Cutaneous lupus erythematosus in dogs: a comprehensive review

Abstract

Since the first description of discoid lupus erythematosus (LE) in two dogs in 1979, the spectrum of canine cutaneous lupus erythematosus (CLE) variants has expanded markedly.In this review, we first propose an adaptation of the Gilliam-Sontheimer classification of CLE for dogs. We then review the signalment, clinical signs, laboratory and histopathology and treatment outcome of the currently recognized variants of canine CLE, which are vesicular CLE, exfoliative CLE, mucocutaneous LE and facial or generalized discoid LE. We end with a short description of the rare cutaneous manifestations of systemic LE in dogs.Canine CLE variants are heterogeneous, some of them mirror their human counterparts while others appear-thus far-unique to the dog. As most CLE subtypes seem to have a good prognosis after diagnosis, veterinarians are encouraged to become familiar with the spectrum of often-characteristic and unique clinical signs that would permit an early diagnosis and the rapid implementation of an effective treatment.

Keywords: Auto-immune skin diseases; Auto-immunity; Canine; Dermatology; Lupus; Skin.

Fig. 1

Classification of skin manifestations of lupus erythematosus in humans and dogs. a Gilliam-Sontheimer classification of human cutaneous lupus erythematosus variants; b: proposed classification of canine cutaneous lupus erythematosus variants

Fig. 2

Clinical characteristics of canine vesicular cutaneous lupus erythematosus. a, b, c: erythematous macules progress to annular-to-polycyclic lesions with central flaccid vesiculation and peripheral erythema; skin lesions predominate on the ventral abdomen, medial thighs and axillae. d: with chronicity, ulceration can become more prominent. e, f: erosions at mucocutaneous junctions can be seen in some dogs

Fig. 3

Histopathology of canine vesicular cutaneous lupus erythematosus. a: cell-rich, lymphocytic interface dermatitis is present. Marked basal keratinocyte apoptosis has caused a secondary cleft (vesiculation) through the epidermal basal cell layer, which is typical of the disease. 100X (b): inset box from image “a”, lymphocytes infiltrate the basal layer and are associated with basal cell vacuolation, apoptosis, loss and disorganization at the cleft margin. 200X (c): dermal lymphocytic inflammation can be mild, lacking a clear subepidermal band-like (lichenoid) pattern, but lymphocytes are still observed in the basal epidermal layer in association with basal cell loss. 200X (d): chronic lesions can develop epidermal hyperplasia, a prominent dermal infiltrate of lymphocytes and plasma cells and thickening of the basement membrane zone. 200X

Fig. 4

Clinical characteristics of canine exfoliative cutaneous lupus erythematosus in German shorthaired pointers. a, b: poor hair coat, scaling and follicular casts are visible from a distance. c, d, e, f: irregular plaques with hyperpigmentation and scaling can be seen on closer examination - (d-f) courtesy of Petra Bizikova, NC State University

Fig. 5

Clinical characteristics of canine exfoliative cutaneous lupus erythematosus in Magyar viszlas. a, b: multifocal, often coalescing, patches of alopecia are noted from afar. c, d: atrophic scars and follicular casts and large scales develop in alopecic areas - courtesy of Émilie Vidémont, University of Lyon, France

Fig. 6

Histopathology of canine exfoliative cutaneous lupus erythematosus. a: cell-rich, lymphocytic interface dermatitis is present with a distinct band-like (lichenoid) dermal infiltrate of lymphocytes, plasma cells and a few histiocytes. 100X (b): in an area of well-developed interface dermatitis, laminated, orthokeratotic hyperkeratosis (exfoliation) is present, which is typical of the disease. 200X. c: lymphocytic interface folliculitis and mural folliculitis involve the infundibulum (upper-right) as well as the isthmus and inferior segments (lower-left) of hair follicles. Sebaceous glands are absent in this biopsy, as is reported in some cases. 200X (d): lymphocytic interface folliculitis and mural folliculitis are present in the external root sheath of anagen hair follicles. Telogen hair follicles can also be affected (not shown). 200X

