Dermatophytosis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2]


Dermatophytes mode of transmission is direct (or)indirect contact with skin (or) scalp lesions of infected people,animals (or) fomites. Following transmission, the dermatophytes use proteases to adhere to the stratum corneum of the skin. Penetration by dermatophytes is achieved by secreting multiple serine-subtilisins and metallo-endoproteases (fungalysins) formerly called keratinases that are found only in the dermatophytes. Acutely, the host responds to fungal invasion by Type IV delayed type hypersensitivity reaction (also known as "Trichophytin reaction") leading to a cell mediated response. Fungus secreted proteases are one of the most important virulence factors of dermatophytes and are thought to be responsible for evasion from host defense mechanisms. Secreted subtilisin proteases expressed in the dermatophytes could play a role in keratin degradation. Dermatophyte infections of the skin surface (tinea corporis and tinea faciei) mostly present as erythematous, scaly papules that gradually progress to annular or circular red patches or plaques, with central clearing and scaling at the periphery. On microscopic examination of the skin, there may be neutrophils retained in the stratum corneum, parakeratosis, spongiosis and dermal edema.



After the inoculation in the host skin, suitable conditions favor the infection to progress through the following stages:



Host response


Gross Pathology

Tinea corporis, source:

Microscopic Pathology

The following features may be seen on microscopic examination of the skin in dermatophytosis:[12]

H&E section on skin showing the sandwich sign, source:
H&E section on skin showing the sandwich sign, source:
KOH prep of Tinea capitis infecting hair, source:
KOH prep of Tinea capitis infecting hair, source:


  1. Samdani AJ (2005). "Dermatophyte growth and degradation of human stratum corneum in vitro (pathogenesis of dermatophytosis)". J Ayub Med Coll Abbottabad. 17 (4): 19–21. PMID 16599028.
  2. Aljabre SH, Richardson MD, Scott EM, Rashid A, Shankland GS (1993). "Adherence of arthroconidia and germlings of anthropophilic and zoophilic varieties of Trichophyton mentagrophytes to human corneocytes as an early event in the pathogenesis of dermatophytosis". Clin. Exp. Dermatol. 18 (3): 231–5. PMID 8348716.
  3. 3.0 3.1 Vermout S, Tabart J, Baldo A, Mathy A, Losson B, Mignon B (2008). "Pathogenesis of dermatophytosis". Mycopathologia. 166 (5–6): 267–75. doi:10.1007/s11046-008-9104-5. PMID 18478361.
  4. 4.0 4.1 Dahl MV (1994). "Dermatophytosis and the immune response". J. Am. Acad. Dermatol. 31 (3 Pt 2): S34–41. PMID 8077506.
  5. Almeida SR (2008). "Immunology of dermatophytosis". Mycopathologia. 166 (5–6): 277–83. doi:10.1007/s11046-008-9103-6. PMID 18478362.
  6. Brasch J (2009). "Current knowledge of host response in human tinea". Mycoses. 52 (4): 304–12. doi:10.1111/j.1439-0507.2008.01667.x. PMID 19207841.
  7. 7.0 7.1 Tainwala R, Sharma Y (2011). "Pathogenesis of dermatophytoses". Indian J Dermatol. 56 (3): 259–61. doi:10.4103/0019-5154.82476. PMC 3132899. PMID 21772583.
  8. de Jonge R, Thomma BP (2009). "Fungal LysM effectors: extinguishers of host immunity?". Trends Microbiol. 17 (4): 151–7. doi:10.1016/j.tim.2009.01.002. PMID 19299132.
  9. Burmester A, Shelest E, Glöckner G, Heddergott C, Schindler S, Staib P, Heidel A, Felder M, Petzold A, Szafranski K, Feuermann M, Pedruzzi I, Priebe S, Groth M, Winkler R, Li W, Kniemeyer O, Schroeckh V, Hertweck C, Hube B, White TC, Platzer M, Guthke R, Heitman J, Wöstemeyer J, Zipfel PF, Monod M, Brakhage AA (2011). "Comparative and functional genomics provide insights into the pathogenicity of dermatophytic fungi". Genome Biol. 12 (1): R7. doi:10.1186/gb-2011-12-1-r7. PMC 3091305. PMID 21247460.
  10. Martinez DA, Oliver BG, Gräser Y, Goldberg JM, Li W, Martinez-Rossi NM, Monod M, Shelest E, Barton RC, Birch E, Brakhage AA, Chen Z, Gurr SJ, Heiman D, Heitman J, Kosti I, Rossi A, Saif S, Samalova M, Saunders CW, Shea T, Summerbell RC, Xu J, Young S, Zeng Q, Birren BW, Cuomo CA, White TC (2012). "Comparative genome analysis of Trichophyton rubrum and related dermatophytes reveals candidate genes involved in infection". MBio. 3 (5): e00259–12. doi:10.1128/mBio.00259-12. PMC 3445971. PMID 22951933.
  11. Stein DH (1998). "Tineas--superficial dermatophyte infections". Pediatr Rev. 19 (11): 368–72. PMID 9805462.
  12. Stein DH (1998). "Tineas--superficial dermatophyte infections". Pediatr Rev. 19 (11): 368–72. PMID 9805462.

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