It is an exclusively clonal,[2] anthropophilic saprotroph that colonizes the upper layers of dead skin, and is the most common cause of athlete's foot, fungal infection of nail, jock itch, and ringworm worldwide.

[3] Trichophyton rubrum was first described by Malmsten [sv] in 1845 and is currently considered to be a complex of species that comprises multiple, geographically patterned morphotypes, several of which have been formally described as distinct taxa, including T. raubitschekii, T. gourvilii, T. megninii and T.

[7] Trichophyton rubrum grows slowly in culture with sparse production of teardrop or peg-shaped microconidia laterally on fertile hyphae.

[5] Different members of the T. rubrum complex are endemic to different regions; isolates previously referred to T. megninii originate from Portugal, while T. soudanense and T. gourvilii are found in Sub-Saharan Africa.

[7] Trichophyton raubitschekii, which is common from northwestern India and southeast Asia as well as parts of West Africa, is characterized by strongly granular colonies and is the only variant in the complex that reliably produces urease.

of varying species of the genus can have multiplicative effects that are invisible to the host immune system, resulting in potentially chronic infection.

[9] As a preliminary test indicating infection, plucked hairs and skin and nail scrapings can be directly viewed under a microscope for detection of fungal elements.

In this test, medium supporting T. rubrum remains sky blue, indicating neutral pH, until 7 to 10 days after inoculation.

Red pigment production can be restored in such contaminated isolates using casamino acids erythritol albumin agar (CEA).

[5] Trichophyton rubrum has also been known to cause folliculitis in which case it is characterized by fungal element in follicles and foreign body giant cells in the dermis.

[10] Mannan, a component of the fungal cell wall, can also suppress immune responses, although the mechanism of action remains unknown.

Infections cause reddish brown lesions mainly on the upper thighs and trunk, that are border by raised edge.

[10] Once considered a rare causative agent,[12] T. rubrum is now the most common cause of invasive fungal nail disease (called onychomycosis or tinea unguium).

[12] It is thought that Trichophyton rubrum evolved from a zoophilic ancestor, establishing itself ultimately as an exclusive agent of dermatophytosis on human hosts.

[13] These proteases allow T. rubrum to digest human keratin, collagen and elastin; they have an optimum pH of 8 and are calcium dependent.

[18] Tinea unguium presents a much greater therapeutic challenge as topical creams do not penetrate the nail bed.