History
A 6-year-old male castrated Tenterfield Terrier was evaluated because of an approximately 4-month history of progressive erythema and pruritus. Lesions started on the dog's head, then progressed to the body and limbs. Prior treatments included lokivetmab (2.6 mg/kg, SC), cefovecin (8 mg/kg, SC), doxycycline (7.5 mg/kg, PO, q 12 h), ketoconazole (7.5 mg/kg, PO, q 24 h), 4% chlorhexidine–containing shampoo, and a strict prescription hydrolyzed diet trial without noticeable or lasting improvement. The owner and patient had moved from Australia to California about 4 years earlier.
Clinical Gross Findings
At the dermatologic evaluation, the patient was bright, alert, and responsive and had heart and respiratory rates within reference limits with no murmur or arrhythmia auscultated. Abnormal physical examination findings were limited to the integumentary system. Multifocal, annular to coalescing serpiginous areas of hypotrichosis to alopecia with erythema and scale were observed on the dorsal aspect of the head, medioventral aspect of the concave side of the pinnae, dorsal aspect of the trunk, and ventral aspects of the thorax and abdomen and were observed circumferentially on all limbs, the inguinal region, and the axilla (Figure 1). In some areas, alopecia was targetoid with a circumferential ring of alopecia enclosing a central area of normal-appearing haired skin. The affected skin of the head and pinnae was hyperpigmented. Punch biopsy samples for histologic evaluation were collected from the dorsal aspect of the head, left shoulder, and right hind limb.
Photographs of the left front limb and shoulder (A) and ventral aspects of the thorax and abdomen (B) of a 6-year-old male castrated Tenterfield Terrier, showing erythema and multifocal annular to coalescing serpiginous areas of hypotrichosis to alopecia. Suture at the biopsy site (arrow) is evident.
Citation: Journal of the American Veterinary Medical Association 260, 13; 10.2460/javma.20.01.0040
Histopathologic Findings
Skin biopsies were fixed in neutral-buffered 10% formalin and routinely processed for histologic evaluation. Sections were stained with H&E stain. On histologic examination, throughout all sections, a predominantly pyogranulomatous nodular infiltrate was associated with pilosebaceous units with diffuse absence of sebaceous glands (Figure 2). The inflammatory infiltrate was composed of macrophages, neutrophils, lymphocytes, and occasional plasma cells and was present in a lopsided distribution or surrounding the hair follicle at the isthmus. In areas, lymphocytes and macrophages extended into the outer aspect of the follicular epithelium (mural folliculitis), but luminal folliculitis was absent. Segmental mild epidermal and follicular hyperplasia and orthokeratotic hyperkeratosis were observed. Follicular activity was adequate. Mild separation of superficial dermal collagen (interpreted as edema) and a mixed superficial perivascular infiltrate were also observed. No bacteria or fungal agents were noted on slides prepared with H&E or special stains, including tissue Gram stain (Brown and Brenn), periodic acid–Schiff stain, and Ziehl-Neelsen acid-fast stain.
Photomicrographs of a tissue section from a punch biopsy of haired skin from an erythematous and alopecic region of the dog in Figure 1. A—Periadnexal pyogranulomatous inflammation is present at the area of sebaceous glands with complete loss of the sebaceous glands. The infiltrate is lopsided (asterisk) or surrounding hair follicles. H&E stain; bar = 100 μm. B—Nodular inflammatory infiltrate composed primarily of macrophages, lymphocytes, and neutrophils with extension of mononuclear cells into the outer wall of the follicular isthmus. H&E stain; bar = 50 μm.
Citation: Journal of the American Veterinary Medical Association 260, 13; 10.2460/javma.20.01.0040
Microbiological and Cytologic Findings
Results were negative for culture on dermatophyte test medium. Superficial cytology and skin scrape revealed corneocytes, no infectious organisms or inflammatory cells, and no mites.
Morphologic Diagnosis and Case Summary
Morphologic diagnosis: multifocal, chronic pyogranulomatous sebaceous adenitis with mild epidermal hyperplasia and orthokeratotic hyperkeratosis.
Case summary: sebaceous adenitis (synonym: granulomatous [nodular] sebaceous adenitis) in a dog.
