By Ted Rosen
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Additional resources for Dermatologic Clinics (Infectious Diseases, Volume 21, Number 2, April 2003)
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Colonies of species causing human infection are fast growing and white to pale purple, pale tan, or (less commonly) orange on the surface, with colony reverse colors becoming vinaceous, purple, tea brown, chestnut red – brown, orange, or (rarely) carmine on potato dextrose agar [29]. Many isolates rapidly form typical canoe-shaped, multi-celled macroconidia with a distinctive foot cell within 7 to 14 days on potato dextrose or specialized Fusarium media [29]. Nearly all human pathogenic species also form copious single-celled, ellipsoidal, club- or sausage-shaped microconidia.
Baran and Dawber’s Diseases of the Nails and their management. Oxford, UK: Blackwell Science Ltd; 2001. p. 129 – 71. [11] Tosti A, Baran R, Piraccini BM, et al. ‘‘Endonyx’’ onychomycosis: a new modality of nail invasion by dermatophytes. Acta Derm Venereol 1999;79:52 – 3. [12] Baran R, Hay R, Haneke E, et al, editors. Onychomycosis the current approach to diagnosis and therapy. UK: Martin Dunitz; 1999. p. 10 – 9. [13] Gupta AK, Elewski BE. Nondermatophyte causes of onychomycosis and superficial mycoses.
Some organisms such as Scytalidium species produce infections that clinically mimic the signs and symptoms seen in dermatophyte infections. Correct identification becomes imperative because many non-dermatophyte molds respond poorly to therapy [1]. Unlike tinea unguium, non-dermatophyte onychomycosis is often diagnosed inaccurately. In such cases, stringent criteria are required for the attribution of etiology to non-dermatophyte molds and yeasts. Direct microscopic examination (ie, potassium or sodium hydroxide, or, alternatively, histopathology) is mandatory.
Dermatologic Clinics (Infectious Diseases, Volume 21, Number 2, April 2003) by Ted Rosen
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