Fig. 7

Clinical characteristics of canine mucocutaneous lupus erythematosus. a: anal erosions with peripheral hyperpigmentation in a German shepherd dog; (b): multifocal perigenital erosions with peripheral hyperpigmentation are often seen in female German shepherd bitches; (c): erosions on the lateral sides of the vulva in a German shepherd bitch (courtesy of Pablo Del Mestre, Mar Del Plata Argentina); (d): periocular erosions in a German shepherd – these lesions were bilateral (courtesy of Petra Bizikova, NC State University, Raleigh; (e): erosion abutting the lip in the same German shepherd dog as in (a); (f): same dog as in (b) – large perilabial erosion; this lesion was also symmetric

Fig. 8

Histopathology of canine mucocutaneous lupus erythematosus. a: cell-rich, lymphocytic interface dermatitis is present with numerous plasma cells, including Mott cells, which is common with inflammation in perimucosal skin and is exacerbated by secondary bacterial infection. 100X (b): inset box from image “a”, lymphocytes infiltrate the basal and suprabasal layers of the epidermis in association with multifocal basal cell apoptosis. 400X (c): basement membrane thickening (arrows) is present and is usually patchy and multifocal. 400X (d): lymphocytic interface folliculitis and mural folliculitis involve the infundibulum and extend to the isthmus (not shown) of a hair follicle. 400X (e): lymphocytic mural folliculitis of the inferior hair follicle (external root sheath), with apoptosis and follicular atrophy. 200X

Fig. 9

clinical characteristics of canine facial discoid lupus erythematosus. a, b: erythematous, depigmented, ulcerated, crusted and scarred nasal lesions of FDLE in a rough collie; a discoid lesion is visible in the proximal dorsal muzzle; (c, d): during the chronic phase of FDLE, depigmentation and scarring without inflammation are present; (e): erosions leading to scars in a Labrador with active FDLE; (f) depigmentation, scarring and crusting in a dog with FDLE. The presence of prominent inflammation often heralds a secondary bacterial colonization, like in the so-called MCP (courtesy of Petra Bizikova, NC State University, Raleigh)

Fig. 10

Clinical characteristics of canine generalized discoid lupus erythematosus. a, b: disc-shaped, annular and polycyclic plaques with hyperpigmentation, focal depigmentation and scarring on the thorax of a Chinese crested dog with GDLE; (c): large irregular plaque with dyspigmentation, scarring and erythema on the lateral knee of the same dog as in (a, b); d: reticulated depigmentation with occasional plaques and focal ulceration on the abdomen; (e): unusual “mask-like” bilateral and symmetric hyperpigmentation and dorsal proximal ulceration and scarring in another Chinese crested dog with GDLE; (f): same dog as in (e) – classic disc-shaped dyspigmented plaque with scarring and focal ulceration and crusting; (g): same dog as in (e) – anal and perianal dyspigmentation and scarring with focal ulceration; (h): large polycyclic hyperpigmented and scaly plaque on the abdomen of a crossbred dog with GDLE

Fig. 11

Histopathology of facial canine discoid lupus erythematosus. a: in a biopsy from the nasal planum, cell-rich, lymphocytic interface dermatitis is present with a prominent band-like (lichenoid) dermal infiltrate of lymphocytes and plasma cells. Pigmentary incontinence is moderate. 100× (b): inset box from image “a”, a short epidermal segment with well-developed interface change, where lymphocytes infiltrate predominantly the basal layer in conjunction with basal cell vacuolation, apoptosis, and loss. 400X (c): a similar interface reaction pattern affects the epidermis of haired skin in the dorsal nasal area. 200X (d): lymphocytic interface folliculitis and mural folliculitis of the hair follicle infundibulum. 200X

Fig. 12

Histopathology of generalized canine discoid lupus erythematosus (a): in a skin biopsy from the trunk, a cell-rich lymphocytic interface dermatitis is present with prominent pigmentary incontinence. While epidermal atrophy (not shown) is classically seen in areas of prominent interface change, epidermal hyperplasia (shown here) can occur in chronic smoldering areas of lesions. 200X (b): inset box from image “a”, lymphocytes infiltrate predominately the basal layer in conjunction with basal cell vacuolation, apoptosis, and loss. 400X (c): some chronic lesions develop mild subepidermal fibrosis with a paucity of inflammation, while retaining pigmentary incontinence. 100X (d): inset box from image “c”, higher magnification image shows mild subepidermal fibrosis, few inflammatory cells and prominent pigmentary incontinence. 400X