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Tinea pedis: The etiology and global epidemiology of a common fungal

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ISSN: 1040-841X (print), 1549-7828 (electronic)

Crit Rev Microbiol, Early Online: 1–15

! 2014 Informa Healthcare USA, Inc. DOI: 10.3109/1040841X.2013.856853

REVIEW ARTICLE

Tinea pedis: The etiology and global epidemiology of a common fungal

infection
Macit Ilkit1 and Murat Durdu2
1
Department of Microbiology, Faculty of Medicine, University of Cukurova, Adana, Turkey and 2Department of Dermatology, Başkent University
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Adana Hospital, Adana, Turkey

Abstract Keywords
Tinea pedis, which is a dermatophytic infection of the feet, can involve the interdigital web Dermatophyte, epidemiology, Trichophyton
spaces or the sides of the feet and may be a chronic or recurring condition. The most common rubrum
etiological agents are anthropophiles, including Trichophyton rubrum sensu stricto, which is the
most common, followed by Trichophyton interdigitale and Epidermophyton floccosum. There has History
been a change in this research arena, necessitating a re-evaluation of our knowledge on the
topic from a multidisciplinary perspective. Thus, this review aimed to provide a solid overview Received 1 July 2013
of the current status and changing patterns of tinea pedis. The second half of the twentieth Revised 4 October 2013
century witnessed a global increase in tinea pedis and a clonal spread of one major etiologic Accepted 15 October 2013
agent, T. rubrum. This phenomenon is likely due to increases in urbanization and the use Published online 4 February 2014
of sports and fitness facilities, the growing prevalence of obesity and the aging population.
For optimal patient care and management, the diagnosis of tinea pedis should be verified by
For personal use only.

microbiological analysis. In this review, we discuss the epidemiology, clinical forms, compli-
cations and mycological characteristics of tinea pedis and we highlight the pathogenesis,
prevention and control parameters of this infection.

Introduction tinea pedis to be a rare infection caused by the same organism

that produced tinea capitis; however, the former frequently
Dermatophytosis, which is a fungal infection common
remained undiagnosed and was often treated inadequately
worldwide, occurs in all age and sex groups and more than
(Merlin et al., 1999).
70% of the population will experience this infection during
The reliable diagnosis and efficient treatment of tinea
their lifetime (Brooks & Bender, 1996). Over $500 000 000
pedis is important. First, tinea pedis mimics many dermato-
per year is spent globally on medications that target derm-
logic diseases of the foot (Brod et al., 2007; Lin et al., 2011).
atophytosis (Kane et al., 1997). Tinea pedis, an infection of
Second, tinea pedis is also an important reservoir for
the feet and toes, is the most common form of dermatophyt-
dermatophytosis in other parts of the body. This infection is
osis in the post-pubescent period; this condition is a public
often transmitted by autoinoculation, which causes the
health problem because of its contagious and recurrent nature
additional conditions of tinea manuum, tinea inguinalis and
(Merlin et al., 1999). Rippon (1988) revealed that 70% of the
tinea unguium (Daniel et al., 1997; Daniel & Jellinck, 2006;
population is infected with athlete’s foot or tinea pedis, at
Daniel & Lawson, 1987). Third, when inappropriate treatment
some point in their life. Although tinea pedis has afflicted
is received, it can lead to secondary bacterial infections and
humanity for centuries, it was first described by Pellizzari in
various allergic diseases (Al-Hasan et al., 2004; Woodfolk,
1888 (Pellizzari, 1888). Djélaleddin-Moukhtar (1892), a
2005). Last, tinea pedis is the most common entry point for
famous Ottoman Empire dermatologist in Paris, studied the
bacteria in cellulitis of the leg (Baddour & Bisno, 1985;
dermatomycotic infection known today as ‘‘tinea pedis et
Semel & Goldin, 1996) and is the most common cause of id
manuum’’ or ‘‘Celal Muhtar’’ disease. Terming the infection
reactions (Ilkit et al., 2012a). In this review, we aimed to
‘‘trichophytosis’’, Djélaleddin-Moukhtar (1892) described its
provide a broad update of the epidemiology, pathogenic
etiology, differential diagnosis, prognosis and therapy.
mechanisms, clinical forms and complications of tinea pedis.
Subsequently, Whitfield (1908) and also Sabouraud believed
In addition, we provide a comprehensive overview of accurate
and reliable diagnostic and management protocols as well as
prevention and control strategies for allergists, clinical
microbiologists, dermatologists, family physicians, general
Address for correspondence: Macit Ilkit, Department of Microbiology,
Faculty of Medicine, University of Cukurova, Adana 01330, Turkey. practitioners, infectious disease clinicians, public health
E-mail: milkit@cu.edu.tr workers and sports medicine specialists.
 2 M. Ilkit & M. Durdu
Methods
We searched PubMed/MEDLINE and Google Scholar for
clinical and mycological studies published in English (prior to
July 2013) using the following search terms: ‘‘tinea pedis’’,
‘‘athlete’s foot’’, and ‘‘foot diseases’’. We then reviewed the
retrieved reports to determine whether they should be
included in the present study. We excluded papers that
focused on other foot diseases, such as erythrasma, contact
dermatitis or pemphigus. The scope of this review is therefore
limited to tinea pedis studies and not all foot diseases are
discussed herein.
