Case Presentation: Disseminated histoplasmosis occurs in about one in two thousand patients affected with acute infection. In most immune competent hosts, histoplasmosis is a self-limited disease contained by our cellular immunity. Disseminated histoplasmosis is seen in heavily immunocompromised hosts and can present with multi-organ system involvement, leading to lethal consequences if left untreated.A 33-year-old Hispanic man from Texas with history of fifteen pack year smoking and alcohol dependence presented with fever, chills, malaise, decreased appetite and thirty-pound weight loss for 3 weeks. He also had a two-day history of shortness of breath with productive cough of yellow-green sputum, and abdominal pain associated with watery bowel movements. Patient denied sick contacts or history of travel but he lived on a ranch in southeast Texas where he had with farm animals. On physical exam, he was febrile, tachycardic, but normotensive. He was initially alert, oriented, and had no nuchal signs. Pulmonary exam revealed decreased breath sounds in mid and lower lung fields. His abdomen was tender to palpation in the left and right upper quadrants and he had associated hepatosplenomegaly. Initial laboratory studies revealed pancytopenia (WBC 2190, Hemoglobin 8.1, and Platelet 19,000), elevated LDH (402), ferritin (5396), and severe hypoalbuminemia (1.3). Rapid HIV 1&2 and HIV-1 confirmatory tests were positive with CD4 count of 10 and vial load (PCR) of 889,000 copies/ml. Due to hypoxic respiratory failure and extensive bilateral patchy pulmonary infiltrates on chest imaging, he underwent bronchoscopy, which bronchoalveolar lavage cytology with GMS stain showing Histoplasma species and culture growing Histoplasma capsulatum. Further investigation revealed positive blood culture, urine and serum Histoplasma antigen as well as serum Histoplasma antibody titers to mycelial and yeast. He was started on liposomal amphotericin B induction for 2 weeks that was subsequently deescalated to oral itraconazole upon clinical improvement. Initiation of antiretroviral therapy (tenofovir, emtricitabine, and lopinavir/ritonavir) was not delayed, as well as appropriate prophylaxis for Pneumocystis jirovecii pneumonia and Mycobacterium avium complex. Prior to discharge, patient had dramatic improvement in his respiratory and mental status as well as improved pancytopenia.
Discussion: This case illustrates the importance of early recognition of invasive, disseminated histoplasmosis occurring in the immunocompromised host. Patients most commonly present with fever, fatigue, and weight loss. The common sites of involvement include gastrointestinal tract, central nervous system, and skin. The diagnosis is based upon fungal antigen detection and confirmed by isolation of the organism from culture. Treatment varies depending on the severity of disease. Amphotericin B or itraconazole therapy is highly effective. A vital component of treatment is immediate initiation of antiretroviral therapy in HIV-infected individuals. Physicians should recognize the risk of immune reconstitution inflammatory syndrome, but this should not delay initiation of antiretroviral treatment.
Conclusions: It is imperative to recognize invasive infections, especially in the immunocompromised host, early in the course of disease. Subsequent treatment should never be delayed as it can be potentially life saving.