Library

Notes: Abstract The size of the internal transcribed spacer (ITS) region as measured by gel electrophoresis of PCR products, amplified by primers ITS1 and ITS4, was over 800 bp for all Saccharomyces sensu stricto species, but yeasts belonging to other Saccharomyces species had a shorter ITS region, making this characteristic potentially useful in the identification of Saccharomyces isolates. The ITS product length was homogeneous within the species Saccharomyces cerevisiae.

Notes: A 68-year-old African–American woman was awoken from her sleep by a centipede bite on the dorsum of her left hand. Several days later, the patient presented to the emergency room complaining of fevers, severe itching, swelling, and blistering (〈link href="#f1"〉Fig. 1) of both hands. The past history was unremarkable. There was no history of asthma or use of medications. Physical examination at that time was consistent with a bullous cellulitis of the hands. Laboratory investigations revealed: white blood cell count (WBC), 10.3 (normal, 4–10.5); differential: 54 neutrophils, 15 lymphocytes, and 31 eosinophils. The platelet count was 225,000/mm3. A blood chemistry profile was within normal limits. Blood cultures and stool examination for ova and parasites were negative. The patient was treated with oral cephalexin and diphenhydramine.〈figure xml:id="f1"〉1〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD570:IJD_570_f1"/〉Left hand reveals a bulla and several vesicles at the site of the centipede biteTwo weeks later the patient was seen in the dermatology clinic. She complained of unabated pruritus and extensive new lesions. Physical examination revealed a moderately obese woman with normal vital signs. Firm gray plaques with an irregular contour were present on the left hand. The buttocks (〈link href="#f2"〉Fig. 2) and extensor aspects of her upper arms were strikingly indurated and had a blue–gray discoloration. Violaceous, indurated oval patches were noted on the medial aspect of both knees. Finally, a slate-colored, irregularly outlined plaque on the heel of the right foot was present. Complete blood count revealed: WBC, 16.5; differential, 8 neutrophils, 9 lymphocytes, 81 eosinophils, and 2 monocytes. The differential was repeated and confirmed. The platelet count was 568,000/mm3.〈figure xml:id="f2"〉2〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD570:IJD_570_f2"/〉Blue–gray discoloration and induration of the buttocks as well as the proximal thighs is seen. These changes became apparent several weeks after the initial blistering reaction of the handsA skin biopsy from the patient's left upper arm revealed a superficial and deep perivascular dermatitis. In addition, the dermis had a dense inflammatory infiltrate consisting of numerous interstitial eosinophils, many of which were degranulated. Collagen bundles coated with eosinophilic granules characteristic of flame figures were abundant (〈link href="#f3"〉Fig. 3). The changes were consistent with eosinophilic cellulitis. Chest X-ray revealed no evidence of infiltrates.〈figure xml:id="f3"〉3〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD570:IJD_570_f3"/〉There is a dense infiltration of eosinophils in the dermis, many of which have degranulated. Several collagen bundles coated by an extracellular amorphous material (flame figures, arrow) are evident in the center (hematoxylin and eosin stain; original magnification, ×100)A course of oral corticosteroids was prescribed. One week later, the lesions were substantially less indurated, but otherwise similar in appearance. Complete blood count revealed: WBC, 9.9; differential: 21 neutrophils, 19 lymphocytes, 1 basophil, 51 eosinophils, and 8 monocytes. The platelet count was 408,000/mm3. Hematologic consultation was arranged for bone marrow biopsy and examination. Unfortunately, the patient did not return for subsequent appointments.

