Disseminated cutaneous histoplasmosis in newly diagnosed HIV Gabriela M. Soza, BS, Mahir Patel, MD, Allison Readinger, MD, and Caitriona Ryan, MD
We present a woman with a widespread severe papulopustular eruption, fever, and fatigue of 5 weeks’ duration. HIV infection was diagnosed, with an absolute CD4+ count of 3 cells/μL. The eruption was consistent with disseminated cutaneous histoplasmosis. The clinical manifestations and management of cutaneous histoplasmosis are reviewed.
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CASE DESCRIPTION A 55-year-old white woman presented to the emergency department reporting a rash of 5 weeks’ duration, severe fatigue, and a fever. Initially the rash was present on a localized area of her back, but it rapidly progressed to involve her trunk, face, arms, and legs. She had presented to the emergency department on four separate occasions and Figure 1. (a) The truck showing scattered erythematous papules and plaques with central necrosis and ulceration was prescribed multiple courses of and some cases of secondary impetiginization. (b) A few larger plaques on the left shoulder. antibiotics, antihistamines, and corticosteroids without significant improvement. Review of systems showed multifocal nodular opacities and mediastinal lymphwas negative for cough, myalgias, arthralgias, and weight loss. adenopathy. The patient was initiated on intravenous liposomal + A rapid HIV test was positive with an absolute CD4 count amphotericin B for histoplasmosis and antiretroviral therapy for HIV. Itraconazole was commenced a few days later for long-term of 3 cells/μL. treatment of histoplasmosis. Amphotericin B was discontinOn examination, the patient had a widespread papulopusued after 3 weeks due to acute kidney injury, and voriconazole tular eruption with lesions coalescing into necrotic plaques with was substituted for itraconazole due to concomitant infection central ulceration over the trunk and extremities. There was with Sporothrix schenckii. There was considerable improvement secondary impetiginization in places (Figure 1). Punch biopof the cutaneous lesions, and 1 month after discharge the pasies were obtained for histopathologic examination and culture tient was recommenced on itraconazole for her histoplasmosis. (Figure 2). Histopathology revealed dermal parasitized macrophages with small intracytoplasmic round organisms with surroundFrom the Texas A&M College of Medicine, Bryan, Texas (Soza), and the Department ing mild chronic inflammation. Stains demonstrated periodic of Dermatology, Baylor University Medical Center at Dallas, Dallas, Texas (Patel, acid-Schiff (PAS)–positive and Gomori methenamine silver Readinger, Ryan). (GMS)–positive yeast within macrophages in the dermis, conCorresponding author: Caitriona Ryan, MD, Department of Dermatology, Baylor sistent with histoplasmosis. A Fungitell blood test (1,3 beta-DUniversity Medical Center, 3900 Junius Street, Suite 145, Dallas, TX 75246 glucan) was positive. Computed tomography (CT) of the chest (e-mail: [email protected]). 50
Proc (Bayl Univ Med Cent) 2016;29(1):50–51
with varying degrees of respiratory, hepatic, and reticuloendothelial system involvement (3). The nonspecific skin lesions in disseminated cutaneous histoplasmosis (DCH) can make the diagnosis challenging; thus, a high index of suspicion is necessary. Histopathologic examination of cutaneous lesions is the gold standard diagnostic test, in combination with culture, and is done using special stains including PAS and GMS. These stains highlight numerous intracellular yeast forms 2 to 4 μm in diameter that fill a macrophage and appear as basophilic dots with a pseudocapsule (2, 4). There are a wide variety of histopathologic features, such as necrotizing “tuberculoid” and nonnecrotizing granuFigure 2. Punch biopsy from a vesicle on the back. (a) Superficial dermal and perivascular diffuse histiocytic infiltrate lomas with small intracellular yeasts, (hematoxylin and eosin [H&E], original magnification ×40). (b) Superficial dermis filled with parasitized macrophages diffuse dermal histiocytosis, and difwith small round organisms stuffing their cytoplasm (H&E, original magnification ×200). fuse dermal karyorrhexis (2). This appearance of karyorrhexis may mimic leukocytoclastic vasculitis at first glance (4, 5). These varied After 3 months of follow-up, the patient had minimal scattered findings, in addition to the range of clinical manifestations in papules and pustules on the face and extremities. DCH, demonstrate a wide spectrum of reaction patterns in this AIDS-defining illness (2). DISCUSSION Histoplasma antigen detection, which can be performed on Histoplasmosis, the most common endemic mycosis in samples of urine, serum, cerebrospinal fluid, and bronchoalAIDS patients, is caused by the dimorphic fungus H. capsuveolar lavage fluid, is the most sensitive method of diagnosing latum, a primary pathogen that can cause opportunistic infecdisseminated disease (1). Radiographic imaging should be pertions in immunocompromised hosts. In the United States, it is formed to assess for pulmonary involvement, although initial prevalent in the Mississippi and Ohio River valleys; worldwide radiographs may be normal. Common radiographic findings it is endemic in areas of Mexico, Central and South America, include diffuse interstitial or reticulonodular infiltrates, while Africa, and Asia. The fungus is found in soil enriched with pleural effusions, mediastinal adenopathy, and calcified granubird or bat excreta and is acquired via inhalation of microcolomas can also be observed (3). nidia into the alveoli, where they convert to the yeast form. In immunocompetent hosts, histoplasmosis can present as a 1. Chang P, Rodas C. Skin lesions in histoplasmosis. Clin Dermatol self-limiting illness (1). Patients with advanced AIDS and CD4 2012;30(6):592–598. lymphocyte counts
We present a woman with a widespread severe papulopustular eruption, fever, and fatigue of 5 weeks’ duration. HIV infection was diagnosed, with an absolute CD4+ count of 3 cells/μL. The eruption was consistent with disseminated cutaneous histoplasmosis. The clinical manifestations and management of cutaneous histoplasmosis are reviewed.
