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Pythium insidiosum is a pathogenic, fungus-like oomycete in the kingdom Stramenopila, primarily known for causing pythiosis, a life-threatening infectious disease in humans and animals (Gaastra et al., 2010). Unlike true fungi, P. insidiosum lacks ergosterol in its cell membrane, substituting it with other sterols such as sitosterol and stigmasterol, which leads to inherent resistance to many common antifungal agents like amphotericin B and most azoles (Mendoza et al., 1996). The organism typically inhabits stagnant water and wet soil in tropical and subtropical regions, infecting hosts through motile, biflagellated zoospores that invade tissues through wounds or ingestion (Krajaejun et al., 2006). In humans, clinical presentations include vascular, ocular, cutaneous, and disseminated forms, with the vascular form often resulting in arterial thrombosis and high mortality rates (Prasertwitayakij et al., 2003). Current therapeutic strategies are often multimodal, involving aggressive surgical resection of infected tissue, immunotherapy with P. insidiosum antigens (PIA) to stimulate a Th1 immune response, and adjunctive combinations of drugs like itraconazole and terbinafine (Mendoza & Newton, 2005).
Traditional antifungal drugs interact with lanosterol 14-alpha-demethylase (azoles) or (1,3)-beta-D-glucan synthase (echinocandins), while immunotherapy (PIA) shifts the host's immune response from a Th2 profile to a Th1 profile (Mendoza & Newton, 2005; Gaastra et al., 2010).
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