Title : Unmasking histoplasma capsulatum: The pulmonary dimorph that mimics tuberculosis
Abstract:
Pulmonary histoplasmosis is a noncontagious, mycotic infection of lungs caused by a thermally dimorphic fungus Histoplasma capsulatum discovered long ago by an American pathologist Samuel Taylor Darling in 1905. H. capsulatum naturally occurs in nitrogen -rich soils with a pH of 5 to 10, but thrives in bird and bat feces, making chicken coops and bat caves common sources of infection. Pathogenesis occurs by inhaling airborne spores(microconidia) which usually circulate in the air after the contaminated soil is disturbed during excavation, demolition of old buildings and cleaning infected sites. It does not spread from person-to person. Spores after entering in the lungs, are transformed into parasitic budding yeast cells by the body temperature, engulfed by alveolar macrophages, where they survive, multiply, and spread through the lymphatic system and blood streams to other organs (e.g., liver, spleen, bone marrow, and CNS), especially in people with weakened immune systems, leading to mortality. Clinically, it is of 3 types: Acute pulmonary histoplasmosis 90% of the individuals experiences no symptoms or cause mild flu-like disease. Chronic cavitary pulmonary histoplasmosis Formation of cavities in the upper lobes of the lungs similar to TB. Progressive disseminated histoplasmosis severe lifethreatening form where the fungus spreads through bloodstream into vital organs damaging liver, spleen, bone marrow, CNS and gastrointestinal tract. Because this disease mimics TB, sarcoidosis, and lung malignancy, accurate laboratory diagnosis and mycological identification remain cornerstone objectives for practicing clinicians and scientists. The clinical presentation of pulmonary histoplasmosis heavily mimics TB caused by the bacterium Mycobacterium tuberculosis, frequently leading to diagnostic delays or misdiagnosis due to 5 issues: Classic triads of symptoms (e.g., chronic fever, drenching night sweats and significant weight loss); respiratory manifestations (e.g., persistent cough, shortness of breath and coughing up blood); cavitary lesions; lymphadenopathy; and granulomatous tissue response. The notable features used to diagnose H. capsulatum are: Thermal dimorphism (fluffy mold phase at 25-30 °C and yeast phase at 37°C); Intracellular yeasts within host macrophages; No true capsule alike M tuberculosis - a faux "halo" appears under staining due to cell wall shrinkage (species name H. capsulatum-a historical misnomer): Culture (mold producing large tuberculate macroconidia and small microconidia; and Galactomannan antigen detection in urine/ serum via enzyme immunoassay. Intravenous Amphotericin B for severe acute pulmonary or progressive disseminated histoplasmosis, and oral Itraconazole for mild- to- moderate acute pulmonary and chronic cavitary pulmonary histoplasmosis, are the wocurrently used antifungal drugs. Therapeutic drug monitoring is a must to avoid toxicity and efficacy of a drug since these are much more dangerous than the antibacterial drugs.
Keywords: Histoplasmosis; Histoplasma Capsulatum; Bird's Guano; Dimorphism; Pathogenesis; Diagnosis; Treatment