a
b
CASE DESCRIPTION A 55-year-old white woman presented to the emergency department reporting a rash of 5 weeks’ duration, severe fatigue, and a fever. Initially the rash was present on a localized area of her back, but it rapidly progressed to involve her trunk, face, arms, and legs. She had presented to the emergency department on four separate occasions and Figure 1. (a) The truck showing scattered erythematous papules and plaques with central necrosis and ulceration was prescribed multiple courses of and some cases of secondary impetiginization. (b) A few larger plaques on the left shoulder. antibiotics, antihistamines, and corticosteroids without significant improvement. Review of systems showed multifocal nodular opacities and mediastinal lymphwas negative for cough, myalgias, arthralgias, and weight loss. adenopathy. The patient was initiated on intravenous liposomal + A rapid HIV test was positive with an absolute CD4 count amphotericin B for histoplasmosis and antiretroviral therapy for HIV. Itraconazole was commenced a few days later for long-term of 3 cells/μL. treatment of histoplasmosis. Amphotericin B was discontinOn examination, the patient had a widespread papulopusued after 3 weeks due to acute kidney injury, and voriconazole tular eruption with lesions coalescing into necrotic plaques with was substituted for itraconazole due to concomitant infection central ulceration over the trunk and extremities. There was with Sporothrix schenckii. There was considerable improvement secondary impetiginization in places (Figure 1). Punch biopof the cutaneous lesions, and 1 month after discharge the pasies were obtained for histopathologic examination and culture tient was recommenced on itraconazole for her histoplasmosis. (Figure 2). Histopathology revealed dermal parasitized macrophages with small intracytoplasmic round organisms with surroundFrom the Texas A&M College of Medicine, Bryan, Texas (Soza), and the Department ing mild chronic inflammation. Stains demonstrated periodic of Dermatology, Baylor University Medical Center at Dallas, Dallas, Texas (Patel, acid-Schiff (PAS)–positive and Gomori methenamine silver Readinger, Ryan). (GMS)–positive yeast within macrophages in the dermis, conCorresponding author: Caitriona Ryan, MD, Department of Dermatology, Baylor sistent with histoplasmosis. A Fungitell blood test (1,3 beta-DUniversity Medical Center, 3900 Junius Street, Suite 145, Dallas, TX 75246 glucan) was positive. Computed tomography (CT) of the chest (e-mail: [email protected]). 50
Proc (Bayl Univ Med Cent) 2016;29(1):50–51
with varying degrees of respiratory, hepatic, and reticuloendothelial system involvement (3). The nonspecific skin lesions in disseminated cutaneous histoplasmosis (DCH) can make the diagnosis challenging; thus, a high index of suspicion is necessary. Histopathologic examination of cutaneous lesions is the gold standard diagnostic test, in combination with culture, and is done using special stains including PAS and GMS. These stains highlight numerous intracellular yeast forms 2 to 4 μm in diameter that fill a macrophage and appear as basophilic dots with a pseudocapsule (2, 4). There are a wide variety of histopathologic features, such as necrotizing “tuberculoid” and nonnecrotizing granuFigure 2. Punch biopsy from a vesicle on the back. (a) Superficial dermal and perivascular diffuse histiocytic infiltrate lomas with small intracellular yeasts, (hematoxylin and eosin [H&E], original magnification ×40). (b) Superficial dermis filled with parasitized macrophages diffuse dermal histiocytosis, and difwith small round organisms stuffing their cytoplasm (H&E, original magnification ×200). fuse dermal karyorrhexis (2). This appearance of karyorrhexis may mimic leukocytoclastic vasculitis at first glance (4, 5). These varied After 3 months of follow-up, the patient had minimal scattered findings, in addition to the range of clinical manifestations in papules and pustules on the face and extremities. DCH, demonstrate a wide spectrum of reaction patterns in this AIDS-defining illness (2). DISCUSSION Histoplasma antigen detection, which can be performed on Histoplasmosis, the most common endemic mycosis in samples of urine, serum, cerebrospinal fluid, and bronchoalAIDS patients, is caused by the dimorphic fungus H. capsuveolar lavage fluid, is the most sensitive method of diagnosing latum, a primary pathogen that can cause opportunistic infecdisseminated disease (1). Radiographic imaging should be pertions in immunocompromised hosts. In the United States, it is formed to assess for pulmonary involvement, although initial prevalent in the Mississippi and Ohio River valleys; worldwide radiographs may be normal. Common radiographic findings it is endemic in areas of Mexico, Central and South America, include diffuse interstitial or reticulonodular infiltrates, while Africa, and Asia. The fungus is found in soil enriched with pleural effusions, mediastinal adenopathy, and calcified granubird or bat excreta and is acquired via inhalation of microcolomas can also be observed (3). nidia into the alveoli, where they convert to the yeast form. In immunocompetent hosts, histoplasmosis can present as a 1. Chang P, Rodas C. Skin lesions in histoplasmosis. Clin Dermatol self-limiting illness (1). Patients with advanced AIDS and CD4 2012;30(6):592–598. lymphocyte counts
