Medical Mycology Q&A Section C — MCQ Bank OmpathStudy

Medical Virology — Section C: Essay Questions Unit: MBMM 3300 Medical Virology & Mycology MBChB Year 3 --- --- Q: Discuss the causative agent, clinical manifestation, and treatment of Histoplasmosis. --- CAUSATIVE AGENT Histoplasma capsulatum — a thermally dimorphic fungus: At 25°C (environmental temperature): grows as a mold producing characteristic tuberculate macroconidia and oval microconidia — these are the infective forms At 37°C (human body temperature): converts to small oval yeast cells (2–4 µm) that reproduce by narrow-based budding and survive intracellularly within macrophages Ecology: Thrives in soil enriched by bird and bat droppings. Endemic to the Ohio and Mississippi River valleys in the USA, parts of East Africa, and Latin America. Associated with chicken coops, caves, construction sites, and air conditioning units exposed to bird roosts. Transmission: Inhalation of microconidia from disturbed contaminated soil or dust. --- CLINICAL MANIFESTATIONS Phase 1 — Acute Pulmonary Histoplasmosis: Mild manifestations occur when microconidia are inhaled and deposited in the alveoli, where macrophages ingest them. H. capsulatum survives intracellularly by converting to yeast forms and resisting macrophage killing. In the early stages, manifestations are mild and include headache, nausea, and a mild fever. Most immunocompetent individuals clear the infection at this stage with minimal or no symptoms — over 90% of infections are subclinical. Phase 2 — Chronic Pulmonary Histoplasmosis: After the initial acute manifestations, the disease progresses to the second phase in which symptoms are now more severe. This is because the fungus is now actively replicating within granulomas in the lung, and the body's immune system is working extremely hard to fight the pathogen. Clinical features at this stage closely resemble pulmonary tuberculosis and include: High fever and night sweats Chronic productive cough Weight loss Vomiting and diarrhoea Cavitary lesions visible on chest radiograph Disseminated Histoplasmosis: Seen predominantly in immunocompromised patients (HIV/AIDS with CD4 count below 150 cells/µL, transplant recipients, those on long-term corticosteroids). Through translocation in white blood cells and haematogenous spread, the yeast is transported throughout the body system. Manifestations include: Hepatosplenomegaly Generalised lymphadenopathy Skin and mucocutaneous lesions Pancytopenia Meningitis and adrenal insufficiency in severe cases --- LABORATORY DIAGNOSIS Microscopy: Wright-Giemsa stain of peripheral blood smear or bronchoalveolar lavage (BAL) showing small yeast cells packed within macrophages Culture: Growth on Sabouraud dextrose agar at 25°C reveals mold with characteristic tuberculate macroconidia — takes 4 to 6 weeks; this is the gold standard Serology: Complement fixation and immunodiffusion tests detect H and M precipitin bands in serum Antigen Detection: Histoplasma polysaccharide antigen in urine or serum by ELISA — rapid and highly sensitive in disseminated disease Histology: GMS or PAS stain of tissue biopsy showing intracellular 2–4 µm yeast cells within macrophages --- TREATMENT Mild to moderate disease: Oral itraconazole for 6 to 12 weeks Severe or disseminated disease: Amphotericin B (liposomal preferred) initially, then step down to oral itraconazole once clinical improvement is achieved HIV/AIDS patients: Lifelong itraconazole suppressive therapy to prevent relapse --- --- Q: An executive in an office in Philadelphia has a window air conditioning unit that is a favourite roost for pigeons. She and her secretary both develop lung disease. (a) What is the most likely causative agent? (b) What is the relationship between the pigeons and the disease? (c) Discuss the pathogenesis and clinical presentation. (d) Laboratory diagnosis. (e) Treatment. --- (a) Most Likely Causative Agent: Histoplasma capsulatum --- (b) Relationship Between the Pigeons and the Disease: Pigeon droppings enrich the surrounding soil and surfaces with nitrogen, creating an ideal growth medium for Histoplasma capsulatum . The fungus grows in the soil and organic debris accumulating around the air conditioning unit used as a roost. When the unit operates, it disturbs this material and circulates air laden with infective microconidia into the office. Both the executive and her secretary inhaled these microconidia, resulting in acute pulmonary histoplasmosis. The pigeons themselves are not infected — they are purely environmental amplifiers of the fungus. --- (c) Pathogenesis and Clinical Presentation: Pathogenesis: Microconidia (2–5 µm) are inhaled and deposited in the terminal bronchioles and alveoli. Alveolar macrophages phagocytose the microconidia, but H. capsulatum resists intracellular killing by raising the phagosomal pH and scavenging reactive oxygen intermediates. Inside the macrophage, microconidia transform into yeast cells that replicate freely. Infected macrophages carry yeast cells to hilar lymp