To rule out demodicosis, numerous deep skin scrapings of the face and body were performed, and the results were negative.
Ear swab cytology revealed mild ceruminous debris. A repeat otic examination again revealed a normal ear canal. Impression
smears of the facial lesions showed a neutrophilic exudate with intracellular and extracellular cocci; Malassezia organisms were not seen, and the results of a bacterial culture of a ruptured papule were positive for Staphylococcus intermedius. The results of a Wood's lamp examination were negative. A toothbrush technique was used to obtain a sample from the face
for fungal culture, and no pathogens were isolated from the culture. Skin biopsy samples were obtained from the face, dorsum,
and inguinal region. Histologic examination of the trunk and inguinal lesions revealed large areas of hypereosinophilic, fragmented
collagen fibers in the dermis (Figure 3). The pathologists reported that this finding is common in cases of calcinosis cutis. Histologic examination of the facial
lesions revealed an ulcerated epidermis, mixed inflammatory infiltrate in the dermis, and small deposits of mineralization;
a von Kossa's stain was positive for calcium.
3. A photomicrograph of dermis with calcinosis cutis. The dark hypereosinophilic areas represent dystrophic mineralization
of collagen (hematoxylin-eosin; original magnification 400X).
The diagnoses were PDH with calcinosis cutis of the face, trunk, and inguinal area and a secondary bacterial infection. The
presence of the neutrophilic exudate with cocci from the face was compatible with a secondary bacterial infection; the diagnosis
of a bacterial infection was further supported by the results of culture and sensitivity testing of the papule. Two possible
causes of the facial pruritus were considered most likely: a staphylococcal bacterial infection secondary to immunosuppression
from the PDH or inflammation from the calcinosis cutis. The problem with the latter diagnosis was that at the original examination
there was no mention of calcinosis cutis on the face and no evidence of pruritus at the two other sites of calcinosis cutis,
the dorsal trunk and inguinal region.
The dog continued receiving maintenance mitotane therapy for the PDH. Cephalexin (30 mg/kg orally every 12 hours for 21 days)
was prescribed along with daily bathing of the face with an antipruritic oatmeal shampoo. Patient reexamination was scheduled
for three weeks later, but after only 10 days of antibiotic and topical therapy, the owner reported that the dog's pruritus
had worsened and that the dog was mutilating its face (Figure 4). In addition, the dorsal and inguinal lesions were pruritic and self-traumatized. The pruritus had become so severe that
the dog was not sleeping or eating. Patient reexamination revealed severe erythema, exudation, and ulceration and a white,
gritty material extruding from the skin in these areas, particularly the face. It was suspected that the original and continuing
cause of the dog's facial pruritus was resolving calcinosis cutis. (Samples of the gritty material were examined histologically
and were confirmed to be calcium deposits.) Twice-daily whole-body hydrotherapy in tepid water was instituted at home until
the dog was able to sleep comfortably and was not observed to mutilate itself (at least three weeks).
4. The lateral aspect of the dog's face after increasingly severe pruritus developed. Note the erythematous alopecic areas.
Treating the pruritus was difficult; it did not respond to antihistamines (neither hydroxyzine nor diphenhydramine 2 mg/kg
orally every eight hours for seven to 10 days), essential fatty acids (Derm Caps—DVM Pharmaceuticals; 1 capsule/5 kg/day for
10 days), or hydrotherapy. Marked relief from the pruritus was obtained only after topical dimethyl sulfoxide (DMSO) and betamethasone
were applied to the affected areas' margins in the evening after the second hydrotherapy. The DMSO and betamethasone were
applied once a day for three weeks and then every other day for three weeks. An Elizabethan collar was not used because the
owner did not permit it. The dog's pruritus decreased markedly over the next six weeks, and a marked decrease in the calcinosis
cutis was noted. Complete resolution of the calcinosis cutis took six months, and after the initial six weeks of DMSO and
betamethasone therapy, the owner used the mixture intermittently when lesions became pruritic. The addition of this topical
treatment did not affect the therapy and monitoring of the PDH. The dog continued to do well while receiving maintenance mitotane