Taxonomy: current state
Dermatophytes are aligned with the family
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Arthrodermataceae, a monophyletic group of filamentous
fungi that are closely related to the dimorphic fungi in the
order Onygenales (most closely related to the genus
Coccidioides) and the class Eurotiomycetes. Three ana-
morphic (asexual or imperfect) dermatophyte genera
(Trichophyton, Microsporum and Epidermophyton) have
been described (Padhye & Summerbell, 2005; Weitzman &
Summerbell, 1995); however, the dermatophytes that are also
capable of reproducing sexually (i.e., able to produce
ascomata with asci and ascospores) are classified in the
teleomorphic genus Arthroderma (Weitzman et al., 1986).
Remarkably, all sexual and asexual dermatophytes are closely
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related and are members of Arthrodermataceae (Padhye &
Summerbell, 2005). Depending on their host preferences and
natural habitats, dermatophytes are also divided into three
ecological groups: anthropophiles, zoophiles and geophiles
(Padhye & Summerbell, 2005; Summerbell et al., 2007;
Weitzman & Summerbell, 1995).
The post-1999 modern systematics of dermatophytes
extensively improved and simplified our knowledge of any
given species in question and greatly increased our under-
standing of population genetics (Abdel-Rahman, 2008; Gräser
et al., 1999a, 2000a, b, 2008). Here, the two major etiologic
agents of tinea pedis, T. rubrum and T. interdigitale, are
discussed. T. rubrum sensu lato is comprised of two
anamorphic taxa, T. rubrum and T. violaceum. Furthermore,
T. rubrum, which was found to be genetically uniform,
includes several morphotypes (e.g., ‘‘raubitschekii’’ or
‘‘megninii’’). It has also been suggested that T. gourvilii,
T. soudanense and T. yaoundei are biologically equivalent to
T. violaceum but have been given different names (Gräser
et al., 2000a).
T. mentagrophytes sensu lato consists of anthropophilic
and zoophilic species; therefore, reliable identification is
essential for the selection of a relevant management strategy.
Currently, the T. mentagrophytes complex is designated as
follows: (i) the zoophilic T. mentagrophytes sensu stricto
(phylogenetically related to the teleomorphic species
Arthroderma simii), (ii) the zoophilic T. erinacei (hedgehog-
specific species), (iii) the zoophilic Trichophyton anamorph of
A. benhamiae (both related to A. benhamiae) and (iv) the
zoophilic and anthropophilic strains of T. interdigitale (related
to A. vanbreuseghemii). (Beguin et al., 2012; Gräser et al.,
1999a, 2008; Heidemann et al., 2010; Sun et al., 2010).
Beguin et al. (2012) also noted that some strains of
Crit Rev Microbiol, Early Online: 1–15
T. interdigitale belong to A. benhamiae, according to their
mating behavior and geographical origin.
Molecular studies have revealed that T. mentagrophytes is
only synonymous with the zoophilic subspecies T. menta-
grophytes var. quinckeanum. The anthropophilic subspecies of
T. mentagrophytes and many of the zoophilic strains were
formerly differentiated as var. ‘‘mentagrophytes’’ or var.
‘‘granulosum’’; however, these varieties are indistinguishable
from one another and are thus designated T. interdigitale,
which has a worldwide distribution (Beguin et al., 2012;
Gräser et al., 1999a, 2008; Heidemann et al., 2010; Trotha
et al., 2003). Differentiation between the zoophilic strains of
T. interdigitale and T. mentagrophytes is not possible using
conventional methods (Heidemann et al., 2010).
Emergence of T. rubrum and the T. mentagrophytes
complex
Anthropophilic dermatophytes are primarily associated with
humans and rarely infect other animals (Weitzman &
Summerbell, 1995). The changing incidence of dermatophyte
colonization and their associated dermatophytoses, as well as
their potential for spreading throughout the population,
became evident after the two world wars (Rippon, 1985).
The change in the dermatophyte spectrum over the last
century has been extensively reviewed (Philpot, 1977;
Rippon, 1985; Seebacher et al., 2008). Although the
anthropophiles T. rubrum, T. interdigitale and E. floccosum
are the major agents of tinea pedis, zoophiles and geophiles
have also been recovered from foot lesions, albeit less
frequently (Borman et al., 2007; Summerbell et al., 2007).
By the late 1960s, the anthropophilic species that cause tinea
pedis (T. rubrum and T. interdigitale) were solidly estab-
lished and tinea capitis had become a relatively rare infection
(Aly, 1994; Philpot, 1977; Rippon, 1985; Seebacher et al.,
2008). In addition, anthropophilic T. interdigitale has been
progressively replaced by T. rubrum as the primary etiologic
agent of tinea pedis and tinea unguium (Seebacher et al.,
2008). For example, in the British Isles, these two common
causes of foot infection comprised 80% of all dermatophytes
isolated in 1980 and 90% of the isolates in 2005 (Borman
et al., 2007). This trend is also typical in central and northern
Europe and is linked to the increased incidence of tinea pedis
(Seebacher et al., 2008). In Germany, T. rubrum increased
from 41.7% of all dermatophyte isolates in 1950 (Götz,
1952) to 82.7% in 1993 (Tietz et al., 1995). Although the
exact reasons for the predominance of these two organisms
remain unclear, their increased prevalence and continued
dominance may be related to genuine changes in lifestyle,
including increased urbanization and ready access to com-
munal sports facilities (Borman et al., 2007). Seebacher et al.
