[7] In previous publications, Naim-Ur-Rahman misidentified the fungus in the genus Cladosporium, while Al-Hedaithy et al (1988) considered it synonymous with Fonsecaea pedrosoi.

[5][10] It is considered endemic throughout the Middle East, specifically Saudi Arabia, Kuwait, and Qatar,[10][5] and infections by this species have been observed in individuals from Afghanistan,[11] Iran,[10] and India.

Due to the lack of knowledge about its environmental niche, it has been difficult to isolate R. mackenziei; and selective techniques such as the use of high temperatures, mouse vectors, alkyl benzenes and mineral oils are required.

Histologically, infection by this agent causes the cerebrospinal fluid to become blackish and necrotic, pus-filled lesions to develop in brain tissue.

[6][8][5][10][11][12][14][15] R. mackenziei is mostly found in brain abscesses of immunocompetent patients,[5][10] however infection has been reported in conjunction with primary central nervous system lymphoma (PCNSL).

[10][14] Diagnosis of cerebral phaeohyphomycosis by R. mackenziei is confirmed by the microscopic observation of pigmented fungal elements in affected tissues combined with the identification of the agent by culture or genetic sequencing.

[14] The basis for the affinity of R. mackenziei for brain tissue is unknown but has been hypothesized to involve the fungal melanin which acts as a virulence factor by allowing it to evade a human host's immune system and cross the blood–brain barrier.

[3] Untreated cerebral phaeohyphomycosis caused by Rhinocladiella mackenziei has a mortality rate of nearly 100%,[10] although some case reports exist of documented survival of patients.

[15][19] Rhinocladiella mackenziei has been shown to be resistant to Amphotericin B, an antifungal drug commonly used to treat fungal infections, both in vivo and in vitro.