Trichophyton rubrum is a dermatophytic fungus in Ascomycota phylum, class Euascomycetes. This is an exclusive, clonal anthroprophic saprotroph that colonizes the top layers of dead skin, and is the most common cause of athlete's foot, nail fungus infections, itchy athletes, and ringworm all over the world. Trichophyton rubrum was first described by Malmsten in 1845 and is now considered a complex species consisting of many geographically motivated morphotypes, some of which have been formally described as different taxa, including T. raubitschekii , T. gourvilii , T. megninii and T. soudanense .
Video Trichophyton rubrum
Growth and morphology
Typical isolates of T. rubrum are white and seedy on the surface. The colonies below are usually red, although some of the isolates appear to be more yellowish and others are more brownish. Trichophyton rubrum grows slowly in culture with the faint production of teardrops or laterally wedge-shaped microconidia on a fertile hyphae. Macroconidia, currently, is smooth and shaped like a club, although most of the isolates are deficient in macroconidia. Growth is inhibited by the presence of certain sulfur, nitrogen, and phosphorus-containing compounds. Isolates from T. rubrum are known to produce penicillin in vitro and in vivo .
Variant
The strain T. rubrum forms two distinct biogeographic subpopulations. One of these is largely confined to parts of Africa and southern Asia, while others are composed of populations that have spread throughout the world. Afro-Asiatic subpopulation is most commonly manifested clinically as tinea corporis and tinea capitis. In contrast, globally distributed subpopulations manifest mostly in tinea pedis and tinea unguium. Different members of the complex T. rubrum are endemic in various regions; the isolates formerly called T. megninii are from Portugal, while T. soudanense and T. gourvilii are found in Sub-Saharan Africa. All species belonging to the complex T. rubrum are the "-" type of marriage with the exception of the T. megninii representing "" marriage and auxotropic for L -histidine. The identity of the mating type from T. soudanense is still unknown. Trichophyton raubitschekii, commonly from northwestern India and Southeast Asia and parts of West Africa, is characterized by very granular colonies and is the only variant in the complex that reliably produces urease.
Maps Trichophyton rubrum
Diagnostic test
As a preliminary test showing infection, picked hair and skin and nail scrapings can be directly seen under a microscope to detect the fungus. T. rubrum can not be distinguished from other dermatophytes in this direct examination. It can distinguish in vitro from other dermatophytes by characteristic micromorphology in culture, usually consisting of small tear-shaped microcidias, as well as red blood colonic pigment in most growing media.. In addition, the purple Bromocresol milk glucose glucose test (BCP) can be used to differentiate it. Various species of Trichophyton emit different ammonium ions, changing the pH of this medium. In this test, the support being T. rubrum remains sky blue, indicating a neutral pH, up to 7 to 10 days after inoculation. In the main growth of Sabouraud dextrose agar with cycloheximide and antibacterial, contaminated organisms may cause confusion, such as
T. rubrum colonies lacking glucose by competing contaminants can grow without forming a species-specific red pigment. Antibiotic-resistant bacteria and saprotrophic fungi can beat T. rubrum for glucose if they contaminate the sample. Red pigment production can be recovered in contaminated isolates using casamino erythritol albumin (CEA) acid. T. rubrum can be isolated on media containing cycloheximide and cycloheximide-free media. The latter is conventionally used to detect nail infections caused by non-dermatophytes such as Neoscytalidium dimidiatum . Skin testing is not effective in diagnosing active infection and often results in false-negative results.
Pathology
Trichophyton rubrum is rarely isolated from animals. In humans, men are more often infected than women. Infection can manifest as a chronic and acute form. Typically T. rubrum infection is limited to the epidermal upper layers; however, deeper infections may occur. About 80-93% of chronic dermatophyte infections in many parts of the developing world are estimated to be caused by T. rubrum including tinea pedis, tinea unguium, tinea manuum, tinea cruris and tinea corporis cases, as well as some cases of tinea barbae. Trichophyton rubrum has also been known to cause folliculitis characterized by fungal elements in the follicles and giant bodies of foreign bodies in the dermis. A T. rubrum infection can also form granulomas. Extensive granuloma formation may occur in patients with immune deficiency (eg Cushing's syndrome). Immunodeficient neonates are susceptible to systemic T. rubrum infection.
