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Microconidia of T. rubrum
Scientific classification
Kingdom:	Fungi
Phylum:	Ascomycota
Subphylum:	Pezizomycotina
Class:	Eurotiomycetes
Order:	Onygenales
Family:	Arthrodermataceae
Genus:	Trichophyton
Species:	T. rubrum
Binomial name
Trichophyton rubrum (Castell.) Sabour.
Synonyms
Trichophyton megninii R. Blanch. (1895) Trichophyton fischeri J. Kane (1977) Trichophyton raubitschekii J. Kane, Salkin, Weitzman & Smitka (1982) Trichophyton kanei Summerbell (1987)

Trichophyton rubrum is a dermatophytic fungus in the phylum Ascomycota, class Euascomycetes. It is an 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. Trichophyton rubrum was first described by Malmsten in 1845 and is currently recognized to be a complex of species that comprises multiple, geographically patterned morphotypes several of which have been formally described as distinct taxa, including T. violaceum (which is mainly found in Africa), T. raubitschekii, T. gourvilii, T. megninii, T. soudanense, T. violaceum.

Growth and morphology

Colonies of Trichophyton rubrum isolated from toenail (left-right): Primary isolation from scrapings on Sabouraud's dextrose agar with cycloheximide, chloramphenicol and gentamicin (14 d); Greenish colonies on Littman Oxgall agar (14 d); Restricted, red colony without pH change on Bromocresol Purple Milk Solids Glucose agar (10 d).

Typical isolates of T. rubrum are white and cottony on the surface. The colony underside is usually red, although some isolates appear more yellowish and others more brownish. Trichophyton rubrum grows slowly in culture with sparse production of teardrop or peg-shaped microconidia laterally on fertile hyphae. Macroconidia, when present, are smooth-walled and narrowly club-shaped, although most isolates lack macroconidia. Growth is inhibited in the presence of certain sulfur-, nitrogen- and phosphorus-containing compounds. Isolates of T. rubrum are known to produce penicillin in vitro and in vivo.

Epidemiology

It is thought that Trichophyton rubrum evolved from a zoophilic ancestor, establishing itself ultimately as an exclusive agent of dermatophytosis on human hosts. Genetic analyses of T. rubrum have also revealed the presence of heat shock proteins, transporters, metabolic enzymes and a system of up regulation of key enzymes in the glyoxylate cycle. It secretes more than 20 different proteases, including exopeptidases and endopeptidases that allow T. rubrum to digest human keratin, collagen and elastin, these proteases have an optimum pH of 8 and are calcium dependent. Although T. rubrum shares phylogenetic affiliations with other dermatophytes, it has a distinctive protein regulation system.

Variants

Strains of T. rubrum form two distinct biogeographical subpopulations: one restricted to Africa, the population spread throughout the remainder of the world. Isolates of the African subpopulation report clinically as Tinea corporis and Tinea capitis. In contrast, the globally-distributed subpopulation occurs predominantly in Tinea pedis and Tinea uniguium. Members of the T. rubrum complex are endemic to different regions; isolates previously referred to T. megninii originate from Portugal, T. soudanense is found in Sub-Saharan Africa, T. violaceum was originally restricted to South Asia but has recently become more widespread in the global population. All species included in the T. rubrum complex are "–" mating type with the exception of T. megninii which represents the "+" mating type and is auxotrophic for L-histidine. The mating type identity of T. soudanense remains unknown. Trichophyton raubitschekii is characterized by strongly granular colonies and is the only variant in the complex that produces urease.

Diagnostic tests

Colonies of Trichophyton mentagrophytes (left), T. rubrum (center) and T. violaceum (right) showing differential responses on Bromocresol Purple Milk Solids Glucose agar (7 d). Trichophyton mentagrophytes shows unrestricted growth with alkaline (purple) colour change, T. rubrum shows restricted growth with no pH change, and T. violaceum produces weak growth accompanied by clearing of the milk solids and a purple colour change.

Dermatophytes can usually be identified using microscopy; hair and nail scraping can be directly viewed under a microscope for identification. It can differentiated from other dermatophytes by the Bromocresol purple (BCP) milks as different Trichophyton species release different amounts of ammonia, T. rubrum will remain sky blue after 10 to 14 days indicating neutral pH. However, contaminations can easily cause false positives when T. rubrum is grown on cycloheximide, as the distinctive red pigment in T. rubrum will not form in the absence of glucose. Bacteria and saprotrophic fungi will out compete T. rubrum for glucose if they contaminate the sample, the red pigment can be restored using casamino acids erythritol agar (CEA), which reliably induces the formation the red pigment. Cultures isolated using both cycloheximide-containing media and cycloheximide-free media are necessary for the verification of dermatophytic nail infections, especially when systemic treatment is being considered, given the propensity of these infections to involve non-dermatophytes. A skin test is ineffective in diagnosing active infection and often yields false negative results.