(2008) suggested that the predominance of T. rubrum could
be explained by the wide distribution of tinea pedis and tinea
unguium. Conversely, the relative prevalence of E. floccosum
decreased 11-fold from 1980 (7.31%) to 2000 (0.63%) in the
UK (Borman et al., 2007). However, a different spectrum of
dermatophytes was reported in an Iranian study in which
E. floccosum was the predominant dermatophyte species
(31.4%) over a three-year period (1999–2001) (Falahati
et al., 2003).
 DOI: 10.3109/1040841X.2013.856853
Sex in dermatophytes
Many fungi have the ability to reproduce both sexually and
asexually (Coppin et al., 1997). Fungi have been hypothesized
to preferentially clonally expand through asexual reproduction
in stable environmental niches; however, they may also
undergo genetic exchange via sexual reproduction in response
to stressful conditions, such as new environments or changes
in the human host, including the use of antimicrobial therapy
(Coppin et al., 1997; Nielsen & Heitman, 2007).
Sexual reproduction has also been reported in a large
number of dermatophytes, predominantly in geophilic spe-
cies, although the genomic basis of the mating type has not
been studied (White et al., 2008). Li et al. (2010) frequently
observed sexual reproduction in one geophilic dermatophyte
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(M. gypseum) but did not often observe it in zoophilic
(M. canis and T. equinum) or anthropophilic (T. rubrum and
T. tonsurans) dermatophytes. Sexual reproduction is particu-
larly rare in anthropophilic dermatophytes. However, the
identification of mating type (MAT) loci in five dermatophyte
species has indicated that most anthropophilic dermatophytes
retain a MAT locus and extant sexual or parasexual cycles.
Molecular typing strategies
With the introduction of molecular methods such as the
sequencing of the internal transcribed spacer (ITS) region for
the differentiation of dermatophytes, it has become clear that
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the phenotypes and genotypes of this group of fungi are not
always congruent (Gräser et al., 1999a, 2000a,b). According
to genetic and phylogenetic studies, dermatophytes are a
homogeneous group with recent evolutionary divergence,
despite their diverse morphological and host characteristics
(Gräser et al., 2006, 2008; Kanbe, 2008).
Ohst et al. (2004) identified two strains from among 124
isolates of T. rubrum using a single microsatellite marker
(T1). Gräser et al. (2007) described 55 unique genotypic
combinations in 233 isolates of T. rubrum and three multi-
locus genotypes in T. violaceum using seven microsatellite
markers, including the T1 marker. In one study, T. rubrum
tinea pedis isolates were inoculated onto a single plate and
two to five colonies per plate were typed using a PCR-based
analysis of repeats in the rRNA intergenic spacer.
Interestingly, each patient was colonized by only a single
isolate (Rad et al., 2005). Using PCR fingerprinting, 19
profiles were observed among 42 isolates of T. mentagro-
phytes var. interdigitale (Jackson et al., 2006). Several studies
have attempted to address numerous relevant clinical and
epidemiological questions concerning dermatophytes (Gräser
et al., 1999b, 2007; Guoling et al., 2006; Gupta et al., 2001;
Jackson et al., 2006; Ohst et al., 2004; Rad et al., 2005).
In general, molecular typing strategies are used to explore the
population structure and regional distribution of dermato-
phyte strains, such as T. rubrum (Abdel-Rahman, 2008).
The T. rubrum complex
Anthropophilic T. rubrum (Castellani) Semon 1910, which is
the most prevalent species of this complex, was first
discovered and described as Epidermophyton rubrum
(Castellani, 1910), after the other primary dermatophytes
Tinea pedis: common fungal infection 3
had already been recognized for several decades. T. rubrum
typically causes chronic infections and may have a tendency
to spread to other anatomical sites (Zaias & Rebell, 2003).
This species was suggested to have evolved in the late 19th
century as a cause of chronic tinea corporis from the endemic
areas of Southeast Asia. T. rubrum has since spread through-
out the world as the predominant etiological agent of tinea
pedis and tinea unguium (Rippon, 1988). Its prevalence is
related to increases in traveling, sporting events, the use of
occlusive footwear and the use of public facilities, such as
communal showers and swimming pools (Havlickova et al.,
2008; Lacroix et al., 2002; Seebacher et al., 2008; Weitzman
& Summerbell, 1995). Most notably, T. rubrum can survive
(without propagation) up to 18 months in its arthroconidial
form (Baer et al., 1955), which may be responsible for its
clonal spread. However, as noted by Rippon (1988), the
arthroconidia (hyphal fragments) of T. rubrum do not survive
as long as those of other species (e.g., E. floccosum).