Trichophyton rubrum does not cause a strong inflammatory response, as it suppresses cellular immune responses involving T cell lymphocytes. Mannan, the fungal cell wall component, may also suppress the immune response, although the mechanism of action is still unknown. Trichophyton rubrum infection has been associated with induction of an id reaction in which infection in one part of the body induces an immune response in the form of a sterile rash in a remote place. The most common clinical form of T. rubrum is described below.
Leg
Trichophyton rubrum is one of the most common causes of chronic tinea pedis commonly known as athlete's foot. Chronic tinea pedis infections cause moccasin feet, where the entire foot forms scaly white patches and the infection usually affects both legs. Individuals with tinea pedis tend to have infections on some sites. Infection can be spontaneously cured or controlled by topical antifungal treatments. Although tinea pedal tinea pedis in children is very rare, it has been reported in children aged two years. Hands
Tinea manuum is commonly caused by T. rubrum and is characterized by a unilateral palm infection.
Groin
Along with E. floccosum , T. rubrum is the most common cause of this disease, also known as 'jock itch.' Infection causes reddish brown lesions mainly in the upper thighs and stems, which border on raised edges.
Nail
Having been considered a rare cause agent, T. rubrum is now the most common cause of invasive fungal nail disease (called onikomikosis or tinea unguium). Nail invasion by T. rubrum tends to be limited to the bottom of the nail plate and is characterized by the formation of white plaque on the lunula which can spread throughout the nail. Nails often thicken and become brittle, turn brown or black. Infection by T. rubrum is often chronic, remaining confined to one or two-digit nails for years without development. Spontaneous healing is rare. This infection is usually unresponsive to topical treatment and responds only to systemic therapy. Although most commonly seen in adults, T. rubrum nail infections have been noted in children.
Epidemiology
It is thought that Trichophyton rubrum evolved from a zoophilic ancestor, in itself an exclusive agent of dermatophytosis in the human host. Genetic analysis of T. rubrum has revealed the presence of heat shock proteins, transporters, metabolic enzymes and key enzyme regulation systems in the glyoxylate cycle. This species emits more than 20 different proteases, including exopeptidase and endopeptidase. This protease allows T. rubrum to digest human keratin, collagen and elastin; they have an optimal pH of 8 and depending on calcium. Although T. rubrum shares phylogenetic affiliations with other dermatophytes, it has a typical protein regulatory system.
Transmission
This species has a tendency to infect bald (not hairy) skin and is only very well known from other sites. Transmission occurs through an infected towel, linen, clothing (contributing factors are high humidity, heat, sweat, diabetes mellitus, obesity, friction from clothing). Infection can be avoided by lifestyle modification and hygiene such as avoiding barefoot walking on the wet floor especially in communal areas.
Treatment
Treatment depends on locus and severity of infection. For tinea pedis, many antifungal creams such as miconazole nitrate, clotrimazole, tolnaftate (synthetic thiocarbamate), terbinafine hydrochloride, butenafine hydrochloride and undecylenic acid are effective. For more severe or complicated infections, oral ketoconazole has historically proven to be an effective treatment for T. rubrum infection but is no longer used for this indication because of the risk of liver damage as a side effect. Oral terbinafine, itraconazole or fluconazole have all been shown to be safer, effective treatments. Terbinafine and naftifine (topical cream) have been successfully treated tinea cruris and tinea corporis caused by T. rubrum . Trichophyton rubrum infections have been found to be susceptible to photodynamic treatments, laser irradiation, and photoactivation of rosy dye roses by green laser beams.
Tinea unguium presents a much larger therapeutic challenge because topical creams do not penetrate nails. Historically, systemic griseofulvin treatment showed improvement in some patients with tinea unguium; However, failure often occurs even in long treatment programs (eg, & gt; 1 yr). Current treatment modalities include oral terbinafine, oral itraconazole, and intermittent "pulse therapy" with oral yeast itraconazole fungal infections can be treated in 6-8 weeks while nail infections may last up to 12 weeks to achieve healing. Topical treatment with an occlusive dressing that incorporates a 20% urea paste with 2% tolnaftate has also been promising in softening the nail plate to encourage penetration of the antifungal agent to the nail bed.
References
Source of the article : Wikipedia
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