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South America is the likely source of the virulent<jats:named-content content-type=\"genus-species\">C. gattii<\/jats:named-content>VGII molecular types that have emerged in North America.<jats:named-content content-type=\"genus-species\">C. gattii<\/jats:named-content>shares major virulence determinants with<jats:named-content content-type=\"genus-species\">C. neoformans<\/jats:named-content>, although genomic and transcriptomic studies revealed that despite similar genomes, the VGIIa and VGIIb subtypes employ very different transcriptional circuits and manifest differences in virulence phenotypes. Preliminary evidence suggests that<jats:named-content content-type=\"genus-species\">C. gattii<\/jats:named-content>VGII causes severe lung disease and death without dissemination, whereas<jats:named-content content-type=\"genus-species\">C. neoformans<\/jats:named-content>disseminates readily to the central nervous system (CNS) and causes death from meningoencephalitis. Overall, currently available data indicate that the<jats:named-content content-type=\"genus-species\">C. gattii<\/jats:named-content>VGI, VGII, and VGIII molecular types more commonly affect nonimmunocompromised hosts, in contrast to VGIV. New, rapid, cheap diagnostic tests and imaging modalities are assisting early diagnosis and enabling better outcomes of cerebral cryptococcosis. Complications of CNS infection include increased intracranial pressure, severe neurological sequelae, and development of immune reconstitution syndrome, although the mortality rate is low.<jats:named-content content-type=\"genus-species\">C. gattii<\/jats:named-content>VGII isolates may exhibit higher fluconazole MICs than other genotypes. 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