For many years, no studies have identified any related
teleomorphic species suggestive of clonal reproduction
associated with the T. rubrum complex (Gräser et al., 2007).
In one study, Gräser et al. (1999b) analyzed 57 DNA loci
representing 12 markers of 96 T. rubrum strains and
remarkably, none of the methods revealed DNA polymorph-
isms, indicating a strictly clonal mode of reproduction
and a strong adaptation to human skin. This high degree of
morphological diversity contrasts with the homogeneity of the
genome, as revealed by anonymous DNA markers. T. rubrum
strains were later distinguished by polymorphisms in the
number of subrepeat elements in the ribosomal nontran-
scribed spacer region (Gupta et al., 2001; Jackson et al., 2000;
Rad et al., 2005). In addition, T. rubrum showed a wide
variety of phenotypic features, including the presence or
absence of reflexively branching hyphae, micro- and macro-
conidia, red colony pigmentation and urease activity, whereas
its genotype was reported to be stable (Guoling et al., 2006).
Subsequently, Gräser et al. (2007) verified this lack of
correlation between the multilocus genotypes and any of the
phenotypical characteristics. Within the T. rubrum complex,
although the urease-positive and granular T. raubitschekii are
more strongly associated with tinea corporis, cases of tinea
pedis have already been described (Kane, 1990). T. megninii
is almost exclusively confined to Portugal, Corsica and
Sardinia and has been recovered from a well-defined foot
lesion in a patient in Canada (Kane & Fischer, 1975).
Recently, the genome sequencing of T. rubrum and four
related species (T. equinum, T. tonsurans, M. canis and
M. gypseum) was described by Martinez et al. (2012).
The T. mentagrophytes complex
T. mentagrophytes (Robin) Blanchard 1853 was first
described in the follicles of a man’s beard (Robin, 1853).
This isolate likely corresponded to the granular type of the
species belonging to A. simii (Gräser et al., 1999a).
Subsequently, the T. mentagrophytes complex was shown to
be heterogeneous, containing several species and varieties
that broadly differ in their ecology and have a wide range of
hosts, including humans and animals (Beguin et al., 2012;
Georg, 1954; Gräser et al., 1999a; Heidemann et al., 2010;
 4 M. Ilkit & M. Durdu
Sun et al., 2010). Members of T. mentagrophytes sensu lato
frequently cause more inflammatory types of infections
compared with T. rubrum, which typically causes chronic
infections (Zaias & Rebell, 2003). The downy-type (cottony
and velvety) and granular-type isolates of T. mentagrophytes
sensu lato differ in their clinical, epidemiological and
virulence properties (Georg, 1954; Ota, 1933). The downy-
type isolates were primarily isolated from chronic, low-grade
infections and were more commonly involved in tinea pedis in
city dwellers, whereas the granular-type infections were more
acute and suppurative and were generally observed in rural
settings (Georg, 1954).
A decade ago, a deep absceding case of tinea barbae,
caused by a zoophilic strain of T. interdigitale, was also
reported (Trotha et al., 2003). Consistent with these findings,
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Sun et al. (2010) reported that the downy-type isolates from
human tinea pedis and onychomycosis shared the same
sequence as type CBS 428.63, the anthropophilic strain of
T. interdigitale, whereas the granular-type isolates of tinea
faciei, tinea capitis and tinea corporis were compatible with
the zoophilic strain of T. interdigitale (T. mentagrophytes
CBS 318.56). The authors recovered T. erinacei from only
two human cases, one with tinea faciei and the other with
tinea manuum, which were compatible with T. erinacei
CBS 511.73.
Epidemiology
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Several researchers have used different study sizes, designs
and target groups to examine the epidemiological character-
istics of tinea pedis and have found that its incidence is not
associated with a specific racial or ethnic group (Götz &
Hantschke, 1965; Ilkit et al., 2005; Lacroix et al., 2002;
Noguchi et al., 1995; Perea et al., 2000; Triviño-Duran et al.,
2005). The prevalence of tinea pedis increases with age and it
is more frequent in adults aged 31–60 years, followed by
adults aged 460 years (Drakensjö & Chyrssanthou, 2011;
Szepietowski et al., 2006); it is rare in children (Andrews &
Burns, 2008). The risk of tinea pedis has been shown to be
higher in men than in women (Drakensjö & Chyrssanthou,
2011) and it is more common in developed countries. It is
clear that certain occupational groups are exposed to a
particularly high risk of infection. For example, up to 72.9%
of miners (Götz & Hantschke, 1965), 58% of soldiers
(Noguchi et al., 1995) and 31% of marathon runners
(Lacroix et al., 2002) examined had mycologically proven
tinea pedis. The prevalence of tinea pedis was 29.5% in
mosque attendees (Ilkit et al., 2005). The exposure of these
specific populations to sweating, trauma, occlusive footwear
and communal areas predisposes these groups to an increased
incidence of tinea pedis (Field & Adams, 2008). In an elegant
study, Szepietowski et al. (2006) reported that tinea pedis was
the most common concomitant dermatomycosis, found in
33.8% of all of patients with toenail onychomycosis. The
authors noted that the interdigital subtype was the most
common form of tinea pedis and was present in 65.4% of
participants. In one study, the prevalence of palmoplantar
keratoderma in Sézary syndrome was reported to be 61.6%
and co-existing tinea pedis was present in 52.9% of partici-
pants (Martin & Duvic, 2012).
