Fungal killers. Or not.

Histoplasma capsulatum A couple of nice recent papers about fungi and disease – or not:

 

Pathogens are often described by the nature of their relationship with their hosts. At one extreme are species that are entirely dependent on their host to complete their life cycle (often called obligate parasites). At the other are opportunistic species, which live as saprobes on dead organic matter, but can also invade living organisms (often called facultative pathogens). In between lies an array of combinations ranging in their degree of host dependency and ability to cause disease.

Another way to categorize pathogens is according to their pathogenic lifestyle and disease characteristics. In this case, different terminology is used for plant and animal pathogens: plant-attacking fungi are usually categorized according to the way they feed on the host, e.g., biotrophic or necrotrophic pathogens. Fungi that cause disease in animals are usually described according to the type of disease they cause, e.g., superficial or invasive mycoses. Therefore, we tend to think about fungal pathogens of plants and animals in different terms and treat them separately. Yet fungi attacking animals or plants are actually closely related. Moreover, close examination of animal and plant pathosystems reveals that fungal pathogens in both groups share similar infection strategies and sometimes even cause similar symptoms (although similarity in symptoms doesn’t necessarily indicate similar mechanism). For example, pH-lowering molecules, such as oxalic acid, are virulence factors against plant, animal, and insect hosts. This warrants revisiting the terminology and the way in which we think about fungal pathogens of animals and plants.

Fungi Infecting Plants and Animals: Killers, Non-Killers, and Cell Death. (2013) PLoS Pathog 9(8): e1003517. doi:10.1371/journal.ppat.1003517

 

And on to:

 

The yeast Candida albicans is well known as the most common agent of symptomatic fungal disease, but its more typical role is as a permanent resident of the healthy gastrointestinal microbiome. Longitudinal molecular typing studies indicate that disseminated C. albicans infections originate from individuals’ own commensal strains, and the transition to virulence is generally thought to reflect impaired host immunity. Nevertheless, the ability of this commensal pathogen to thrive in radically different host niches speaks to the existence of functional specializations for commensalism and disease. To investigate the C. albicans commensal lifestyle, researchers developed a mouse model of stable gastrointestinal candidiasis in which the animals remain healthy, despite persistent infection with high titers of yeast. Using this model, they found that a C. albicans mutant lacking the Efg1 transcriptional regulator had enhanced commensalism, such that mutant cells strongly outcompeted wild-type cells in mixed infections.

Passage through the mammalian gut triggers a phenotypic switch that promotes Candida albicans commensalism. (2013) Nature Genetics 45, 1088–1091. doi:10.1038/ng.2710
Among ∼5,000,000 fungal species, C. albicans is exceptional in its lifelong association with humans, either within the gastrointestinal microbiome or as an invasive pathogen. Opportunistic infections are generally ascribed to defective host immunity but may require specific microbial programs. Here we report that exposure of C. albicans to the mammalian gut triggers a developmental switch, driven by the Wor1 transcription factor, to a commensal cell type. Wor1 expression was previously observed only in rare genetic backgrounds, where it controls a white-opaque switch in mating. We show that passage of wild-type cells through the mouse gastrointestinal tract triggers WOR1 expression and a novel phenotypic switch. The resulting GUT (gastrointestinally induced transition) cells differ morphologically and functionally from previously defined cell types, including opaque cells, and express a transcriptome that is optimized for the digestive tract. The white-GUT switch illuminates how a microorganism can use distinct genetic programs to transition between commensalism and invasive pathogenesis.

 

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