antinuclear anti-
body test, and direct immunofluorescent test on skin biopsies. 1· 35• 38 The
clinical signs and physical findings should dictate which tests should
be used.
Fine needle aspiration from intact nodules usually reveals numerous
neutrophils, foamy macrophages, and no microorganisms. 1· 35• 38 A few
bacteria may be present if the sample is collected by impression smear of
a ruptured nodule. 1 Bacterial and fungal cultures of intact subcutaneous
nodules yield no growth. The definitive diagnosis of SNP can be
achieved only by histopathological examination. Biopsies must be exci-
sional, because punch biopsies may not contain adequate diagnostic
material. 1· 35• 38 Special stains that can be used to help eliminate bacteria
and fungi as causative agents include Ziehl-Neelsen acid-fast stain,
Brown-Brenn Gram stain, Giemsa stain, periodic acid-Schiff stain, and
Gomori' s methenamine silver stain. 1· 35
In the early disease stages, the histological findings are characterized
by lobular inflammation and necrosis of the panniculus associated with
a cellular infiltrate of predominantly neutrophils and macrophages in
the deep portions of the dermis and subcutis. 3• 10· 35• 38 As the disease
progresses, the involvement becomes diffuse, and the inflammatory pro-
cess is generally mixed, with the presence of macrophages, neutrophils,
lymphocytes, and plasma cells in varying numbers and distribution.
Chronic lesions have few neutrophils and variable fibrosis, which re-
places the panniculus. 10 Unless ulceration has occurred, the lesions are
confined to the subcutis and deeper portions of the dermis, leaving the
overlying epidermis unaffected. 3• 35• 38
1314 TORRES

The evaluation of serum amylase and lipase concentrations is espe-

cially important when gastrointestinal signs are concurrently present.l
Measurement of the serum alpha1 antitrypsin concentration should ide-
ally be evaluated in cases of SNP to help understand the pathogenesis
of this disorder.

Treatment

Surgical excision of single nodules is curative in most cases of SNP.35

Systemic glucocorticoids constitute the primary therapy for cases with
multiple lesions. 35, 38 Prednisone or prednisolone at a dose of 0.5 to 1
mg/kg of body weight administered twice daily is given until all lesions
are healed. 3' 23, 34, 35, 38 At this point, the therapy can be discontinued or
can be tapered off over a period of a few weeks. Immature dogs usually
enter long-term or permanent remission. Adult dogs have a tendency to
relapse when corticosteroids are reduced or discontinued, however, and
need to be maintained on long-term therapy (and may need periodic
adjustment of the dosage). 35, 38 A few cases may benefit from oral vitamin
E at a dose of 400 IU administered every 12 hours. 35, 38 Vitamin E must
be given at least 2 hours before or after a meal for maximal results, and
its effectiveness has a lag phase of 1 to 2 months. Vitamin E is useful as
an antioxidant and anti-inflammatory agent. Oral potassium iodide also
has been used successfully in cases of SNP in people. It has been
indicated to work well in two canine cases of SNP. 35 Appropriate antibi-
otic therapy should be instituted to treat any secondary infection.

CUTANEOUS STERILE PYOGRANULOMAI

GRANULOMA SYNDROME

Canine SPGS, also called idiopathic periadnexal multinodular granulo-

matous dermatitis, is considered to be an uncommon disorder. The cause
and pathogenesis of SPGS remain unknown, but the histiocytic nature
of the inflammatory infiltrate, the failure to demonstrate a causative
agent, and the good to excellent response to glucocorticoids and other
immunomodulating drugs suggest that an immune-mediated process
plays a role in the pathogenesis of this condition. 12' 13, 22, 30, 35

Clinical Signs

Skin lesions are characterized by firm, hair-covered to partially

alopecic erythematous papules, nodules, or plaques most commonly
present on the head (especially the bridge of the nose and muzzle) and
distal extremities. 22, 30, 35 Less frequently, lesions can also develop on the
pinnae, eyes, trunk, and abdomen (Fig. 2). 13, 22, 30 In most cases, lesions
are multiple, and pain or pruritus is not associated with the condition. 13'
 STERILE NODULAR DERMATITIS IN DOGS 1315

Figure 2. Sterile pyogranuloma/granuloma syndrome in a 3-year-old, male castrated,

mixed-breed dog. Multiple plaques and nodules are present on the ventral abdomen
and prepuce.

