- A preview of this full-text is provided by Springer Nature.
- Learn more
Preview content only
Content available from Biological Trace Element Research
This content is subject to copyright. Terms and conditions apply.
Boric Acid Inhibition of Trichophyton rubrum Growth
and Conidia Formation
Martin Schmidt
1
Received: 28 February 2017 /Accepted: 4 April 2017 / Published online: 8 April 2017
#Springer Science+Business Media New York 2017
Abstract Trichophyton rubrum is a common human dermato-
phyte that is the causative agent of 80–93% of fungal infections
of the skin and nails. While dermatophyte infections in healthy
people are easily treatable with over-the-counter medications,
such infections pose a higher risk for patients with compromised
immune function and impaired regenerative potential.
The efficacy of boric acid (BA) for the treatment of vaginal yeast
infections prompted an investigation of the effect of BA on
growth and morphology of T.rubrum. This is of particular inter-
est since BA facilitates wound healing, raising the possibility that
treating athlete’s foot with BA, either alone or in combination
with other antifungal drugs, would combine the benefits of anti-
microbial activity and tissue regeneration to accelerate healing of
infected skin. The data presented here show that BA represses T.
rubrum growth at a concentration reported to be beneficial for
host tissue regeneration. Oxygen exposure increases BA toxicity,
and mycelia growing under BA stress avoid colonizing the sur-
face of the growth surface, which leads to a suppression of aerial
mycelium growth and surface conidia formation. BA penetrates
into solid agar matrices, but the relative lack of oxygen below the
substrate surface limits the effectiveness of BA in suppressing
growth of embedded T.rubrum cells.
Introduction
Superficial infections of the feet (tinea pedis) are a common
nuisance, affecting about 70% of the population at some time
in life. About 90% of tinea pedis cases are caused by derma-
tophytes of the Trichophyton genus, T.rubrum and T.
mentagrophytes [1]. These infections may cause pruritus, er-
ythema, maceration, and scaling of the skin and normally
respond well to standard over-the-counter treatments.
However, drug resistance of Trichophyton strains appears to
be on the increase and can lead to initial treatment failure [2].
Insulin resistance and associated comorbidities (e.g., micro-
vascular and neuropathic problems) aggravate the risk for
more serious Trichophyton infections that can proceed to in-
flammation, erosion, and predispose to secondary bacterial
infections of affected areas [3]. The increase in the prevalence
of diabetes in the population puts more individuals at risk for
complicated Trichophyton infections and increases their al-
ready high liability for permanent damage to the lower limb.
Boric acid (BA) is a mild antiseptic with an unclear mode
of action. It is currently only recommended as a second-line
treatment for complicated vulvovaginal yeast infections [4]
but has shown some promise in the treatment of otitis media
[5]. The use of BA solutions as antiseptic treatments can be
traced back to Lister’s pioneering work reported in 1875 [6]
and is often recommended in the non-scientific literature. For
tinea pedis, folk medicine recommends the use of pure boric
acid powder—but a scientific analysis of the actual effective
dose, required treatment times, and potential interactions with
other drugs has not been conducted. Recent systematic anal-
yses of the antimicrobial activity of BA emphasize the agent’s
value as an inexpensive, non-antibiotic alternative for micro-
bial control [7–9]. Importantly, there does not appear to be a
specific BA detoxification mechanism that could diminish the
agent’s therapeutic potential by giving rise to BA resistance.
Remarkably, in addition to its clear cytotoxic effects, BA
also has beneficial effects on eukaryotic tissues. It has been
demonstrated that in lower doses, BA stimulates the synthesis
of extracellular matrix glycoproteins and proteoglycans
*Martin Schmidt
mschmidt@dmu.edu
1
Department of Biochemistry and Nutrition, Des Moines University,
3200 Grand Avenue, Des Moines, IA 50312, USA
Biol Trace Elem Res (2017) 180:349–354
DOI 10.1007/s12011-017-1019-x
Content courtesy of Springer Nature, terms of use apply. Rights reserved.