Tinea corporis B35.4

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Synonym(s)

circulatory herpes; Dartre furfuracées arrondies (Alibert); Dartres furfuracees arrondies; dermatophyte infection; dermatophytosis; Eccema marginatum (Hebra); fungal infection; impetigo figurata; ringworm; ringworm of the body; squarrus circumscriptum (Gruby); superficial trichophytia corporis; Trichophytia of the hairless skin

Definition
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Mostly chronic, superficial, inflammatory or non-inflammatory tinea of the hairless skin with centrifugal spread.

Pathogen
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The frequency of certain pathogens varies from continent to continent.

In Europe mainly Trichophyton rubrum, Trichophyton mentagrophytes, also Epidermophyton floccosum are detected. S.a.u. Dermatophytes. The Tinea corporis gladiatores is mostly caused by T. tonsurans.

In a larger Persian study, the frequency of the pathogen was found as follows: Trichophyton verrucosum (40.6%), Trichophyton mentagrophytes (17.6%), Trichophyton violaceum (12%)

In an Indian study, the most common was Trichophyton mentagrophytes (63%) followed by Trichophyton rubrum (35%).

Etiopathogenesis
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Frequently infection by domestic animals (cats, cattle, guinea pigs, hamsters - see also zoonoses).
Initially described as folliculitis resulting from the penetration of the fungus into the follicleostium and hair follicles.

The infection spreads exclusively in the stratum corneum with consecutive (optional) infestation of further hair follicles (formation of follicular papules).

Clinically, an inflammatory, slightly scaly, red, roundish plaque with centrifugal expansion and central healing tendency is observed.

As the infection progresses, several such foci may confluent and form polycyclic, large, map-like figures.

Manifestation
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Frequently occurring in children, but also in adults.

Localization
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face ( Tinea faciei), neck ( Tinea colli ), trunk, extremities ( Tinea corporis ), feet/hands( Tinea pedis, Tinea manuum), genital area

Clinical features
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Initially, a circumscribed folliculitis develops as a result of the penetration of the fungus into the follicleostium and hair follicles (clinically rarely observed). The infection spreads exclusively in the stratum corneum and infests other hair follicles.

In general, one or more inflammatory reddened, slightly scaly, border-emphasized plaques with a centrifugal expansion tendency appear at the initial diagnosis. Inflammatory follicular papules are often included.

As the infection progresses, several foci may confluent and form polycyclic, large, map-like figures with central healing.

There is almost always a marked itching, which often leads to pre-treatment with corticosteroids and thus obscures the clinical inflammatory pattern of tinea.

Less frequent is the development of a tinea profunda which is caused by an excessive inflammatory reaction of the organism to the dermatophyenic infection of the skin (analogous to the Kerion Celsi of the capillitium). Clinically impressive are inflammatory, moderately painful, frequently verrucous plaques and nodules which may be interspersed with follicular pustules (see also Granuloma trichophyticum) . Majocchi granuloma is described as granulomatous and pustular tinea caused by Trichophyton rubrum. Nodular abscesses are found mainly in immunocompromised persons.

Under prolonged and severe immunosuppression an erosive and necrotizing tinea corporis is observed, often complicated by a superimposed superinfection by Staphylococcus aureus.

Histology
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Mild to moderate acanthosis of the surface epithelium (see Fig. A-B) with focal cancellous bone disease and parakeratosis. In early stages of infection a rather sparse perivascular lymphocyte infiltrate with papillary oedema, focal epitheliotropy and cancellous vesicles to spongiotic vesicles is found. During prolonged persistence, increasing exocytosis of neutrophil granulocytes, which may condense sub- or intracorneally to small neutrophil abscesses. In the upper dermis there is a dense diffuse, sometimes perivasally accentuated lymphocytic infiltrate with few neutrophils and eosinophilic granulocytes.

In PAS staining (if no antifungal pretreatment has been performed) mycelia can be detected in varying densities at the border between the stratified ortho- and parakeratosis zones.

If the density of mycelia in the stratum corneum and in the follicular keratin is unusual, immunosuppression should be considered.