Crit Rev Microbiol, Early Online: 1–15
In a Spanish study, the prevalence of tinea pedis was
reported to be low (2.9%) in the general adult population;
however, participation in sports and the use of common
showers increased the risk of tinea pedis (p50.05) but not the
presence of concomitant diseases (e.g., diabetes mellitus,
psoriasis or vascular diseases) (p40.05) (Perea et al., 2000).
In line with this finding, a 40% prevalence of tinea pedis has
been reported in patients with pedal interdigital macerations,
although no meaningful difference was observed when
diabetic and non-diabetic participants were compared
(p40.05) (Legge et al., 2008). In addition, dermatophytes
which are strongly associated with the presence of tinea pedis,
have been isolated from normal-appearing toenails (Walling,
2009). Children are exposed to three primary sources
of infection: (i) families, (ii) schools and (iii) swimming
pools. In a previous study, tinea pedis was reported to have
prevalence rates of 6.6% and 1.6% in 11–14-year-old boys and
girls, respectively and 2.2% in 7–10-year-old boys (English &
Gibson, 1959). One study demonstrated that tinea pedis
(2.8%) had a higher prevalence than tinea capitis (0.23%) in
3–15-year-old children (Triviño-Duran et al., 2005).
Pathogenesis
Dermatophyte infections are caused by arthrospores or
asexually reproducing conidia. High temperatures, an alkaline
pH and hyperhidrosis facilitate pedal infections by these
organisms. Host factors that can enhance these infections
include broken skin, maceration of the skin and immunosup-
pression. However, Pseudomonas aeruginosa, transferrin,
natural killer cells and CD14-positive monocytes inhibit
fungal invasion (Brasch, 2009). The most common dermato-
phyte infections are due to the absence of sebum, which is a
natural inhibitory secretion; sebum is not present in the
plantar region due to the absence of sebaceous glands.
Dermatophytes release various enzymes (e.g. keratinases,
metalloproteases, cysteine dioxygenase and serine proteases),
produce lipases and ceramides and invade the superficial
keratin (Grumbt et al., 2013; Mendez-Tovar, 2010).
Keratinocytes not only constitute a physical barrier against
dermatophytes but also play a role in cutaneous immune
reactions (Tani et al., 2007). They express pattern recognition
receptors, such as Toll-like receptors (TLRs) and dectin-1,
which promote the release of various proinflammatory
cytokines and chemotactic factors and cause inflammatory
reactions, such as redness and swelling (Brasch, 2010).
Keratinocytes also release antimicrobial peptides, including
defensins, cathelicidins and psoriasin, which prevent fungal
invasion (Brasch, 2009; López-Garcı́a et al., 2006). The
release of beta-defensins is decreased in patients with atopic
dermatitis, which leads to frequent dermatophyte infections.
Dermatophyte infections are considered to be rare in psoriatic
patients; these individuals have no greater prevalence of tinea
pedis and tinea unguium compared to control patients
(p40.05) (Hamnerius et al., 2004).
Chemotactic factors recruit neutrophils and monocytes
(macrophages), which are inflammatory phagocytes that
engulf dermatophytes and release cytokines (Almeida,
2008). They also produce reactive oxygen species (ROS),
such as superoxide, hydrogen peroxides and hydroxyl
 DOI: 10.3109/1040841X.2013.856853
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For personal use only.
Figure 1. Pathogenesis of tinea pedis. IL, interleukin; TLR, Toll-like receptor; TNF, tumor necrosis factor; GM-CSF, granulocyte-macrophage colony-
stimulating factor; INF, interferon; Th, T helper; Tc, cytotoxic T-lymphocyte; B cell, plasma cell; CXCL-8F, chemokine receptors.
radicals, that result in damaged proteins, lipids and DNA,
thereby destroying the phagocytosed pathogens (Ozturk et al.,
2013). However, the cell wall mannans of T. rubrum decrease
the lymphoproliferative response (Mendez-Tovar, 2010).
Local fungal infections induce the production of circulating
antibodies and activate T-lymphocytes, leading to various
localized or generalized inflammatory reactions called ‘‘id
reactions’’ (Ilkit et al., 2012a). The pathogenesis of tinea
pedis is illustrated in Figure 1 (Brasch, 2010; Fritz et al.,
2012; Grumbt et al., 2013; Martinez et al., 2012; Tani et al.,
2007; Woodfolk, 2005).