22• 30• 35 Occasionally, draining tracts and ulcerated areas can be observed,

especially on lesions localized to the feetY· 22• 35 Lymphadenopathy has

been reported to occur in 31% of 29 reviewed cases. 22 No systemic signs
are associated with this syndrome, and the condition may spontaneously
resolve or may take a waxing and waning course. 12• 30 SGPS has been
reported in several breeds, but it appears to occur more commonly in
Collies, Weimaraners, Great Danes, Boxers, Golden Retrievers, English
Bulldogs, Doberman Pinchers, and Dachshunds. No age predilection has
been noted, and despite the fact that most reports mention no gender
predisposition, a retrospective analysis of 29 cases indicated that 24
(82.8%) were male dogs. 12• 13• 22• 3o. 3s

Diagnosis

The clinical differential diagnosis includes granulomatous and pya -

granulomatous disorders caused by bacteria, fungi, or foreign material;
cutaneous xanthomas; cutaneous eosinophilic granuloma; SNP; cutane-
ous histiocytosis; sterile sarcoidal granulomatous skin diseases; and cuta-
neous neoplasms. 12• 22• 35 A definitive diagnosis is based on the history,
clinical signs, cytological examination, bacterial and fungal cultures, and
skin biopsy.U· 35 A cytological examination of fine needle aspirations
obtained from nonruptured lesions reveals pyogranulomatous or granu-
lomatous inflammation with no microorganisms.35 Samples obtained by
aseptic surgical biopsy techniques yield no growth of bacterial or fungal
agents.Iz. 35
The histopathological findings are characterized by multifocal, nod-
1316 TORRES

ular to diffuse, granulomatous to pyogranulomatous dermatitis. Early

lesions have a unique histological appearance consisting of elongated
and vertically oriented (sausage-shaped) perifollicular granulomas or
pyogranulomas that track hair follicles. 5 ' 12' 13' 22' 30' 35 In the later stages of
the disease, the inflammatory infiltrates coalesce to form more diffuse
infiltrates that can extend into the subcutis and through the panniculus
adiposus. 5 ' 12, 13, 22, 35 In advanced lesions, adnexal structures can be totally
replaced by the diffuse cellular infiltrates resembling cutaneous histio-
cytosis.13' 22, 30 The inflammatory cells are composed predominantly of
histiocytes, lymphocytes, and neutrophils. Occasionally, plasma cells and
multinucleated histiocytic giant cells are seen. 13' 22 Special stains (i.e.,
acid orcein-Giemsa, Brown-Brenn Gram, periodic acid-Schiff, Gomori's
methenamine silver, and Ziehl-Neelsen acid-fast stains) and polarization
microscopy reveal no organisms or foreign material. 5, 13, 22, 3o, 35

Treatment

Treatment of SGPS may consist of surgical excision of solitary le-

sions or use of systemic glucocorticoids for multiple lesions (or when-
ever surgery is not recommended)P' 22' 30' 35 Prednisone or prednisolone
is given orally at a dose of 2.2 to 4.4 mg/kg administered every 24 hours
until the lesions have resolved, usually in 7 to 14 days. 13, 22, 30, 35 Most
dogs require prolonged alternate-day glucocorticoid therapy. 35 Cases
unresponsive, poorly responsive, or refractory to glucocorticoid therapy
can be treated with azathioprine (Imuran) at a dose of 2.2 mg/kg
administered every 24 hours until remission and then on alternate
days. 13' 22, 30, 35 Tetracycline and niacinamide have various immunomodu-
lating effects and have been successfully used to manage discoid lupus
erythematosus in dogs. 43 In dogs under 10 kg, the dose is 250 mg of
each drug given orally every 8 hours, and in dogs over 10 kg, the dose
is 500 mg of each drug given every 8 hours. It may take 8 weeks before
any results can be obtained. 30' 43 Recently, tetracycline and niacinamide
have been used with good results to treat a single case of SGPS.30

CUTANEOUS HISTIOCYTOSIS

Cutaneous histiocytosis is an uncommon to rare benign histiocytic

proliferative disorder of dogs_12, 32, 36 The etiopathogenesis of this condi-
tion is unknown, butit has been proposed that this proliferative disorder
of histiocytes may represent an immune dysfunction associated with
persistent antigenic stimuli. 12, 36

Clinical Signs

Clinical signs are characterized by the presence of multiple erythem-

atous dermal to subcutaneous plaques or nodules varying in size from
 STERILE NODULAR DERMATITIS IN DOGS 1317

