The patient is 62-yr-old woman with skin changes which started 3 yr ago with diffuse erythematous, slightly infiltrated plaques on her trunk and extremities, with no clear borders, associated with moderate pruritus. Because she had been suffered from hypothyroidosis for 20 yr, at the first dermatological examination, she was misdiagnosed and her skin changes were thought to be in relation with the endocrine disorder. First, she was treated with topical potent corticosteroids (Betametasone valerate 0.1%, triamcinolone acetonide 0.1%, fluocinonide 0.05%), in 1 to 2 weeks repeated courses, over five months, without effect. In next six months her skin changes became more extensive, erythrodermic with scaling and showed tendency for generalization, and then her diagnosis was erythroderma, also thought to be secondary to her hypothyreoidism. Pruritus was persistently present and intensive. In that time, she began with systemic corticosteroid therapy in medium doses (40 mg/day of prednisone). In first month of therapy her skin changes improved, and erythema and pruritus became less intensive, but every time with reduction of dose of steroids, she had an exacerbacion. Sistemic corticosteroid therapy lasted almost one year with pauses and with doses between 20 and 40 mg of prednisone daily. Biopsy specimens were taken several times, but on microscopic examination there were only signs of nonspecific inflammation. Suddenly, she came to a hospital with widespread skin eruptions which had developed during previous few weeks.
Examination showed generalized erythema and scaling of the whole body and face with large hyperkeratotic plaques on her trunk and limbs and crusted lesions on her scalp and external ears (Fig. 1, 2). Also, she had fever and raised body temperature. Laboratory examination showed an elevated sedimentation rate (46 mm) and leukocgtosis with eosinophilia (1.3x109/L). The haematologic (urea, creatinine, hepatic enzimes, glukose level) and urine analyses were normal. Pruritus was very intensive, so she could not sleep. At this time crusted scabies was suspected and microscopical examination of scrapings from the hyperkeratotic lesions from trunk (we did not examined tips of fingers and toes) showed numerous mites and eggs (Fig. 3). In that time we did not perform biopsy, because we made diagnosis. She was treated first with 1% lindane (one application, left on skin 24 hr) with remarkable improvement. After treatment no live mites were found on microscopic examination, but after three days we repeated antiscabiotic treatment first with 25% benzyl benzoat and then with 10% precipitated sulphur ointment (for three consecutive days). At the follow up controls after one, three and six months she had no signs of skin disease.
Maybe the reason of these serious infection is that patient lives in poor hygiene and socioeconomic conditions, she lives alone,without any human care. We have not data about affected neighbors.
There had been outbreak of scabies among the staff (2 doctors, 5 nurses), and 14 patients who were in clinic in the same time.