Trichophyton rubrum is a dermatophytic fungus in the phylum
Ascomycota, class Euascomycetes. It is an exclusively clonal,
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 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.
1 Growth and morphology
2 Diagnostic tests
Growth and morphology
Bottom view of a Sabouraud agar plate with a colony of Trichophyton
rubrum var. rodhainii.
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.
Strains of T. rubrum form two distinct biogeographical subpopulations.
One is largely restricted to parts of Africa and southern Asia, while
the other consists of a population that has spread around the world.
Isolates of the Afro-Asiatic subpopulation most commonly manifest
clinically as tinea corporis and tinea capitis. In contrast, the
globally-distributed subpopulation manifests predominantly in tinea
pedis and tinea unguium. 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. 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, 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.
Colonies of T. 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).
Colonies of T. mentagrophytes (left), T. rubrum (center) and T.
violaceum (right) showing differential responses on Bromocresol Purple
Milk Solids Glucose agar (7 d). T. 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
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. T. rubrum cannot be distinguished from other
dermatophytes in this direct examination. It can distinguished in
vitro from other dermatophytes by means of characteristic
micromorphology in culture, usually consisting of small,
tear-drop-shaped microconidia, as well as its usual blood-red colony
reverse pigmentation on most growth media. In addition, the
Bromocresol purple (BCP) milk solid glucose agar test can be used to
distinguish it. Different
Trichophyton species release different
amounts of ammonium ion, altering the pH of this medium. In this test,
medium supporting T. rubrum remains sky blue, indicating neutral pH,
until 7 to 10 days after inoculation. In primary outgrowth on
Sabouraud dextrose agar with cycloheximide and antibacterials,
contaminating organisms may cause confusion, as T. rubrum colonies
deprived of glucose by competing contaminants may grow without forming
the species' distinctive red pigment. Both antibiotic-resistant
bacteria and saprotrophic fungi may outcompete T. rubrum for glucose
if they contaminate the sample. Red pigment production can be restored
in such contaminated isolates using casamino acids erythritol albumin
agar (CEA). T. rubrum cultures can be isolated on both
cycloheximide-containing media and cycloheximide-free media. The
latter are conventionally used for the detection of nail infections
caused by non-dermatophytes such as Neoscytalidium dimidiatum. A
skin test is ineffective in diagnosing active infection and often
yields false negative results.
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 in many parts of the developed world are
thought to be caused by T. rubrum including cases of tinea pedis,
tinea unguium, tinea manuum, tinea cruris, and tinea corporis, as well
as some cases of tinea barbae.
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. 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 strong 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.
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 two years of age.
Tinea manuum is commonly caused by T. rubrum and is characterized by
unilateral infections of the palm of the hand.
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
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 thickens and becomes brittle, turns 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 to
systemic therapy. Although it is most frequently seen in adults,
T. rubrum nail infections have been recorded in children.
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
revealed the presence of heat shock proteins, transporters, metabolic
enzymes and a system of up-regulation of key enzymes in the glyoxylate
cycle. The species secretes more than 20 different proteases,
including exopeptidases and endopeptidases. These proteases allow
T. rubrum to digest human keratin, collagen and elastin; they 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.
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 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 was historically shown to be an effective treatment for
T. rubrum infections but is no longer used for this indication due to
the risk of liver damage as a side effect. Oral terbinafine,
itraconazole or fluconazole have all been shown to be safer, effective
Terbinafine and naftifine (topical creams) have been
successfully treated tinea cruris and tinea corporis caused by T.
Trichophyton rubrum infections have been found to be
susceptible to photodynamic treatment, laser irradiation, and
photoactivation of rose bengal dye by green laser light.
Tinea unguium presents a much greater therapeutic challenge as topical
creams do not penetrate the nail bed. Historically, systemic
griseofulvin treatment showed improvements in some patients with tinea
unguium; however, failure was common even in lengthy treatment courses
(e.g., > 1 yr). Current treatment modalities include oral
terbinafine, oral itraconazole, and intermittent "pulse therapy" with
oral itraconazole 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 shown promise in softening
the nail plate to promote penetration of the antifungal agent to the
^ Gräser, Y; Kühnisch, J; Presber, W (1999). "Molecular markers
reveal exclusively clonal reproduction in
Journal of Clinical Microbiology. 37 (11): 3713–7.
PMC 85735 . PMID 10523582.
^ a b Zaugg, C; Monod, M; Weber, J; Harshman, K; Pradervand, S;
Thomas, J; Bueno, M; Giddey, K; Staib, P (2009). "Gene expression
profiling in the human pathogenic dermatophyte
during growth on proteins". Eukaryotic cell. 8 (2): 241–50.
doi:10.1128/EC.00208-08. PMC 2643602 .
^ William Williams, The Principles and Practice of Veterinary Surgery,
p.734, W.R. Jenkins, 1894, from the collection of the University of
^ a b c d e Gräser, Y; Scott, J; Summerbell, R (2008). "The new
species concept in dermatophytes-a polyphasic approach".
