- What type of inflammatory process is present? Describe the
features of this process.
The process is granulomatous. The well-formed granulomas are formed by palisading epithelioid macrophages and chronic inflammatory cells with surrounding fibroblasts and collagen. The macrophages are large pink cells, oval to spindled, which line up around the center, and Langhans giant cells are also seen.
- What is the differential diagnosis? Which of these is most likely given the history? What organism do you see?
The differential diagnosis includes tuberculosis, which
causes caseating granulomas, and the various fungal organisms that can cause pulmonary disease, including histoplasmosis, cryptococcosis, blastomycosis, coccidioidomycosis, and paracoccidioidomycosis. The organisms for each of these diseases has a fairly distinctive morphologic appearance on Gomori methenamine silver (GMS) staining, which highlights the walls of fungal organisms in black, on a green background. The historical findings and the morphology in this case are classic for coccidioidomycosis.
- How would the histopathology differ if the patient had underlying HIV infection with AIDS?
If the patient were immunocompromised, particularly with AIDS, the histopathology of C. immitis infection may be less granulomatous and more suppurative (acute inflammatory cells.) because of reduced cell mediated immunity.
- What proportion of normal hosts exposed to this agent develop clinical symptomatology? What are the possible outcomes/sequelae?
Only about 10% of the people exposed develop clinically evident disease. Of those, the vast majority resolve completely either spontaneously or with antifungal treatment. From 2 to 4% of infected persons may go on to develop systemic dissemination, with worsening pulmonary involvement and spread to skin, bones, CNS and other organs.
- What therapy is available?
Primary pulmonary coccidioidomycosis usually resolves spontaneously. Resection of chronic progressive pulmonary lesions, particularly those limited to a single lobe of the lung, can aid pharmacologic therapy. Patients with very severe or protracted primary infection at risk for disseminated disease or chronic infection may require treatment with intravenous amphotericin B or itraconazole for several weeks. Patients with severe or rapidly progressing disseminated coccidioidomycosis are started on intravenous amphotericin B for 2 to 3 months, and those who improve may be placed on oral itraconazole or fluconazole therapy for long-term suppression, continued for years.
