FosterKW, GhannoumMA, ElewskiBE: Epidemiologic surveillance of cutaneous fungal infection in the United States from 1999 to 2002. J Am Acad Dermatol50: 748, 2004.1509795910.1016/S0190-9622(03)02117-0)| false
TostiA, PiracciniBM, LorenziS: Onychomycosis caused by nondermatophytic molds: clinical features and response to treatment of 59 cases. J Am Acad Dermatol42: 217, 2000.10.1016/S0190-9622(00)90129-410642676)| false
BontemsO, HauserPM, MonodM: Evaluation of a polymerase chain reaction-restriction fragment length polymorphism assay for dermatophyte and nondermatophyte identification in onychomycosis. Br J Dermatol161: 791, 2009.
BontemsO, HauserPM, MonodM: Evaluation of a polymerase chain reaction-restriction fragment length polymorphism assay for dermatophyte and nondermatophyte identification in onychomycosis. Br J Dermatol161: 791, 2009.1955859710.1111/j.1365-2133.2009.09291.x)| false
BaranR, KaoukhovA: Topical antifungal drugs for the treatment of onychomycosis: an overview of current strategies for monotherapy and combination therapy. J Eur Acad Dermatol Venereol19: 21, 2005.10.1111/j.1468-3083.2004.00988.x15649187)| false
FrassinettiS, FalleniA, Del CarratoreR: Effect of itraconazole on Staphylococcus aureus biofilm and extracellular vesicles formation. Microb Pathog147: 104267, 2020.3246430310.1016/j.micpath.2020.104267)| false
SimanskiM, ErkensAS, RademacherF, et al.: Staphylococcus epidermidis-induced interleukin-1 beta and human beta defensin-2 expression in human keratinocytes is regulated by the host molecule A20 (TNFAIP3). Acta Derm Venereol99: 181, 2019.
SimanskiM, ErkensAS, RademacherF, : Staphylococcus epidermidis-induced interleukin-1 beta and human beta defensin-2 expression in human keratinocytes is regulated by the host molecule A20 (TNFAIP3). Acta Derm Venereol99: 181, 2019.3032847110.2340/00015555-3073)| false
Background: Historically recalcitrant to treatment, infection of the nail unit is a pervasive clinical condition affecting approximately 10% to 20% of the US population; patients present with both cosmetic symptomatology and pain, with subsequent dystrophic morphology. To date, the presumptive infectious etiologies include classically reported fungal dermatophytes, nondermatophyte molds, and yeasts. Until now, the prevalence and potential contribution of bacteria to the clinical course of dystrophic nails had been relatively overlooked, if not dismissed. Previously, diagnosis had largely been made by means of clinical presentation, although microscopic examinations (potassium hydroxide) of nail scrapings to identify fungal agents and, more recently, panel-specific polymerase chain reaction assays have been used to elucidate causative infectious agents. Each of these tools suffers from test-specific limitations.
Methods: Molecular-age medicine now includes DNA-based tools to universally assess any microbe or pathogen with a known DNA sequence. This affords clinicians with rapid DNA sequencing technologies at their disposal. These sequencing-based diagnostic tools confer the accuracy of DNA-level certainty, and concurrently obviate cultivation or microbial phenotypical biases.
Results: Using DNA sequencing-based diagnostics, the results in this article document the first identification and quantification of significant bacterial, rather than mycotic, pathogens to the clinical manifestation of dystrophic nails.
Conclusions: In direct opposition to the prevailing and presumptive mycotic-based causes, the results in this article invoke questions about the very basis for our current standards of care, including effective treatment regimens.
Corresponding author: Stephanie C. Bishop, PhD, South University School of Pharmacy, 709 Mall Blvd, Savannah, GA 31406. (E-mail: firstname.lastname@example.org)