1 to 5 em in diameter. 12• 17• 32• 36• 40 These lesions have been reported to
occur on the face, neck, back, trunk, feet, and nasal mucosa. Involvement
of the nasal mucosa may result in difficulty in breathing. 12• 17• 32• 36 The
lesions tend to develop in regional clusters, but a more random general-
ized distribution is also seen.U· 17• 36 Larger nodules and plaques may
become alopecic and umbilicated or ulcerated. 12• 17 Pruritus is usually not
a feature of this disorder. 17• 40 Older lesions may regress spontaneously as
new lesions develop, but most persist with a variable waxing and
waning course. 12• 36• 40 Prolonged but temporary periods of total remission
may be observedY· 40 Systemic involvement or lymphadenopathy has
not been reported. 17• 40 There is no evidence of age or gender predilection;
however, Collies and Shetland Sheepdogs may be predisposed to de-
velop cutaneous histiocytosis. 12• 36

Diagnosis

The clinical differential diagnosis should include neoplasms (espe-

cially canine cutaneous histiocytomas and cutaneous lymphoma), infec-
tious granulomatous dermatitis, SNP, and SPGS.U· 17• 40 The rapid re-
sponse to glucocorticoid therapy distinguishes cutaneous histiocytosis
from neoplasms and infectious granulomas. Cutaneous histiocytosis can
be difficult to differentiate clinically and histologically (late-phase le-
sions) from SPGS; however, discrete granulomas or pyogranulomas are
not present histologically in cutaneous histiocytosis.U Fat necrosis with
formation of draining tracts, which are typical features of SNP is not
seen in cutaneous histiocytosis. The definitive diagnosis is based on the
history, clinical signs, bacterial and fungal cultures to rule out infectious
agents, and multiple skin biopsies. 12
Cutaneous histiocytosis is histopathologically characterized by ex-
tensive infiltrates of large histiocytes (often vacuolated and "foamy" in
appearance) within the deep dermis and also sometimes within the
underlying panniculus. The histiocytes may be organized in trabeculated
sheets that obscure the normal dermal architecture and associated ad-
nexa.U· 17• 40 Mitotic figures vary from few to numerous.U· 17• 40 Variable
numbers of lymphocytes, neutrophils, and plasma cells may be intermin-
gled with the histiocytes.U· 17• 40 Distinct granulomas or pyogranulomas
are not observed. 12
In a few cases, the histopathological features of cutaneous histio-
cytosis closely resemble those of solitary canine cutaneous histiocytoma.
In these forms of cutaneous histiocytosis, a diffuse infiltrate of large
uniform histiocytes with oval granular nuclei and pale eosinophilic or
amphophilic cytoplasm is associated with smaller numbers of mature
lymphocytes, especially at deep margins. 12 In these cases, the infiltrate
extends into the superficial dermis, attenuating the overlying epidermis,
and also into the panniculus. A tendency for the infiltrate to invade the
epidermis can also be seen with canine cutaneous histiocytosis. 17 The
main histopathological differential diagnosis for this histiocytoma-like
1318 TORRES

form of cutaneous histiocytosis is malignant lymphoma. Immunohisto-

chemistry may be necessary for accurate differentiation.U

Treatment

Most cases of cutaneous histiocytosis respond to immunosuppres-

sive doses of prednisone or prednisolone (i.e., 2.2-4.4 mg/kg/ d orally). 17•
36• 40 Prolonged remissions are frequently followed by recurrencesP· 36

Chemotherapy protocols for lymphomas, including prednisolone, can be

effective in some casesY

CANINE EOSINOPHILIC GRANULOMA

Canine eosinophilic granuloma refers to a rare and somewhat het-

erogeneous group of diseases affecting the oral cavity and skin. 6• 9 • 15• 21 • 27•
28• 31 • 35• 41 • 42 The cause and pathogenesis of eosinophilic granulomas are

unknown. The occurrence of tissue eosinophilia or occasional blood

eosinophilia and the responsiveness of the lesions to glucocorticoid
therapy may indicate a hypersensitivity response most likely related to
a variety of different etiological stimuli-6· 21 • 31• 35• 42 The tendency for
Siberian Huskies to develop the oral form of the disease suggests that
hereditary factors may also be involved in the pathogenesis. 6• 15• 21 • 31• 35• 41