Differential diagnosis
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  • Clinical differential diagnoses:
    • Eczema, nummular: Eczematous plaques without prominent border stress; mostly disseminated, no mycelia in the PAS preparation.
    • Seborrhoeic eczema: No itching; in marginal plaques these are indistinguishable from tinea corporis by differential diagnosis! Typical is the recurrent course of the disease with aggravation in the winter months and possibly complete healing under summer, maritime climate. This course completely excludes a tinea corporis. Neither culturally nor histologically, mycological pathogen detection is successful.
    • Psoriasis vulgaris: Typical plaque psoriasis as important DD. The prying out phenomenon is always negative in tinea corporis!
    • Parapsoriasis en plaques: No stress on the edges, usually no scaling. Pseudoatrophy! No itching!
    • Mycosis fungoides: No accentuation of the edges; initially little or no itching; histology is diagnostic!
    • Erythema anulare centrifugum: Very prominent anular configurations; mostly free of scales. Itching is absent or very mild. The marginal zone is very clearly indurated (wet wool thread). Neither culturally nor histologically a mycological pathogen detection is possible.
    • Early syphilis: Syphillis are usually accompanied by swelling of the LK. Distribution pattern: Often infestation of palms and face. Serology is conclusive! Histology is groundbreaking (plasmacellular dermatitis).
  • Histological differential diagnoses (often difficult to distinguish from tinea and to evaluate definitively only in the context of the clinical picture; good clinical data are therefore important):
    • Acute and subacute eczema: spongiosis, extensive parakeratosis, in atopic eczema possible prominent eosinophilia. Often indistinguishable.
    • Psoriasis vulgaris: The acanthosis is usually more pronounced than in tinea. Extensive hyper- and parakeratosis with neutrophil inclusions. The histological picture is very similar. No evidence of mycelia.
    • Parapsoriasis en plaques: Fibrosis of the papillary stratum. The surface epithelium is rather atrophic. Epidermotropy is present. Hardly any spongiosis. No parakeratosis!
    • Impetigo contagiosa: Subcorneal fissure formation with accumulation of neutrophilic granulocytes. No evidence of mycelium!
    • Pityriasis rosea: Non-specific superficial dermatitis with moderate acanthosis. Sometimes erythrocyte extravasations appear, which are missing in tinea. No mycelia.
    • Allergic contact dermatitis: Clinically clearly distinguishable! Prominent, flat spongiosis; acanthotic surface epithelium; long hills of parakeratosis. Histological differentiation can only be made in connection with clinical data.
    • Erythema anulare centrifugum: Histological differentiation only in connection with clinical data! Mostly dense perivascular infiltrate sheaths.
    • Early syphilis: interface dermatitis with psoriasiform epidermal reaction. Dense, band-shaped infiltrate in the upper and middle dermis (lymphocytes, histiocytes and plasma cells. Extension of the infiltrate to the deep vascular plexus.

Therapy
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Antimycotic therapy with topical antimycotics. In case of extensive infestation or resistance to therapy, additional antimycotic systemic therapy, see below tinea.

General therapy
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For extensive mycoses:

Terbinafine systemic: In Switzerland and Austria Terbinafine is approved for oral use in children, in Germany however not yet (off-label use). A careful documentation and education of parents about the off-label use and the effect of Terbinafine in studies should be carried out.

The following dosage recommendations apply: Children with 10-20 kg bw: 62.5 mg/day; 21-40 kg bw: 125 mg/day; > 40 kg bw: 250 mg/day. 2-3 weeks of therapy are usually sufficient.

Alternatively: Itraconazole 100mg p.o./day (Sempera®) over a period of 2-4 weeks.

Alternative: Fluconazole 50mg p.o./day (Diflucan®) over a period of 2-7 weeks.

Progression/forecast
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Highly inflammatory forms have a tendency to spontaneous healing. If left untreated, the course is generally highly chronic. Quoad vitam always favourable.

Naturopathy
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In some naturopathic approaches, the use of tea tree oil recipes is recommended as a support. S.a.u. Tea Tree Oil.

Aftercare
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In order to avoid recurrences, local treatment, especially of tinea pedis, should be continued for about 3-4 weeks beyond clinical healing until the dormant arthrospores are eliminated by the physiological renewal process of the skin with the upper layers of the stratum corneum.

Note(s)
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Occupational disease Dermatomycosis: Dermatophyte infections transmitted from animals to man may be recognised and compensated as occupational diseases in accordance with point 3102 of the list of occupational diseases, provided that a causal link with the occupational activity can be demonstrated (see occupational disease of the skin) Infectious diseases that are transmitted from person to person and affect insured persons who work in the health care system or are exposed to a similar degree to the risk of infection through another activity can be compensated in accordance with BK number 3101.

Fungus detection. In individual cases, the inspection of the entire integument by means of UV light (wood light) has also proved useful for detecting clinically only discretely affected areas with certain dermatophytes or Malassezia species.

Tinea genitalis as venereal disease (especially in tropical zones): Trichophyton interdigitale can be transmitted during sexual intercourse. It can lead to massive infections, especially in patients who shave regularly in the genital area (damage to the epidermal barrier).

Literature
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  1. Angerstein JH (1977) How tea tree oils heal. With formulations for the most common complaints. Midens publishing house, Augsburg
  2. Bhatia VK et al (2014) Epidemiological studies on dermatophytosis in human patients in Himachal Pradesh, India. Springerplus. 3:134
  3. Chadeganipour M et al (2015) A 10-Year Study of Dermatophytosis in Isfahan, Iran. J Clin Lab Anal doi: 10.1002/jcla.21852
  4. Kassem MA et al (2007) Efficacy of topical griseofulvin in treatment of tinea corporis. Mycoses 49: 232-235
  5. Leiva-Salinas M et al (2014) Tinea capitis in schoolchildren in a rural area in southern Ethiopia. Int J Dermatol 54: 800-805
  6. Luchsinger I et al (2015) Tinea genitalis: a new entity of sexually transmitted infection? Case series and review of the literature. Sex Transm Infect 91:493-496.
  7. Seebacher C et al. (2007) Tinea of the free skin. J Dtsch Dermatol Ges 11: 921-926
  8. Thakur R (2015) Spectrum of dermatophyte infections in Botswana. Clin Cosmet Investig Dermatol 8:127-133
  9. Wilmer A et al (1998) Systemic terbinafine treatment of dermatophytoses in children. Mycoses 41: 54-57
  10. Young Woon Park et al (2014) Clues' for the Histological Diagnosis of Tinea: How Reliable Are They?
    Ann Dermatol 26:286-288

Disclaimer

Please ask your physician for a reliable diagnosis. This website is only meant as a reference.

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Last updated on: 29.10.2020