A 14-YEAR-OLD, 41-lb (18.5-kg), spayed female collie-mix presented to the Veterinary Medical Teaching Hospital at the University of Wisconsin-Madison for evaluation of intense pruritus and gradually worsening skin disease of more than one year's duration. The skin lesions had begun on the face, ventrum, and feet as diffuse erythema and pruritus. The dog had a history of seasonal pruritus in the fall, and, based on that history, seasonal atopic dermatitis had been presumptively diagnosed. The dog had been treated symptomatically and effectively with oral glucocorticoids and essential fatty acids. But more recently, the pruritus had become unresponsive to therapy, including various combinations of antibiotics, ketoconazole, glucocorticoids, antihistamines, and shampoos. As the pruritus worsened, the dog received increasing doses of glucocorticoids. Unfortunately, the lesions progressed, and the dog's skin was now very pruritic and painful.
In addition to the skin disease, the owner reported that the dog had exhibited polyuria and polydipsia (PU/PD) since it was 11.5 years of age. The PU/PD had been extensively investigated two years earlier at a referral hospital, and pertinent findings included isosthenuria (urine specific gravity = 1.009), a low normal serum albumin concentration (2.5 g/dl; normal = 2.5 to 4 g/dl), and a small nodule on the spleen. At that time, the owner had declined further evaluation of the PU/PD but had authorized an ovariohysterectomy and splenic mass removal. Histopathologic examination of the splenic nodule had revealed benign hyperplasia. The PU/PD had continued over the past two years, and a month before referral, the dog's serum albumin concentration was subnormal at 2 g/dl.
The owner also reported that the dog was depressed, had not been eating or drinking regularly, and was losing weight. Upon further questioning, we discovered the dog would eat if food was presented to it, but it was unwilling to walk to its food bowl, presumably because of its painful footpads.
The owner had acquired the dog when it was 8 months old. The dog's vaccination status was current. The dog had been regularly tested for heartworm disease and had received a preventive monthly.
PHYSICAL EXAMINATION AND INITIAL DIFFERENTIAL DIAGNOSES
On physical examination, the dog was afebrile, depressed, mildly dehydrated, and thin. It was reluctant to walk, and its skin was extremely malodorous. The dog also had severe gingivitis and dental tartar. Ocular and dermatologic lesions included moist periocular erythema and alopecia, mucopurulent conjunctivitis, seborrheic otitis externa, facial excoriations with broken whiskers, lip fold pyoderma, dorsal scaling and thinning of the coat, multifocal areas of deep pyoderma on the dorsum and ventrum characterized by hair matted with blood and pus, and severe pododermatitis. The pododermatitis was characterized by severe interdigital ulceration, erythema, swelling, and exudation. The hair between the footpads was matted with dried exudate and blood, and the footpads were severely crusted and painful when examined. The dog exhibited intense pruritus by rubbing its face and chewing its feet.
Because of the dog's multiple medical problems, we took a practical approach to the differential diagnoses (Table 1). The dog's weight loss and dehydration may have been from the lack of intake (i.e. reluctance to walk to the food and water bowls) or may have resulted from the PU/PD. In an older dog, the most common differential diagnoses for PU/PD and concurrent skin disease include renal disease, diabetes mellitus, hyperadrenocorticism, severe liver disease, hypercalcemia, or a paraneoplastic syndrome. The hypoalbuminemia could have resulted from a protein-losing nephropathy, a protein-losing enteropathy, liver disease, exudative skin disease, vasculitis from an autoimmune disease, or a lack of dietary protein intake.