Comments
The macroscopic and microscopic features were consistent with a diagnosis of sebaceous adenitis. In veterinary medicine, sebaceous adenitis is most commonly diagnosed in dogs; however, the syndrome has also been reported in cats, rabbits, and horses.1–5 The pathogenesis is poorly understood, with hypotheses including an immune-medicated destruction of sebaceous glands, a primary keratinization defect resulting in sebaceous duct obstruction and subsequent inflammation, an anatomic defect in the structure of the sebaceous duct or gland resulting in lipid leakage, and abnormal lipid metabolism resulting in abnormal keratinization and sebum production.1–3,6 In dogs, strong breed predilections, particularly in Standard Poodles and Akitas, suggest a genetic predisposition, although nongenetic factors likely also contribute.3,7,8
Sebaceous adenitis has been reported in over 50 dog breeds, with common breeds including the Standard Poodle, Akita, Springer Spaniel, Chow Chow, Samoyed, Vizsla, Lhasa Apso, and Havanese1–3,9 To the authors' knowledge, this is the first report describing an affected Tenterfield Terrier. Onset is typically young adult to middle age with a slight sex predilection in males for some breeds.3 Clinical lesions can vary based on the breed affected. Generalized hypotrichosis with bilaterally symmetric multifocal patchy alopecia, easily broken dry brittle hair, and yellow-brown follicular casting with or without alopecia of the tail (“rat tail”) is a more common presentation in Standard Poodles, Akitas, and some of the long-coated breeds.1,2 In the nodular form, such as observed in Vizslas, short-coated breeds, and the dog of the present report, coalescing annular to serpiginous areas of alopecia with scale are more common.1–3 With both presentations, lesions often first develop on the temporal region, pinna, and dorsal aspects of the neck and thorax, and secondary pyoderma is common.1,2 Concurrent pruritis has been reported in up to 55% of dogs in 1 study9 and has been observed in dogs with or without concurrent pyoderma.6,9 Sebaceous adenitis is a disease limited to the integument without systemic effects; however, the disease does require lifelong treatment, often with topical management, and as such can be time-consuming, labor-intensive, and sometimes frustrating for owners.
Definitive diagnosis of sebaceous adenitis is made based on histopathologic findings. Examination of multiple skin punch biopsies is required to capture an adequate number of adnexal units. When selecting biopsy sites, early lesions with scale and follicular casting but without alopecia may be useful as well as multiple samples from hypotrichotic and alopecic sites. Histologically, perifollicular inflammation at the level of the isthmus with absence of sebaceous glands is a characteristic finding. In early lesions, the inflammation consists of lymphocytes, macrophages, neutrophils, plasma cells, and rare eosinophils, whereas in late-stage lesions, inflammation may be scant with small numbers of lymphocytes, perifollicular fibrosis, follicular atrophy or dysplasia, or normal follicular activity.1,2 In the nodular form, inflammation tends to be more consistently prominent and present at all stages. Other changes include epidermal hyperplasia and hyperkeratosis with follicular plugging.1,2 Characteristic follicular casts noted on clinical examination correlate to fronds of keratin that encompass hair shafts as they emerge from the follicular ostia. Immunohistology has shown the mononuclear population within inflamed lesions to be mainly T cells and antigen-presenting dendritic cells, supporting an immune-mediated pathogenesis.1,2
Differential diagnosis for generalized scaling includes primary or secondary seborrhea, zinc or vitamin A–responsive dermatoses, ear margin seborrhea, endocrine alopecias (hypothyroidism), and ichthyosis, whereas considerations for the nodular form should include nodular demodicosis, deep bacterial folliculitis and furunculosis, and dermatophytosis.1,2,10 Negative skin scrape, absence of microscopic organisms on histopathology, negative histochemical stains for infectious agents, and a negative fungal culture (dermatophyte test medium) ruled out parasitic, bacterial and fungal etiologies for the dog in the present report. Nonspecific secondary sebaceous gland destruction can be observed in many inflammatory dermatopathies, including sterile nodular pyogranulomatous dermatitis, leishmaniasis, and uveodermatological syndrome.
