The highest incidences of C.<unk>  infections occur in Papua New Guinea and Northern Australia. Cases have also been reported in other regions, indicating its spread to India, Brazil, Vancouver Island in Canada, and Washington, and Oregon in the United States. Unlike Cryptococcus neoformans, C.<unk>  is not particularly associated with human immunodeficiency virus infection or other forms of immunosuppression. The fungus can cause disease in healthy people, potentially due to its ability to grow extremely rapidly within white blood cells. In the United States, C.<unk>  serotype B, subtype VGIIa, is largely responsible for clinical cases. The VGIIa subtype was responsible for the outbreaks in Canada; it then appeared in the U.S. Pacific Northwest. According to a CDC summary, from 2004 to 2010, 60 cases were identified in the U.S.: 43 in Oregon, 15 from Washington, and one each from Idaho and California. Slightly more than half of these case were immunocompromised; 92% of all isolates were of the VGIIa subtype. In 2007, the first case in North Carolina was reported, subtype VGI, which is identical to the isolates found in Australia and California. In 2009, one case was identified in Arkansas. The multiple clonal clusters in the Pacific Northwest likely arose independently of each other as a result of sexual reproduction occurring within the highly sexual VGII population. VGII C.<unk>  have probably undergone either bisexual or unisexual reproduction in multiple different locales, thus giving rise to novel virulent phenotypes.
Cryptococcus gattii
Cryptococcus neoformans
Aspergillus tubingensis
Paracoccidioides brasiliensis
Talaromyces marneffei
Candida parapsilosis
Mycobacterium canetti
Mycoplasma incognitus