Table 1: Initial Problems and Differential Diagnoses
With regard to the skin disease, there were two principal issues: the pruritus and presumptive pyoderma. Since pruritus can cause pyoderma and pyoderma can cause pruritus, it is difficult to organize a rational diagnostic plan without first eliminating one of these problems. It is usually best to investigate and eliminate the pyoderma first, and then investigate any residual pruritus. In our experience, the hair loss, scaling, seborrhea, crusting, ulceration, and pruritus were likely to be secondary to severe infection. The most common cause of deep pyoderma in a dog is demodicosis. The term pyoderma literally means pus in the skin, so any disease causing a neutrophilic exudate results in pyoderma. In addition to demodicosis and infectious skin diseases (e.g. intermediate and deep mycoses, nonstaphylococcal infections), we also considered neoplasia. Immune-mediated skin diseases, such as lupus erythematosus, were considered possible. Hepatocutaneous syndrome (i.e. profound dermatologic manifestations secondary to severe liver disease) was considered because of the footpad crusting and hypoalbuminemia, but the generalized deep pyoderma was inconsistent with the classic clinical signs of this syndrome.
Although we recommended concurrent investigation of the skin disease and PU/PD, financial constraints and owner concerns necessitated a workup of the dog's skin disease first. Evaluation of multiple skin scrapings from the dog's feet, face, and trunk revealed large numbers of Demodex mites. Cytologic evaluation of impression smears of skin exudate revealed large numbers of degenerate neutrophils, intracellular and extracellular cocci, and five to 10 Malassezia organisms per high-power field. Large numbers of yeast were also found in ear swabs. The dog's packed cell volume was 42% (normal = 37% to 55%), and its total solids measurement was 8.4 g/dl (normal = 5 to 8 g/dl). The owner declined a complete blood count and serum chemistry profile but authorized urine testing. Urinalysis revealed a specific gravity of 1.035 with 4+ protein and a normal urine sediment. Because of the marked proteinuria and historical hypoalbuminemia, we measured the urine protein:creatinine ratio. The result was 5.35 (normal < 1).
DERMATOLOGIC TREATMENT AND FOLLOW-UP
Initial treatment and diagnoses
Our initial diagnosis was adult-onset demodicosis complicated by a deep bacterial and Malassezia species pyoderma. In addition, the urinary protein loss could explain the low serum albumin concentration detected by the referring veterinarian. The owner declined further diagnostic testing for the proteinuria until the dog showed a response to therapy for the skin disease, which was a quality-of-life issue at the time of presentation.
The dog was hospitalized and treated for pain with butorphanol tartrate (0.5 mg/kg orally b.i.d.). We clipped the dog's hair and administered a warm-water whirlpool treatment and chlorhexidine bath to remove the matting and crusts on the face, feet, and trunk. In addition, we addressed supportive nutritional and fluid therapy needs by hand-feeding a high-calorie palatable soft food, administering subcutaneous fluids (lactated Ringer's solution, 30 ml/kg b.i.d.), and directly offering water by hand several times a day. We initiated cephalexin (30 mg/kg orally b.i.d. for 45 days) for the bacterial pyoderma, and itraconazole (5 mg/kg orally once a day for 10 days) for the Malassezia species infection. We chose itraconazole because it is less likely than ketoconazole to cause side effects, including a decreased appetite. The extensive deep pyoderma precluded treatment with amitraz for the demodicosis, so we administered milbemycin oxime (3 mg/kg orally once a day for 30 days pending reevaluation). Amitraz was also avoided because it can cause insulin resistance with subsequent glucosuria and PU/PD. Ivermectin was not used because the dog appeared to be a collie-mix.
Three days after presentation, the dog was discharged from the hospital. The owner was instructed to continue the oral medications and to bathe the dog with chlorhexidine shampoo at least every other day until the skin exudation and hair matting had resolved. Although the dog's pruritus was markedly decreased at discharge, the owner was concerned about the dog's comfort, so we prescribed fexofenadine hydrochloride (Allegra—Aventis; 2 mg/kg orally b.i.d.) until the next recheck examination. At presentation, the dog had been receiving prednisone (0.5 mg/kg orally once or twice a day). After much consideration about whether to taper or simply discontinue this anti-inflammatory dosage of prednisone, we stopped it without tapering. Glucocorticoid use in a patient with severe deep pyoderma, demodicosis, and PU/PD is contraindicated, and we strongly felt it was a contributing factor in the development of adult-onset demodicosis in this dog. During hospitalization, an unquestionably stressful event, the dog became more active, began to eat, and showed no signs of glucocorticoid withdrawal.