Treatment is focused on lifelong topical treatment to remove excess scale and improve coat quality that is often combined with oral treatment, and improvement is often observed in 3 months.10 Topical treatment includes antiseborrheic shampoos, conditioning sprays, topical humectants, and topical oils or fatty acids. Oral treatment most commonly consists of cyclosporine (5 mg/kg, PO, q 24 h), vitamin A supplementation, or oral formulation of fatty acids, alone or in combination, and systemic antimicrobials if indicated due to secondary pyoderma. In 1 study11 of dogs receiving cyclosporine (5 mg/kg, PO, q 24 h) without topical treatment, clinical improvement was observed in 10 of 12 dogs. In a double-blinded, randomized controlled study,12 cyclosporine A in combination with topical treatment showed synergistic benefit on both scaling and alopecia. Increased numbers of sebaceous glands have been observed on repeat biopsy after treatment, particularly with cyclosporine A, suggesting a possibility for gland regeneration.11,12 Varied response to treatment with oral administration of vitamin A has been reported and is commonly utilized as an adjunctive treatment.6,10 Treatment is typically lifelong with recurrence of clinical signs if discontinued; however, some dogs can be maintained on topical treatment alone. The dog of the present report was treated with cyclosporine (Atopica; 5 mg/kg, PO, q 24 h), topical essential oil (Dermoscent Essential 6 spot on; Laboratoire de Derma-Cosmetique Animal; applied twice weekly), topical propylene glycol with water (50:50 ratio, 2 to 3 times weekly), and phytosphingosine-containing shampoo (Douxo Calm Shampoo; Ceva; q 2 wk), with clinical improvement noted at the 1-month recheck examination.
Acknowledgments
The authors declare that there were no conflicts of interest.
The authors thank Derek Fang for photographic assistance.
References
- 1. ↑
Gross TL, Ihrke PJ, Walder EJ, Affolter VK. Diseases with abnormal cornification. In: Gross TL, Ihrke PJ, Walder EJ, Affolter VK, eds. Skin Diseases of the Dog and Cat: Clinical and Histopathologic Diagnosis. 2nd ed. Blackwell Science; 2005:186–188.
- 2. ↑
Gross TL, Ihrke PJ, Walder EJ, Affolter VK. Pustular and nodular diseases with adnexal destruction. In: Gross TL, Ihrke PJ, Walder EJ, Affolter VK, eds. Skin Diseases of the Dog and Cat: Clinical and Histopathologic Diagnosis. 2nd ed. Blackwell Science; 2005:453–457.
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White SD, Linder KE, Schultheiss P, et al. Case report: sebaceous adenitis in four domestic rabbits (Oructatagus cuniculus). Vet Dermatol. 2000;11(1):53–60.
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Lam ATH, Affolter VK, Outerbridge CA, Gericota B, White SD. Oral vitamin A as an adjunct treatment for canine sebaceous adenitis. Vet Dermatol. 2011;22(4):305–311.
- 7. ↑
Pedersen NC, Brucker L, Tessier NG, et al. The effect of genetic bottlenecks and inbreeding on the incidence of two major autoimmune diseases in Standard Poodles, sebaceous adenitis and Addison's disease. Canine Genet Epidemiol. 2015;2:14. doi:10.1186/s40575-015-0026-5
- 8. ↑
Reichler IM, Hauser B, Schiller I, et al. Sebaceous adenitis in the Akita: clinical observations, histopathology and heredity. Vet Dermatol. 2001;12(5):243–253.
- 9. ↑
Tevell EH, Bergvall K, Egenvall A. Sebaceous adenitis in Swedish dogs, a retrospective study of 104 cases. Acta Vet Scand. 2008;50(1):11. doi:10.1186/1751-0147-50-11
- 11. ↑
Linek M, Boss C, Haemmerling R, Hewicker-Trautwein M, Mecklenburg L. Effects of cyclosporine A on clinical and histologic abnormalities in dogs with sebaceous adenitis. J Am Vet Med Assoc. 2005;226(1):59–64.
- 12. ↑
Lortz J, Favrot C, Mecklenburg L, et al. A multicentre placebo-controlled clinical trial on the efficacy of oral ciclosporin A in the treatment of canine idiopathic sebaceous adenitis in comparison with conventional topical treatment. Vet Dermatol. 2010;21(6):593–601.
