Cutaneous Pneumocystis carinii infection in patients with acquired immunodeficiency syndrome.

Extrapulmonary infection with Pneumocystis carinii is an uncommon event in which the skin may be affected rarely. All cases heretofore described in immunocompromised hosts have involved the external auditory canal and mastoid areas. We describe two patients with acquired immunodeficiency syndrome and extrapulmonary cutaneous P carinii infection that involved the glabrous skin. The first was a 31-year-old white man seropositive for human immunodeficiency virus with prior episodes of P carinii pneumonia and infection with Mycobacterium avium-intracellulare evaluated for translucent papules on the skin with an appearance similar to molluscum contagiosum infection. Biopsy confirmed the diagnosis of cutaneous pneumocystosis. The second patient was a 36-year-old homosexual man with long-standing liver disease with a persistent cough, fever, and an abnormal chest roentgenogram. Cutaneous evaluation revealed a bluish macule on the sternal notch that on skin biopsy was diagnostic of cutaneous pneumocystosis. Treatment with intravenous pentamidine resulted in resolution of the pulmonary and cutaneous problems in both cases. Extrapulmonary P carinii infection may involve the skin at sites other than the external auditory canal and may have a nondescript appearance. Histologic findings are similar to those of pneumocystosis found elsewhere. Clinicians should be familiar with the nondescript nature of the eruption as skin biopsy may be helpful in establishing a diagnosis of systemic pneumocystosis.

Erythroderma as the initial presentation of the acquired immunodeficiency syndrome.

A 32-year-old black homosexual man, seronegative for human immunodeficiency virus antibody, presented with erythroderma. His peripheral blood was significant for circulating Sézary-like cells bearing the CD8(+) phenotype. Eighty-eight percent of his lymphocytes were CD8(+) as well. He seroconverted 3 months after the initial presentation. We conclude that erythroderma was the presenting sign of the acquired immunodeficiency syndrome.

Relationship of lumbosacral nevocytic nevi to sun exposure in dysplastic nevus syndrome.

In 104 consecutive Caucasian patients who had histologically proved dysplastic nevi, the number and diameter of nevocytic nevi were determined in two equally sized contiguous rectangles in the lumbosacral region. The cephalad (superior) rectangle was in a relatively sun-exposed site, whereas the caudad (inferior) rectangle was in a relatively sun-protected site. Many of the nevocytic nevi identified in these rectangles had the clinical features of dysplastic nevi. Significantly, more nevi were found in the cephalad rectangle compared with the caudad rectangle. Men greater than or equal to 40 years of age had significantly larger nevi in the cephalad rectangle compared with the caudad rectangle. These data are consistent with the hypothesis that sunlight promotes development of more and larger nevocytic nevi in individuals afflicted with dysplastic nevus syndrome.

Herpes zoster: a possible early clinical sign for development of acquired immunodeficiency syndrome in high-risk individuals.

Zoster is uncommon before the age of 50 years in immunologically normal individuals, but it occurs with increased frequency in people who are immunosuppressed. A retrospective review of 300 patients with acquired immunodeficiency syndrome associated with Kaposi's sarcoma, revealed that 8% had prior zoster, a rate that is sevenfold greater than historic controls of the same age. We prospectively examined forty-eight patients, with no known immunodeficiency or signs of AIDS or AIDS related complex (ARC), who presented with zoster localized to the thoracic region. Forty-one patients had known risk factors for AIDS and thirty-five had antibody to the AIDS-associated virus (AAV) at the time of presentation. One seropositive subject had no known risk factors. Absolute lymphocyte counts, lymphocyte OKT4/OKT8 ratios, and lymphocyte mitogen responses were all depressed in subjects with antibody to AAV when compared with seronegative individuals. Seven of thirty-three AAV antibody-positive subjects, who could be followed longitudinally, developed AIDS from 1 to 28 months (mean = 13) after zoster. One antibody-negative subject seroconverted to become AAV seropositive 16 months after zoster and developed Kaposi's sarcoma 1 month later. These eight subjects had persistently low lymphocyte OKT4/OKT8 ratios and elevated beta-2 microglobulin. In patients at risk for AIDS, the occurrence of zoster may be one sign that heralds the marked depression of cellular immunity associated with AIDS or ARC.