Notes: An 84-year-old Indian woman with no significant past medical history and no known drug allergies had been prescribed clarithromycin (250 mg twice daily) for pneumonia. The patient was receiving no other medications. Ten days after starting treatment, the patient developed a mild fever, eruption, and swelling of the ankles. Several days later, the patient developed a spreading, nonpainful, nonpruritic eruption, joint pain, gastrointestinal bleeding, and general malaise. Skin examination revealed numerous palpable purpuric macules and papules and petechiae on the lower extremities, mostly below the knees, and on the right hand. There were large blistering lesions around both ankles, some of which had ulcerated and had a necrotic center (〈link href="#f1"/〉). Blood streaked stool was noted during rectal examination. Laboratory tests showed a normal white blood cell count, hematocrit, and hemoglobin. Serum urea nitrogen was 22 mg/dL (8–18 mg/dL) and creatinine was normal. Urinalysis revealed proteinuria of 0.9 g/24 h (〈0.15 g/24 h) and a microscopic hematuria. Antistreptolysin O, antinuclear antibodies, cryoglobulins, and hepatitis serologies were all negative. Histology of the skin showed leukocytoclastic〈figure xml:id="f1"〉1〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD741:IJD_741_f1"/〉Extensive purpura on the distal legs. Overlying the medial malleolus of the left ankle is a large crusted erosion. An ischemic but intact blister roof is apparent at the peripheryvasculitis of superficial vessels with extravasation of red blood cells (〈link href="#f2"/〉). Direct immunofluorescence revealed immunoglobulin A (IgA) in superficial dermal vessels. Treatment with prednisone (1 mg/kg/day) was started and the arthralgias, hematochezia, and eruption resolved over the next 3 days. Renal function remained impaired, however, and the patient was discharged with a proteinuria of 0.56 g/24 h (〈0.15 g/day) on prednisone and omeprazole.〈figure xml:id="f2"〉2〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD741:IJD_741_f2"/〉Medium power picture showing fibrinoid necrosis of superficial vessels, neutrophilic infiltrate, and karyorrhectic debris (hematoxylin and eosin, ×100)

Notes: A 57-year-old African–American woman with a history of long-standing asthma, hypertension, and congestive heart failure was referred for an intensely pruritic, blistering eruption of 2 months duration. The blistering began 2 weeks after the initiation of captopril for essential hypertension. It was localized predominantly on the thighs and legs, but had recently spread to the upper extremities. Previously, the patient had been treated with albuterol and furosemide. She had been admitted to the hospital with a diagnosis of acute varicella, which was ruled out by a negative Tzanck preparation. Clarithromycin was prescribed upon discharge.Physical examination revealed multiple healed and crusted erosions ranging in size from 1 to 7 cm on the anteromedial aspect of the thighs and legs (〈link href="#f1"〉Fig. 1). Discrete and confluent tense vesicles, some forming arciform or rosette-like patterns, were noted (〈link href="#f2"〉Fig. 2). Multiple hypopigmented macules and patches were seen. On the flexural aspect of the forearms, there were multiple small erosions, some of which appeared excoriated. There were no urticarial lesions, and the oral mucosa and scalp were spared.〈figure xml:id="f1"〉1〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD544:IJD_544_f1"/〉Multiple healed and crusted erosions on the anteromedial aspect of the left thigh. Hypopigmented macules and patches are also evident〈figure xml:id="f2"〉2〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD544:IJD_544_f2"/〉Confluent tense vesicles in an arciform arrangementA biopsy specimen of lesional skin from the left thigh revealed epidermal detachment at the dermal–epidermal junction with prominent festooning of dermal papillae. A dense, perivascular lymphohistiocytic infiltrate was present in the underlying dermis (〈link href="#f3"〉Fig. 3). Well-defined neutrophilic papillary microabscesses were not identified, nor were eosinophils. Direct immunofluorescence (DIF) staining revealed linear deposition of immunoglobulin A (IgA) at the dermal–epidermal junction (〈link href="#f4"〉Fig. 4). Indirect immunofluorescence studies of the serum were negative for circulating pemphigus and pemphigoid antibodies. On the basis of these findings, a diagnosis of linear IgA bullous dermatosis was made.〈figure xml:id="f3"〉3〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD544:IJD_544_f3"/〉(a) Subepidermal blister with prominent festooning of dermal papillae. (b) Dense, perivascular lymphohistiocytic infiltrate in underlying dermis〈figure xml:id="f4"〉4〈mediaResource alt="image" href="urn:x-wiley:00119059:IJD544:IJD_544_f4"/〉Deposition of IgA in a linear pattern at the dermal–epidermal junctionDespite discontinuation of captopril, the patient continued to develop new blisters. Treatment with dapsone was initiated at a dose of 25 mg t.i.d. Because of continued blister formation, the dose was increased to 50 mg t.i.d. and prednisone was added to the regimen. The latter was tapered over a period of 3 months. For the past year, dapsone has been administered at a dosage of 100 mg b.i.d., and the patient has experienced only occasional blister formation.