Clinical forms
The importance of tinea pedis is two-fold: first, tinea pedis is
a common infection that is becoming more widespread over
time and second, the foot is a pedal fungal reservoir from
which fungi can spread elsewhere (Daniel & Jellinck, 2006;
Daniel & Lawson, 1987). Approximately one-third of patients
with tinea pedis have a concomitant nail infection
(Szepietowski et al., 2006). However, asymptomatic infec-
tions (occult tinea pedis) are common, with a prevalence
of 36-88%, particularly among athletes. Trichophyton
Tinea pedis: common fungal infection 5
interdigitale causes the majority of occult cases of tinea
pedis (Atteye et al., 1990; Auger et al., 1993; Kamihama
et al., 1997) and damp foot conditions may lead to aggravated
symptoms due to mixed infections with bacteria (Auger et al.,
1993). Patients are often unaware of tinea pedis and tinea
unguium and treatments are sometimes insufficient
(Watanabe et al., 2010). Tinea pedis typically presents in
four different forms: (i) interdigital, (ii) inflammatory (ves-
icular), (iii) chronic hyperkeratotic (moccasin) and (iv)
ulcerative.
Interdigital tinea pedis
The most common form is interdigital tinea pedis, which is
predominantly caused by T. rubrum followed by anthropo-
philic T. interdigitale (Havlickova et al., 2008). A more
common role of anthropophilic T. interdigitale among the
members of T. mentagrophytes sensu lato has been reported in
many parts of the world, such as Europe (Beguin et al., 2012;
Heidemann et al., 2010) and East Asia (Sun et al., 2010).
In contrast, T. mentagrophytes sensu stricto is very rare in
western Europe, at least and no association has been reported
with common pets such as guinea pigs, dogs or cats
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Figure 2. Clinical forms of tinea pedis. Interdigital scaling, maceration and fissuring in a patient with interdigital tinea pedis (A); an annular
erythematous scaly plaque on the back of the foot in a patient with tinea incognito (B); maceration with scaling borders between the toes in a patient
with dermatophytosis complex (C); scaling, crust and pustules on the plantar surface of a foot in a patient with vesicular tinea pedis (D); dry
hyperkeratotic scale involving the entire plantar surface in a patient with chronic hyperkeratotic tinea pedis (E); and erythematous scaly plaques in
‘‘two feet-one hand’’ syndrome (F).

(Heidemann et al., 2010). The primary risk factors for the
development of tinea pedis include hot humid climates,
sporting activities and hyperhidrosis (Caputo et al., 2001).
Clinically, interdigital tinea pedis is characterized by inter-
digital erythema, scaling, maceration and fissuring
(Figure 2A). Lesions are typically observed between the
fourth and fifth toes and are collectively called dermatophyt-
osis simplex. The most common reasons for clinical admis-
sion are itching, burning and malodor. The dorsal surface of
the foot is generally unaffected, but adjacent plantar areas
may be involved. If tinea pedis is mistakenly treated with
topical corticosteroids, the corticosteroids suppress the host
immune response, resulting in reduced inflammation and
pruritus. However, this immunosuppressive state leads to the
spread of the fungal infection (tinea incognito) (Glick &
Khachemoune, 2012) (Figure 2B). Extensive spreading to the
dorsum of the feet may be observed in patients with human
immunodeficiency virus (HIV) and in patients with T-cell
function disorders. Tinea pedis may also become resistant to
antifungal therapy in these immunosuppressed patients
(Al-Hasan et al., 2004). Corynebacterium minutissimum,
Gram-negative bacteria and Candida species can cause
interdigital erythema, scaling and maceration, which should
therefore be considered in the differential diagnosis (Lin
et al., 2011).
Interaction with bacteria is also possible in the toe cleft
spaces, with a clinically more severe bacterial infection
having a polymicrobial etiology (complex infection) (Leyden,
 DOI: 10.3109/1040841X.2013.856853
1993). Dermatophytosis complex may cause fissuring in the
interspaces, along with hyperkeratosis, leukokeratosis or
erosions (Al-Hasan et al., 2004; Gupta et al., 2005) (Figure
2C). In the general population, T. rubrum more commonly
causes the simplex interdigital and moccasin types of
infections, whereas the T. mentagrophytes complex causes
the complex interdigital and vesicular types of infections
(Brenner et al., 1994).
Inflammatory or vesicular (vesiculobullous) tinea
pedis
Inflammatory or vesicular tinea pedis, which is typically
caused by anthropophilic T. interdigitale, is characterized by
hard, tense vesicles, bulla and pustules on the instep or mid-
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anterior plantar surface (Figure 2D). The vesicular lesions
settle deep in the epidermis and they typically range in
diameter from 1 to 5 mm. A coalescence of the vesicles may
produce bullae, which are often clinically misdiagnosed. The
contents of the bullae are initially clear or lemon-yellow in
color but may become purulent upon superinfection, most
often with Staphylococcus aureus or group A Streptococcus
(Al-Hasan et al., 2004). The bullae appear in round,
polycyclic, herpetiform or serpiginous clusters with an
erythematous base and are localized to the arches of the
feet, sides of the feet, toes and subdigital creases. New
vesicles develop on the periphery, with fissures often
appearing in the cleft and subdigital creases. An infection
For personal use only.
of the sole by human-adapted forms of T. interdigitale can be
recognized by the formation of bullous vesicles particularly
on the thin skin of the plantar arch and along the sides of the
feet and heel adjacent to the thick plantar stratum corneum.
