Autoimmune Vascular · 2026 · strong signal
Amphotericin B-Resistant Cryptococcus laurentii Meningitis with Concurrent Pulmonary Tuberculosis in a 17-Year-Old Nepali Male on Cyclophosphamide for MPO-ANCA Crescentic Glomerulonephritis — Kathmandu
Key finding
> What did standard medicine miss or get wrong? The organism was **not** *neoformans*. It was *Cryptococcus laurentii*, a non-neoformans species that is uncommon as a human pathogen and — critically — can be **resistant to amphotericin B**, the drug the guideline pathway had committed him to. Four weeks of first-line therapy were spent on an agent the isolate did not respond to. Layered on top of this: **concurrent pulmonary tuberculosis**. In a country where TB is endemic, an immunosuppressed adolescent with fever and pulmonary findings has two competing explanations, and the treatment of one materially interferes with the treatment of the other — rifampicin is a potent CYP3A4 inducer and drives down azole antifungal exposure, while overlapping hepatotoxicity constrains dosing on both sides. The case is therefore a three-way collision: an autoimmune disease requiring immunosuppression,
Framework connections: The Immune Priming, The Undersized Filter (Renal-Metabolic), The Signal Fire (IL-6)
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