Source: University of Birmingham
Summary: Researchers have discovered a unique mechanism that drives the spread of a deadly infection.
Cryptococcosis is a rare and deadly fungal infection that affects the lung and brain and usually only occurs in people with impaired immunity. However, one strain of the fungus, known as the Pacific Northwest strain of Cryptococcus gattii – has gained the ability to infect otherwise healthy individuals. Cryptococcus gattii was considered a tropical fungus primarily found in places like Brazil, New Guinea and Australia, but it was found to be the cause of the Pacific Northwest Outbreak of Cryptococcosis in the US and Canada which began in 1999 and has seen hundreds of humans and animals being infected. Researchers from the University of Birmingham have discovered a unique mechanism that drives the spread of a deadly infection. The study findings were published in the journal Nature Communications.
The infection affects the lungs first because it is acquired by inhaling fungal spores. In the absence of therapy, and sometimes despite it, the infection quickly spreads to the brain and other organs with often fatal consequences. Those infected with the disease have to undergo antifungal drug therapy that can last months but those drugs often fail to curtail the disease and instead surgery is required to remove the infection from the lungs and central nervous system. This latest research has discovered that this ‘division of labour’ can be triggered over large cellular distances and is mediated through the release of microscopic fluid-filled “bags” called extracellular vesicles.
Prof. Robin May said, “Our initial expectation was that the fungus would only be able to communicate within a single host cell, but in fact we discovered that it can communicate over very large – in microbiology terms – distances and across multiple host cell barriers”.
More Information: Ewa Bielska et al, “Pathogen-derived extracellular vesicles mediate virulence in the fatal human pathogen Cryptococcus gattii”, Nature Communications(2018). DOI: 10.1038/s41467-018-03991-6