Pathology

Trichophyton rubrum is rarely isolated from animals. In humans, men are more often infected than women. Infections can manifest as both chronic and acute forms. Typically T. rubrum infections are restricted to the upper layers of the epidermis, however, deeper infections are possible. Approximately 80–93% of chronic dermatophyte infections are thought to be caused by T. rubrum including Tinea pedis, Tinea unguium, Tinea manuum, Tinea cruris, Tinea corporis, some cases of tinea barbae have been also documented. Trichophyton rubrum has also been known to cause folliculitis in which case it is characterized by fungal element in follicles and and foreign body giant cells in the dermis. A T. rubrum infection may also form a granuloma, extensive granuloma formations may occur in patients with immune deficiencies (e.g. Cushing syndrome). Immunodeficient neonates are susceptible to systemic T. rubrum infection.

Trichophyton rubrum infections do not elicit large inflammatory responses as this agent suppresses cellular immune responses involving lymphocytes particularly T cells. Mannan, a component of the fungal cell wall can also suppress immune responses although the mechanism of action remains unknown. Trichophyton rubrum infection has been associated with the induction of an id reaction in which an infection in one part of the body induces an immune response in the form of a sterile rash at a remote site. The most common clinical forms of T. rubrum infection are described below.

Foot

Main article: Tinea pedis

Trichophyton rubrum is one of the most common causes of chronic tinea pedis commonly known as athlete's foot. Chronic infections of tinea pedis result in moccasin foot, in which the entire foot forms white scaly patches and infections usually affect both feet. Individuals with Tinea pedis are likely to have infection at multiple sites. Infections can be spontaneously cured or controlled by topical antifungal treatment. Although T. rubrum Tinea pedis in children is extremely rare, it has been reported in children as young as 2 years of age.

Hand

Main article: Tinea manuum

Tinea manuum is commonly caused by T. rubrum and is characterized by unilateral infections of the palm of the hand.

Groin

Main article: Tinea cruris

Along with E. floccosum, T. rubrum is the most common cause of this disease also known as jock itch. Infections cause reddish brown lesions mainly on the upper thighs and trunk, that are border by raised edge.

Nail

Main article: Onychomycosis

Once considered a rare causative agent, T. rubrum is now the most common cause of invasive fungal nail disease (called Onychomycosis or Tinea unguium). Nail invasion by T. rubrum tends to be restricted to the underside of the nail plate and is characterized by the formation of white plaques on the lunula that can spread to the entire nail. The nail often becomes thickens and brittle, turns the nail brown or black. Infections by T. rubrum are frequently chronic, remaining limited to the nails of only one or two digits for many years without progression. Spontaneous cure is rare. These infections are usually unresponsive to topical treatments and respond only poorly to systemic therapy. Although it is most frequently seen in adults, T. rubrum nail infections have been recorded in children.

Transmission

This species has a propensity to infect glabrous (hairless) skin and is only exceptionally known from other sites. Transmission occurs via infected towels, linens, clothing (contributing factors are high humidity, heat, perspiration, diabetes mellitus, obesity, friction from clothes). Infection can be avoided by lifestyle and hygiene modifications such as avoiding walking barefoot on damp floors particularly in communal areas.

Treatment

Treatment depends on the locus and severity of infection. For Tinea pedis, many antifungal creams such as miconazole nitrate, clotrimazole, tolnaftate (a synthetic thiocarbamate), terbinafine hydrochloride, butenafine hydrochloride and undecylenic acid are effective. For more severe or complicated infections, oral ketoconazole is an effective treatment for T. rubrum infections as this species exhibits greater susceptibility to this agent than other Trichophyton species. Oral terbinafine, itraconazole or fluconazole have also all been shown to be effective treatments. Terbinafine and naftifine (topical creams) have been successfully treated Tinea cruris and Tinea corporis caused by T. rubrum. Recently, general T. rubrum infection have been found to be susceptible to photodynamic treatment and laser irradiation.

Tinea unguium presents a much greater therapeutic challenge as topical creams do not penetrate the nail bed. Systemic griseofulvin treatment have shown improvements in some patients with Tinea unguium; however, treatment failure is common in lengthy treatment courses (e.g., > 1 yr). Current treatment modalities have advocated intermittent "pulse therapy" with oral itraconazole of terbinafine. Fingernail infections can be treated in 6-8 weeks while toenail infections may take up to 12 weeks to achieve cure. Topical treatment by occlusive dressing combining 20% urea paste with 2% tolnaftate have also show promise in softening the nail plate to promote penetration of the antifungal agent to the nail bed.