Histoplasmosis Picture : Learn About Diagnosis And Treatment
- In the vast majority of patients, low-inoculum exposure to H. capsulatum results in mild or asymptomatic pulmonary histoplasmosis. The course of disease is generally benign, and symptoms usually abate within a few weeks of onset. Patients exposed to a higher inoculum during a primary infection or reinfection may experience an acute, self-limited illness with flulike pulmonary symptoms, including fever, chills, headache, myalgia, and nonproductive cough.
- Chronic pulmonary histoplasmosis generally presents as an opportunistic infection imposed on a preexisting structural abnormality such as lesions resulting from emphysema. Patients demonstrate chronic pulmonary symptoms and apical lung lesions that progress with inflammation, calcified granulomas, and fibrosis. Progression of disease over a period of years, seen in 25% to 30% of patients, is associated with cavitation, bronchopleural fistulas, extension to the other lung, pulmonary insufficiency, and often death.
- In patients exposed to a large inoculum and in immunocompromised hosts, progressive illness, disseminated histoplasmosis, occurs. The clinical severity of the diverse forms of disseminated histoplasmosis generally parallels the degree of macrophage parasitization observed.
- Acute (infantile) disseminated histoplasmosis is seen in infants and young children and (rarely) in adults with Hodgkin’s disease or other lymphoproliferative disorders. It is characterized by unrelenting fever; anemia; leukopenia or thrombocytopenia; enlargement of the liver, spleen, and visceral lymph nodes; and gastrointestinal (GI) symptoms, particularly nausea, vomiting, and diarrhea. Untreated disease is uniformly fatal in 1 to 2 months.
- Most adults with disseminated histoplasmosis demonstrate a mild, chronic form of the disease. Untreated patients are often ill for 10 to 20 years, with long asymptomatic periods interrupted by relapses.
- Adult patients with AIDS demonstrate an acute form of disseminated disease that resembles the syndrome seen in infants and children.
- Identification of mycelial isolates from clinical cultures can be made by conversion of the mycelium to the yeast form (requires 3 to 6 weeks) or by the more rapid (2-hour) and 100% sensitive DNA probe that recognizes ribosomal DNA.
- In most patients, serologic evidence remains the primary method in the diagnosis of histoplasmosis. Results obtained from complement fixation, immunodiffusion, and latex antigen agglutination antibody tests are used alone or in combination.
- In the AIDS patient with progressive disseminated histoplasmosis, the diagnosis is best established by bone marrow biopsy and culture, which yield positive cultures in 90% of patients.
- Asymptomatic or mildly ill patients and patients with sarcoid-like disease generally do not benefit from antifungal therapy. Therapy may be helpful in symptomatic patients whose conditions have not improved during the first month of infection.
- Patients with mild, self-limited disease, chronic disseminated disease, or chronic pulmonary histoplasmosis who have no underlying immunosuppression can usually be treated with either oral ketoconazole or IV amphotericin B.
- In AIDS patients, intensive 12-week primary (induction and consolidation therapy) antifungal therapy is followed by lifelong suppressive (maintenance) therapy with itraconazole.
- In AIDS patients, amphotericin B should be administered in patients who require hospitalization. Itraconazole 200 mg twice daily may be used to complete a 12-week course.
- Response to therapy should be measured by resolution of radiologic, serologic, and microbiologic parameters and improvement in signs and symptoms of infection.
- Once the initial course of therapy for histoplasmosis is completed, lifelong suppressive therapy with oral azoles or amphotericin B (1 to 1.5 mg/kg weekly or biweekly) is recommended, because of the frequent recurrence of infection.
- Relapse rates in AIDS patients not receiving preventive maintenance are 50% to 90%.
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