Mycopathologia. 166 (5–6): 239–56. doi:10.1007/s11046-008-9099-y.
^ Makimura, Koichi; Tamura, Y; Mochizuki, T; Hasegawa, A; Tajiri, Y;
Hanazawa, R; Uchida, K; Saito, H; Yamaguchi, H (1999). "Phylogenetic
Classification and Species Identification of
Based on DNA Sequences of Nuclear Ribosomal Internal Transcribed
Spacer 1 Regions". Clinical Mycology. 37: 920–924.
PMC 88625 . PMID 10074502.
^ a b c d e f g h i j Kane, Julius (1997). Laboratory handbook of
dermatophytes : a clinical guide and laboratory handbook of
dermatophytes and other filamentous fungi from skin, hair, and nails.
Belmont, CA: Star Pub. ISBN 978-0898631579.
^ Youssef, N; Wyborn, CH; Holt, G (March 1978). "Antibiotic production
by dermatophyte fungi". Journal of General Microbiology. 105 (1):
105–111. doi:10.1099/00221287-105-1-105. PMID 632806.
^ a b c d e f g h i Weitzman, I; Summerbell, RC (1995). "The
dermatophytes". Clinical Microbiology Reviews. 8 (2): 240–59.
PMC 172857 . PMID 7621400.
^ a b Dahl, MV; Grando, SA (1994). "Chronic dermatophytosis: what is
Trichophyton rubrum?". Advances in dermatology. 9:
97–109; discussion 110–1. PMID 8060745.
^ a b c d e f g h i j k DiSalvo, Edited by Arthur F. (1983).
Occupational mycoses. Philadelphia, Pa.: Lea and Febiger.
ISBN 978-0812108859. CS1 maint: Extra text: authors list
^ a b c d e f Kwon-Chung, K.J.; Bennett, John E. (1992). Medical
mycology. Philadelphia: Lea & Febiger.
^ a b El-Gohary, M; van Zuuren, EJ; Fedorowicz, Z; Burgess, H; Doney,
L; Stuart, B; Moore, M; Little, P (2014). "Topical antifungal
treatments for tinea cruris and tinea corporis". The Cochrane Database
of Systematic Reviews. 8: CD009992.
doi:10.1002/14651858.CD009992.pub2. PMID 25090020.
^ doctorfungus.org/thefungi/trichophyton.php. Missing or empty
title= (help); Missing or empty url= (help)
^ Huang, H (20 June 2017). "Effect of intense pulsed light on
Trichophyton rubrum growth in vitro". Nan Fang Yi Ke Da Xue Xue Bao.
37 (6): 853–857. PMID 28669966.
^ Vural, Emre; Winfield, Harry L.; Shingleton, Alexander W.; Horn,
Thomas D.; Shafirstein, Gal (2007). "The effects of laser irradiation
Trichophyton rubrum growth". Lasers in Medical Science. 23 (4):
349–353. doi:10.1007/s10103-007-0492-4. PMID 17902014.
^ Cronin, L; Moffitt, M; Mawad, D; Morton, OC; Lauto, A; Stack, C
(June 2014). "An in vitro study of the photodynamic effect of rose
bengal on trichophyton rubrum". Journal of biophotonics. 7 (6):
410–7. doi:10.1002/jbio.201200168. PMID 23125143.
^ De Doncker, P; Decroix, J; Piérard, GE; Roelant, D; Woestenborghs,
R; Jacqmin, P; Odds, F; Heremans, A; Dockx, P; Roseeuw, D (January
1996). "Antifungal pulse therapy for onychomycosis. A pharmacokinetic
and pharmacodynamic investigation of monthly cycles of 1-week pulse
therapy with itraconazole". Archives of Dermatology. 132 (1): 34–41.
doi:10.1001/archderm.132.1.34. PMID 8546481.
^ Gupta, AK; Daigle, D; Paquet, M (17 July 2014). "Therapies for
Onychomycosis: A Systematic Review and Network Meta-Analysis of
Mycological Cure". Journal of the American Podiatric Medical
Association. 105: 140717071850003. doi:10.7547/13-110.1.
Fungal infection and mesomycetozoea (B35–B49, 110–118)
Tinea = skin;
endothrix) = hair
Tinea barbae/tinea capitis
Tinea pedis (athlete's foot)
White superficial onychomycosis
Distal subungual onychomycosis
Proximal subungual onychomycosis
Tinea corporis gladiatorum
Coccidioides immitis/Coccidioides posadasii
Primary cutaneous coccidioidomycosis. Primary pulmonary
Primary cutaneous histoplasmosis
Primary pulmonary histoplasmosis
Progressive disseminated histoplasmosis
North American blastomycosis
South American blastomycosis
Congenital cutaneous candidiasis
Erosio interdigitalis blastomycetica
Allergic bronchopulmonary aspergillosis
Primary cutaneous aspergillosis
Fonsecaea pedrosoi/Fonsecaea compacta/Phialophora verrucosa
Conidiobolus coronatus/Conidiobolus incongruus
Enterocytozoon bieneusi/Encephalitozoon intestinalis
Granuloma gluteale infantum