Clinical Signs

In general, canine eosinophilic granuloma does not have a predilec-

tion for any age, gender, or breed; however, male Siberian Huskies less
than 3 years of age are predisposed to develop the oral form of this
disorder. 11 • 21 • 35 Canine eosinophilic granuloma occurs most frequently in
the oral cavity and is usually observed as vegetative and ulcerated
lingual or palatine masses. 9• 15• 21 • 27• 35• 42 Less frequently, the lesions de-
velop as multiple cutaneous papules, nodules, or plaques on the pre-
puce, ventral abdomen, limbs, flanks, dorsal planum nasale, cheek, or
horizontal ear canal.21• 28• 31• 41 Larger and older lesions may ulcerate.U· 35
Pruritus and pain are usually not associated with the cutaneous lesions. 35
In the Siberian Husky, the lesions develop most frequently on the ventral
or lateral aspect of the tongue and occasionally on the palatine mucosa.U·
15 • 21 • 27 Lesions on the palate are usually present on the proximal portion

of the soft palate.27 Palatine lesions are ulcerated and have a well-defined
slightly elevated border.U· 21 • 27 Dogs with lesions confined to the palate
usually are asymptomatic.U· 27 Lesions affecting the lingual mucosa are
firm raised plaques often having an ulcerated surface covered by a
yellow-green exudate. Dogs with lingual lesions frequently have a his-
tory of oral fetor, partial anorexia, weight loss, reluctance to chew dry
food, and a serosanguineous oral discharge.U· 27 Dogs may rarely present
 STERILE NODULAR DERMATITIS IN DOGS 1319

with both lingual and palatine lesions.U' 27 Absolute eosinophilia is not

a consistent finding, and it appears to occur more frequently in dogs
with oral lesions. 27' 31
Complete remission after treatment is commonly observed, but peri-
odic relapses can occur. 6' 9, 15' 21 ' 27' 35, 41 A few cases of canine eosinophilic
granuloma may experience spontaneous resolution15• 27; however, medi-
cal treatment is required in most cases.

Diagnosis

The clinical differential diagnosis should include foreign body reac-

tions, infectious and sterile granulomas, neoplasms, and, for the ulcera-
tive oral form, traumatic ulcer. 11• 35 The diagnosis of canine eosinophilic
granuloma is based on the history, clinical signs, negative bacterial and
fungal cultures, and skin or oral biopsies. The histopathological findings
of oral and cutaneous cases are similar and closely resemble the histopa-
thology of feline linear granuloma. The dermis or submucosa has
multifocal areas of intensely eosinophilic deposits, including degranu-
lated eosinophils and amorphous aggregates of enzymatically degener-
ated collagen.U The associated inflammatory infiltrates are composed
mainly of eosinophils and histiocytes. The histiocytes are often arranged
radially around the foci of collagen degeneration, forming palisading
granulomas. 11 • 21 • 31 • 35 Multinucleated giant cells may be present in some
lesionsY· 15• 31 • 41 Chronic lesions may be associated with prominent
fibrosis. 11

Treatment

Canine eosinophilic granulomas respond well to glucocorticoid

therapy. 21 • 35 Prednisone or prednisolone is given at a dose of 0.5 to 2.2
mg/kg/ d. 15• 27• 35• 41 In most cases, the lesions regress in 10 to 30 days, and
no further therapy is required. 21 • 35 Periodic recurrences and spontaneous
resolution can be observed in some cases. 15• 27• 41

SYSTEMIC HISTIOCYTOSIS OF THE BERNESE

MOUNTAIN DOG

Systemic histiocytosis of the Bernese Mountain Dog is a rare familial

histiocytic proliferative disorder. 12• 18 The cause of systemic histiocytosis
is unknown. The occurrence of the disease in several family members
suggests that genetic mechanisms may play a role in the etiology and
pathogenesis of this disorder. 12• 18 An autosomal recessive mode of inheri-
tance has been proposed. 18 Encouraging results with bovine thymic
extract therapy support the theory that systemic histiocytosis may repre-
sent an immunoregulatory disorder associated with systemic prolifera-
1320 TORRES

