Cryptococcus neoformans variety gattii

Cryptococcus neoformans var. gattii is emerging as a primary human pathogen which is distinct genetically and biochemically from C. neoformans var. ne oformans. There is increasing evidence that it should be reclassified as a separate species within the Tremellales. In nature, C. n. var, gattii has b een consistently isolated from decaying wood in hollows of species of the r ed gum group of eucalyptus trees (Eucalyptus ser. Exsertae Blakely). The ro le that trees play in the life-cycle of C. n. var. gattii is not known, but its association with decaying wood is suggestive of an endophytic existenc e, in common with other wood-rot fungi, Despite the demonstration in the la boratory of sexual reproduction between mating types alpha and n of F. neof ormans var, gattii, this has not been demonstrated in nature. Human cryptoc occosis develops following environmental exposure and inhalation of the inf ectious propagule, Whether this is the basidiospore or dessicated yeast for m is uncertain. The major risk factor for development of disease appears to be exposure, though there is indirect evidence that unidentified host fact ors may contribute to the relatively high incidence of cryptococcosis in Au stralian Aboriginals. The rarity of cryptococcosis due to C. n. var, gattii in immunocompromised patients remains unexplained. Virulence determinants of C. neoformans are currently the subject of intensive investigation, espe cially in C, n. var, neoformans. The best-characterized, major. virulence d eterminants in this variety, the polysaccharide capsule, products of the la ccase enzyme pathway and ability to grow at physiological temperatures, con tribute to its survival in the host. They are also present in C. n. var, ga ttii. A potential determinant of tissue invasion, secreted phospholipase B, is produced in vitro and in vivo by C. n. var. gattii. This enzyme has now been confirmed to play a role in the virulence of C. neoformans serotype A , Disease caused by C. n. var, gattii is distinguished from that due to C. n. var. neoformans by an increased incidence of cryptococcomas in lung and brain, increased neurological morbidity and a slower response to antifungal therapy. The difference in clinical presentation is predominantly due to t he effect of underlying immunocompromise in patients infected with C. n. va r, neoformans.