Risk factors for the disseminated disease include extremes of age, diagnosis of AIDS, hematologic malignancy, history of transplantation, treatment with immunosuppressive agents, and congenital T-cell deficiencies. Patients who develop the progressive, disseminated form of histoplasmosis generally have an underlying condition impairing their ability to defend against these intracellular pathogens. In immunocompetent patients, these defense mechanisms are usually sufficient to control the infection. Once host cellular immunity to Histoplasma develops, the macrophages become activated to kill the organism. The yeast forms are then phagocytized by macrophages, which assist in spreading the organism to various parts of the body. Once inhaled by the susceptible host, the spores transform into budding yeast in warmer climates. In the environment, Histoplasma capsulatum exists as a mold with hyphae, which produce spores that are aerosolized and dispersed. She died 4 days after entering hospice care. During a return admission for complications related to her cirrhosis, the patient and family eventually elected hospice and comfort measures. Because of the persistent-disseminated fungal infection, she was not an appropriate liver transplant candidate. Unfortunately, over the next few weeks, despite appropriate treatment, the patient’s cellulitis worsened, and further decompensation of her cirrhosis occurred. All other antibiotics were discontinued, and since adequate serum concentration was attained, treatment with itraconazole was continued.Īfter a monthlong hospital admission, the patient was finally discharged. Itraconazole was initiated with the recommendation to switch to amphotericin if therapeutic levels of serum itraconazole were not achieved. Approximately 3 weeks after the rash was first noted, the tissue biopsy revealed findings consistent with histoplasmosis. Her regimen was changed to daptomycin and meropenem when both her leukocytosis and skin lesion worsened. For the cellulitis, intravenous vancomycin was added for presumed bacterial infection. Per recommendations of the infectious disease physician, her spontaneous bacterial peritonitis was treated with intravenous piperacillin/tazobactam but was later switched to intravenous cefepime. Histopathology of rash revealing numerous fungal elements in the dermis and subcutis indicative of disseminated histoplasmosis. A skin lesion present on her medial right thigh, measuring approximately 8 cm x 11 cm, had an area of central necrosis with slight purulent drainage surrounded by firm skin without crepitus ( Figure 1). She had a distended abdomen, a positive fluid wave, and bilateral lower extremity edema. Physical examination revealed stigmata of cirrhosis including scleral icterus and spider angiomata. On admission, she was noted to have mild tachypnea with a respiratory rate of 18. The patient was a Dallas County resident and had no history of recent travel, gardening, insect bites, unusual food consumption, or known sick contacts. Several days after admission, she developed a rash on the medial aspect of her right thigh. A 66-year-old Caucasian woman with a past medical history of type II diabetes mellitus and cirrhosis secondary to hemochromatosis presented with symptoms of decompensation including dyspnea, worsening ascites, and lower extremity edema.
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