Athlete's foot pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]

Overview

Athlete's foot is caused by a parasitic fungus and is a communicable disease.[1] It is typically transmitted in moist environments where people walk barefoot, such as showers, bath houses, and locker rooms.[2][3][1] It can also be transmitted by sharing footwear with an infected person, or less commonly, by sharing towels with an infected person.

Pathophysiology

Transmission

  • The various parasitic fungi that cause athlete's foot can also cause skin infections on other areas of the body, most often under toenails (onychomycosis) or on the groin (tinea cruris). It is transmitted even by sharing footwear.

Pathology

  • Majority of the cases of athlete's foot are caused by Trichophyton rubrum. But other organisms such as Epidermophyton floccosum, Trichophyton interdigitale, Trichophyton mentagrophytes are also implicated in development of tinea pedis.
  • Trichophyton tonsurans has been identified as a cause of tinea pedis infections in children. [4]
  • The fungi cause breakdown of superficial skin through secretion of enzymes called keratinises which dissolve keratin.[5]
  • The fungal cell wall of dermatophytes also contain mannans which diminish the body's inflammatory response by decreasing antigen presenting and processing.[6]
  • It is interesting to note thatTrichophyton rubrum often causes chronic and long drawn infection due to increased production of mannans which decrease the turnover and proliferation of keratinocytes.[7]
  • The dermatophytes thrive in a moist and damp environment. Maceration, superficial tears in the skin and chronic occlusive footwear usage for long periods of time increase the chance of getting infected.
  • Several innate factors such as transferrin, beta globulins and sebum have a growth-inhibitory effect on these fungi. Transferrin, particularly the unsaturated form inhibits growth by binding iron which is required for growth and propagation of dermatophytes. [8]
  • A poor immune system such as in immunocompromised individuals also is a predilection for infection with tinea spp.[9]

Histopathology of Tinea pedis

Scrapings of skin affected with tinea pedis prepared with KOH show the following features.

  • Hyperkeratosis
  • Acanthosis
  • Perivascular infiltrate

References

  1. 1.0 1.1 Causes of athlete's foot, at WebMD
  2. "Athlete's foot". Mayo Clinic Health Center.
  3. [1] Risk factors for athlete's foot, atWebMD
  4. Hiruma J, Ogawa Y, Hiruma M (2015). "Trichophyton tonsurans infection in Japan: epidemiology, clinical features, diagnosis and infection control". J Dermatol. 42 (3): 245–9. doi:10.1111/1346-8138.12678. PMID 25736317.
  5. Sharifzadeh A, Shokri H, Khosravi AR (2016). "In vitro evaluation of antifungal susceptibility and keratinase, elastase, lipase and DNase activities of different dermatophyte species isolated from clinical specimens in Iran". Mycoses. 59 (11): 710–719. doi:10.1111/myc.12521. PMID 27291045.
  6. Weitzman I, Summerbell RC (1995). "The dermatophytes". Clin Microbiol Rev. 8 (2): 240–59. PMC 172857. PMID 7621400.
  7. Dahl MV, Grando SA (1994). "Chronic dermatophytosis: what is special about Trichophyton rubrum?". Adv Dermatol. 9: 97–109, discussion 110-1. PMID 8060745.
  8. King RD, Khan HA, Foye JC, Greenberg JH, Jones HE (1975). "Transferrin, iron, and dermatophytes. I. Serum dematophyte inhibitory component definitively identified as unsaturated transferrin". J Lab Clin Med. 86 (2): 204–12. PMID 1151148.
  9. Dai Y, Xia X, Shen H (2019). "Multiple abscesses in the lower extremities caused by Trichophyton rubrum". BMC Infect Dis. 19 (1): 271. doi:10.1186/s12879-019-3897-3. PMC 6425592. PMID 30894136.


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