8-year-old, Rhodesian Ridgeback, canine (Canis familiars).Five skin punch biopsies were submitted from the nasal planum and lips. The clinician reported a one-month duration of crusting, scaling and depigmentation of the affected areas with some vesicles. 

Histopathologic Description:

Haired skin: The epidermis is thickened (acanthotic) and there is a broad zone of plasma cells with some lymphocytes in the superficial dermis and occasionally infiltrating into the basal layer of the epidermis (interface lichenoid inflammation). Many scattered dermal macrophages contain somewhat coarsely granular melanin pigment (pigmentary incontinence). Scattered individual eosinophilic, shrunken, basal cells (apoptotic cells) are present and suggestive of an autoimmune condition.

Morphologic Diagnosis:  

Discoid lupus erythematosus (DLE).


Discoid lupus erythematosis

Contributor Comment:  

This is probably the most common autoimmune disease we see in our submissions and is most common in Collies and Shetland sheepdogs.(3) Typically, it involves the nose, lips, and periorbital skin but may involve the trunk, distal limbs, footpads, genitals and perianal area.(1,3,4) Systemic lupus (SLE) is similar or identical microscopically but is usually more widespread and may have more apoptotic basal cells but less of the lichenoid inflammation than DLE.(4) SLE should have a positive anti-nuclear-antibody serology as well and it may be associated with systemic illness. Vogt-Koyangi-Harada-like syndrome of melanin autoimmunity has more dermal macrophages with finer melanin clumps in them and it is most common in Akitas, Siberian Huskies, Alaskan Malamutes, Chow Chows, and their mixes; it is also limited to the face, but with uveitis. Mucocutaneous pyoderma of the lips also has heavy lichenoid plasma cell dermatitis with pigmentary incontinence; it may have neutrophils as well, and the apoptotic cells are more superficial keratinocytes rather than basal cells.

The dog was treated with short term prednisolone and doxycycline and long-term niacinamide (all 3 are presumed immunosuppressors used to treat DLE and SLE)5and the dog was normal in about one month.

JPC Diagnosis:  

Haired skin: Dermatitis, lichenoid interface, lymphoplasmacytic, neutrophilic and histiocytic, diffuse, marked with epidermal acanthosis, spongiosis, parakeratosis, and rare apoptotic basal cells.

Conference Comment:  

Participants and the moderator were hesitant to assign the specific diagnosis of discoid lupus erythematosus (DLE) in this case due to the variation in specimen quality and the presence of only rare basal cell apoptosis. Many conference participants experienced difficulty in separating tissue processing artifact from pathological changes. Participants agreed with the contributor that several histologic features are suggestive for DLE, although the basal cell apoptosis is not as conspicuous in this dog as would be expected for most animals with the condition. The additional history of clinical response to immunomodulatory treatment supports an underlying autoimmune process, such as DLE.

The moderator commented that the differential diagnosis for superficial lymphoplasmacytic dermatitis with neutrophilic inflammation includes lupus (systemic lupus erythematosus or discoid lupus erythematosus) and mucocutaneous pyoderma (MP). A retrospective study by Weimelt et. al.(8) demonstrated the difficulty in differentiating these two conditions, as the histopathological features of both frequently overlap making treatment modality and clinical response difficult to determine and predict. Whereas mucocutaneous pyoderma responds well to antibiotics, treatment of lupus involves immunomodulatory drugs. 

Since DLE and SLE are nearly indistinguishable histologically, it is worthwhile to briefly review the pathogenesis of SLE. Lymphopenia and an overall decrease in the numbers of T-lymphocytes occurs, and there is an imbalance in the ratio of CD4+:CD8+ T-lymphocytes, with an increase up to 6 to 1 (in healthy dogs the ratio is 2.3 to 1); this favors B-cell stimulation and antibody production.(2) In addition to the imbalance in T-cell populations, there is loss of self-tolerance in both B-cells and T-cells.(2,6) After massive cell death due to exogenous (e.g. ultraviolet light, environmental) insults or endogenous (metabolic, hormonal, genetic) triggers, there is defective clearance of cellular debris, resulting in increased amounts of nuclear antigen.(6) The altered B-cells are stimulated by the released nuclear antigens to produce anti-nuclear antibodies. The anti-nuclear antibodies then bind additional antigen, and the resulting antigen-antibody complexes then bind to Fc receptors on B-cells and antigen-presenting cells (APC). The stimulated APCs secrete type 1 interferon, which is autostimulatory (including for other B-cells).(6)

Antinuclear antibodies have been shown to bind to one of four nuclear components: DNA, histones, non-histone proteins bound to RNA, and nuclear antigens.(6) Generalized tissue damage ensues as part of a Type III hypersensitivity reaction whereby antigen-antibody complexes deposit in the kidney, skin, blood vessels etc.(2,6) The antibody-antigen complexes lodge beneath the basement membrane of the epidermis.(2)

As part of the continuous review and study of the complex pathology of DLE, some authors recommend referring to the lesion as photosensitive nasal dermatitis, suggesting the nomenclature of this entity should change as the pathogenesis is further elucidated.(2) In the skin, DLE and SLE are both photoresponsive, and ultraviolet (UV) light aggravates the autoimmune condition by causing translocation of intracellular antigens (frequently nuclear antigens) to the keratinocyte cell membrane. Autoantibodies then bind the translocated cell membrane antigens, and the keratinocytes are subsequently killed by T-cells or monocytes (antibody dependent cellular cytotoxicity).(2) Injured and necrotic keratinocytes release cytokines (IL-1, IL-2, IL-6, and TNF-β), which then recruit and activate B-cells and histiocytes to the sites of injury.(2)

The use of mouse models for human SLE has been recently reviewed and readers are encouraged to consult the article for a thorough discussion of the pathogenesis of SLE.(7)


1. Gerhauser I, Strothmann-L+â-+erssen I, Baumg+â-ñrtner W. A case of perianal dermatitis in a dog: is this an unusual manifestation of lupus erythematosus? Vet Pathol. 2006;43:761-764.

2. Ginn PE, Mansell JEKL, Rakich PM. Skin and appendages. In: Maxie MG, ed. Jubb, Kennedy and Palmers Pathology of Domestic Animals. Vol. 1, 5th ed. Philadelphia, PA: Elsevier Ltd; 2007:652-654.

3. Goo, M-J, Park, J-K, Hong, I-H, et al. Discoid lupus erythematosus (DLE) in a Spitz dog. J Vet Med Sci. 2008;70:633-635.

4. Gross TL, Ihrke P, Walder EJ, Affolter VK. Skin Diseases of the Dog and Cat. 2nd ed. Ames, IA: Blackwell Publishing; 2005:52-55, 263-265.

5. Kahn CM, ed. The Merck Veterinary Manual. 9th ed. Westhouse Station, NJ: Merck & Co; 2005:2012-2013.

6. Kumar V, Abbas AK, Fausto N, Aster JC. Diseases of the immune system. In: Kumar V, Abbas AK, Fausto N, Aster JC, eds. Robbins and Cotran Pathologic Basis of Disease. 8th ed. Philadelphia, PA: Elsevier Saunders; 2009:213-217.

7. Rottman JB, Willis CR. Mouse models of systemic lupus erythematosus reveal of complex pathogenesis. Vet Pathol. 2010;47:664-676. 

8. Wiemlet SP, Goldschmidt MH, Greek JS, Jeffers JG, Wiemelt AP, Mauldin EA. A retrospective study comparing the histopathological features and response to treatment in two canine nasal dermatoses, DLE and MCP. Vet Dermatol. 2004;15:341-348.

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