Trichophyton rubrum may also produce vesicular lesions, but
these lesions typically settle on the thick plantar surface of the
feet (Zaias & Rebell, 2003). The tops of the vesicles become
detached after a few days, likely because of abrasion,
exposing a red and oozing surface surrounded by a ring of
dry scales that detach readily. Itching may be severe, with
burning and pain and varying degrees of intensity and
inflammation may make walking difficult. These lesions
develop rapidly and typically occur during the summer. In
addition, lesions may be accompanied by a vesicular hyper-
sensitivity (dermatophytid or id) reaction. Occasionally, the
inflammatory response is incapacitating and includes cellu-
litis, adenopathy and lymphangitis (Grigoriu et al., 1987).
Chronic hyperkeratotic (moccasin) tinea pedis
Chronic hyperkeratotic or moccasin, tinea pedis, which is
typically caused by T. rubrum, is characterized by chronic
plantar erythema ranging from slight scaling to diffuse
hyperkeratosis. Typically, the dry hyperkeratotic scaling
may involve the entire plantar surface, extending to the
lateral foot, whereas the dorsal surface of the foot is usually
clear. However, in immunocompromised patients and patients
who receive topical corticosteroid therapy, lesions may spread
across the dorsal surface of the foot. The erythema is mild and
the condition may be asymptomatic; occasionally, however,
thick hyperkeratotic scales with fissures may develop.
Pruritus can be mild or severe and fissures can be painful
while walking (Grigoriu et al., 1987). One or both feet may be
Tinea pedis: common fungal infection 7
involved and the frequency of toenail infections increases
with the duration of the disease (Figure 2E). Approximately
50% of these patients have (only) one palm involved, which
leads to the ‘‘two feet-one hand’’ syndrome (Figure 2F).
Several nails of the involved hand may also be infected. The
clinical features of tinea manuum are similar to those of
moccasin tinea pedis; this syndrome is common, but the cause
of the unilateral involvement of the hands is unknown. In a
study of 80 patients with this syndrome (90% men and 10%
women), tinea was found to begin in the feet (Daniel et al.,
1997). One molecular study, which included 113 cases of
‘‘two feet-one hand’’ syndrome, showed that 94.5% of paired
isolates from the feet and the hand were composed of the
same species and that 80% of these pairs had the same
genotypes. This syndrome can be found in patients with
lowered immunocompetence, such as diabetics and the
condition is frequently associated with T. rubrum (Zhan
et al., 2010). Tinea manuum most likely develops as a result
of scratching the foot (Daniel et al., 1997).
Ulcerative tinea pedis
Ulcerative tinea pedis, which is typically caused by anthro-
pophilic T. interdigitale, is characterized by rapidly spreading
vesiculopustular lesions, ulcers and erosions and is often
accompanied by a secondary bacterial infection. The lesions
are usually macerated and have scaling borders. This infection
typically begins in the third and fourth interdigital spaces and
extends to the lateral dorsum and the plantar surface and
occasionally, large areas, even the entire sole, can be
sloughed. This type of tinea pedis is commonly observed in
immunocompromised and diabetic patients (Legge et al.,
2008). The most common complications are cellulitis,
lymphangitis, fever and malaise (Grigoriu et al., 1987).
In addition to these common forms, verrucous and pustular
forms have also been reported (Figure 3A and B). Qiangqiang
et al. (2001) reported the case of an 8-year-old boy with
verrucous tinea pedis caused by E. floccosum. The lesions
initially occurred on his right heel but spread to involve the
lower extremities. He was treated with oral ketaconazole for
four months. In another study, Hirschmann & Raugi (2000)
reported a 78-year-old man with pustular tinea pedis due to
T. rubrum. Bacterial cultures of his pustular lesions were
sterile and these lesions subsequently resolved within six
weeks of griseofulvin treatment.
Complications of tinea pedis
Tinea pedis can lead to several complications, including id
reactions, bacterial superinfection, Majocchi’s granulomas,
tinea incognito, lymphangitis and cellulitis and can spread to
the nails, other skin areas and scalp (Figure 4A and B)
(Degreef, 2008).
Cellulitis
The most common entry point for bacteria in cellulitis of the
lower extremities is tinea pedis, particularly the interdigital
type (Figure 4C). Two case-control studies have demonstrated
a significantly higher rate of tinea pedis in patients with
cellulitis (Baddour & Bisno, 1985; Semel & Goldin, 1996).
 8 M. Ilkit & M. Durdu Crit Rev Microbiol, Early Online: 1–15
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Figure 3. A verrucous plaque on the lateral side of the heel due to T. rubrum (A); dry, hyperkeratotic scale involving the entire plantar surface in a
patient with chronic hyperkeratotic tinea pedis and verrucous plaque (arrow) due to verruca plantaris (B).
For personal use only.

Figure 4. Complications from tinea pedis. Vesicles on the back of a foot from a patient infected with tinea pedis (A); an erythematous, scaly, crusted
patch on the back of the foot due to tinea pedis, with onychomycosis presenting as subungual hyperkeratosis of the ‘‘hallux’’ (B); maceration between
the toes from secondary tinea pedis in a patient with cellulitis presenting as erythema and edema of the leg and foot (C); and vesicles and crusts on the
wrists due to interdigital tinea pedis (D).
