Malassezia species fungal metabolism

Malassezia species are a genus of lipophilic yeasts that are part of the normal human skin flora but can become pathogenic under certain conditions (Saunders et al., 2012). Their metabolism is characterized by a unique inability to synthesize fatty acids de novo due to the absence of a fatty acid synthase gene (Xu et al., 2007). Consequently, they rely on extracellular lipases and phospholipases to hydrolyze host sebum into essential fatty acids (Park et al., 2017). The metabolic byproducts, such as oleic acid, can disrupt the skin barrier and trigger inflammatory responses, leading to diseases like seborrheic dermatitis and pityriasis versicolor (Gupta et al., 2004). Pharmacological intervention typically targets specific components of this metabolism, most notably the ergosterol biosynthesis pathway. Azole antifungals inhibit the enzyme lanosterol 14-alpha demethylase, which is critical for maintaining fungal cell membrane integrity (Gupta et al., 2004). Other agents, such as zinc pyrithione, are thought to disrupt fungal metabolism by interfering with membrane transport and mitochondrial function (Reeder et al., 2011). Understanding the metabolic requirements of Malassezia is crucial for developing targeted therapies that minimize impact on the host microbiome.

Other names

Malassezia lipid metabolismMalassezia metabolic pathways

Inhibition of ergosterol biosynthesis via lanosterol 14-alpha demethylase (CYP51) inhibition; disruption of fungal cell membrane integrity; inhibition of extracellular lipases and proteinases (Gupta et al., 2004; Park et al., 2017).