tion of histiocytes. 18 Systemic histiocytosis has some clinical and histo-

pathological similarities to the histiocytosis X complex in man. 18

Clinical Signs

Systemic histiocytosis has been described in closely related predomi-

nantly male Bemese Mountain Dogs. 18 The reported age of the affected
dogs ranged from 2 to 8 years. 18 Clinical signs are characterized by
anorexia, weight loss, stertorous respiration, and conjunctivitis as well
as multiple cutaneous papules, plaques, and nodules involving the entire
bodyP, 18, 36 The cutaneous nodules are firm poorly circumscribed masses
measuring up to 4 em in diameter. 18 Larger and older lesions become
alopecic and subsequently erode and ulcerate. 12, 18 Chronic ulcerated
lesions may have a crater-like appearanceP Cutaneous lesions are ob-
served most commonly on the muzzle, planum nasale, eyelids, and
scrotum. 12' 18 Involvement of the eyelids may be associated with severe
conjunctivitis, chemosis, and corneal edema. 18 The skin of the neck,
limbs, and trunk is less frequently affected. 18 Mild peripheral lymphade-
nopathy is associated with the cutaneous lesions. 18 The clinical course of
the disease is often characterized by periods of remission and relapse
and. can be of long duration if the animals are not euthanatized. 18 In
some cases, the disease progresses rapidly and aggressively without
remissionP, 18' 36 Eventually, most dogs are euthanatized, and postmor-
tem examinations have revealed widespread histiocytic infiltrates in
lungs, liver, spleen, bone marrow, kidneys, testes, orbital soft tissue, and
lymph nodes. 18

Diagnosis

Clinically, systemic histiocytosis of the Bemese Mountain Dog

should be differentiated from cutaneous neoplasms (especially lympho-
sarcoma), cutaneous histiocytosis, and infectious and sterile granulomas.
The diagnosis should be based on the history, clinical signs, cytology,
bacterial and fungal cultures, and histopathological findings.
Histopathologically, the cutaneous lesions are characterized by a
nodular or diffuse infiltrate of predominantly large histiocytic cells with
a perivascular orientation in the dermis and panniculus. 12, 18, 36 The infil-
trates are usually most intense in the panniculus and least intense in the
superficial dermis. 12, 18 Small numbers of lymphocytes, neutrophils, and
occasionally plasma cells or eosinophils often accompany the histiocytic
infiltrate. 12' 18 Histiocytes frequently invade blood vessel walls and occa-
sionally cause thrombosis and ischemic necrosis of infiltrated vessels. 18
Fibrosis is present in chronic lesions_12, 18 Large multinucleated histiocytes
are only rarely observed, and the mitotic index is low. 12
The histiocytic lineage of the infiltrating cells should be confirmed
by immunohistochemistry and electron microscopy. Immunohistochemi-
 STERILE NODULAR DERMATITIS IN DOGS 1321

cal studies show that the predominant infiltrating cells are positive for
typical histiocytic markers such as acid phosphatase, nonspecific ester-
ase, and lysozyme. 18• 19 Electron microscopic studies reveal a range of
histiocytic cell types in many stages of differentiation. 18 The nuclei are
often convoluted, with nuclear chromatin varying from euchromatic to
heterochromatic, and the plasmalemma of many cells have numerous
microvilli. The lysosomal granules can be few, and the granular endo-
plasmic reticulum can be abundant in some cells, although other cells
may have abundant lysosomal granules and less extensive granular
endoplasmic reticulum. 18
A nonneoplastic etiopathogenesis is suggested by the prolonged
course of systemic histiocytosis, the frequent occurrence of periods of
temporary remission, and the absence of cytological atypia of the infil-
trating histiocytes. Future investigations, including cytogenetic and
transplantation studies, are required before we can completely exclude
a neoplastic basis for this disorder.

Therapy

Treatment with high doses of glucocorticoids and cytotoxic agents

has resulted in a poor response. In two cases, preliminary results using
bovine thymosin fraction 5 were encouraging, however. 18

SUMMARY

The types of canine sterile nodular dermatitis discussed in this

article have in common the clinical presentation of nodules or plaques;
however, they differ in many aspects such as breed predilection, distribu-
tion and evolution of cutaneous lesions, systemic involvement, response
to therapy, and prognosis. The definitive diagnosis should be based on
multiple skin biopsy results. Other ancillary tests may be indicated in
cases of systemic involvement. In addition, serum alpha1 antitrypsin can
be measured to demonstrate the association between nodular pannicul-
itis arid serum alpha 1 antitrypsin deficiency.
A better understanding of the etiopathogenesis of each of these
interesting skin conditions necessitates extensive and systematic diag-
nostic approaches.

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Address reprint requests to

Sheila M.F. Torres, DVM, MS, PhD
Department of Comparative Dermatology
College of Veterinary Medicine
C339 Veterinary Hospitals
1352 Boyd Avenue
St. Paul, MN 55108