 DOI: 10.3109/1040841X.2013.856853
Although dermatophytes do not cause cellulitis, they lead to
scaling and fissuring, which impair the skin barrier and
provide a suitable niche for bacterial entry (Björnsdóttir et al.,
2005). Tinea pedis has also been associated with an increased
incidence of cellulitis in patients with saphenous venectomy.
In one study, 40 of 42 patients had tinea-pedis-associated
cellulitis following saphenous venectomy; however, add-
itional episodes were prevented by antifungal treatment
(Hirschmann & Gaugi, 2012). These studies have shown
that patients with lower-limb cellulitis should be examined for
tinea pedis and, if positive, that antifungal treatments should
be administered to prevent the development of recurrent
episodes. Furthermore, underlying causes, such as diabetes
mellitus, obesity and poor hygiene, should also be investi-
gated (Al-Hasan et al., 2004; Bristow & Spruce, 2009). In
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several patients with dermatophytosis complex, the genera of
Pseudomonas, Proteus and Klebsiella led to Gram-negative
cellulitis. In these patients, demonstration of the fungal
elements may be difficult because an excess of Gram-negative
bacteria may inhibit fungal growth, making it more difficult
to detect fungal pathogens upon potassium hydroxide (KOH)
examination. For this reason, bacterial cultures of the skin
may detect Gram-negative bacteria, but fungal cultures are
typically negative. Treatment of these underlying fungal and
Gram-negative bacterial infections can lead to faster improve-
ment of the cellulitis (Day et al., 1996).
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Id reaction
The id reaction is a type of secondary immunological reaction
caused by a local inflammatory infection at a distant site
(Figure 4D). Local infections activate circulating antibodies
or activated T-lymphocytes, leading to various localized or
generalized inflammatory reactions. Various fungal, bacterial,
viral and parasitic infections can cause id reactions (Ilkit
et al., 2012a); however, the most common cause is a
superficial fungal infection, particularly tinea pedis. The
incidence of dermatophytids due to tinea pedis has been
reported to be 17%. Dermatophytids are often observed on the
hands and sides of the fingers (Veien et al., 1994) and in some
patients, the lesions are initially dominated by vesicles and
bullae. Subsequently, papules or pustules appear at a second-
ary site, typically the fingers or palmar surfaces and the
interdigital spaces (Brlyd et al., 2003; Kaaman & Torssander,
1983; Veien et al., 1994). Generalized follicular papules have
rarely been reported (Iglesias et al., 1994).
Majocchi’s granuloma
Dermatophytes can invade the hair follicles and cause
perifollicular granulomatous inflammation or Majocchi’s
granuloma. Predisposing factors include the long-term use
of potent topical corticosteroids or chemotherapeutic agents
as well as systemic immunosuppression (Ilkit et al., 2012b).
The papules and nodules can occur alone or on the more
active borders of erythematous plaques. These lesions can
also mimic Kaposi’s sarcoma (Brod et al., 2007).
Asthma and atopic diseases
Dermatophytic infections may induce a T-helper type 2
response (Th2) that can aggravate atopy; therefore, these
Tinea pedis: common fungal infection 9
infections may complicate allergies and asthma and may
contribute to refractory atopic disease (Al-Hasan et al., 2004;
Woodfolk, 2005). Ward et al. (1989) described ‘‘Trichophyton
asthma’’ in 12 adult patients with chronic rhinitis and asthma,
demonstrating an immediate hypersensitivity to Trichophyton
spp. in 10 of the 12 patients. Mungan et al. (2001) showed that
the rates of sensitivity to T. rubrum were higher in patients
with intrinsic asthma than in the control groups and they
suggested that these patients should be examined for signs of
fungal infection and tested to determine their immediate
hypersensitivity to dermatophyte antigens. Furthermore,
superficial fungal infections can trigger atopic dermatitis
and antifungal treatment improves these dermatitis symptoms
(Klein et al., 1999).
Laboratory methods
In this review, we present a brief update on the practical
data and experiences of several groups. To avoid misdiag-
noses, the identification of dermatophytic infections
requires both a fungal culture and the microscopic exam-
ination of skin scrapings or culture-independent molecular
tools (Arabatzis et al., 2007; Bergmans et al., 2010; Verrier
et al., 2013). The collection, transport, storage and handling
of specimens; diagnostic techniques; and methods for the
identification of dermatophytes are well described in
several reviews (Robert & Pihet, 2008; Weitzman &
Summerbell, 1995) and textbooks (Kane et al., 1997;
Padhye & Summerbell, 2005; Rippon, 1988; Summerbell
et al., 2007).
In clinical practice, tinea pedis is treated by dermatologists,
family physicians and occasionally, general practitioners. With
the exception of dermatologists, tinea pedis is routinely
diagnosed without mycological information and its diagnosis
is typically based on clinical findings. However, tinea pedis
can mimic various vesiculobullous and scaly erythematous
diseases, such as psoriasis, herpetic infections, cellulitis,
contact dermatitis, erythrasma, impetigo, bacterial toe-web
infections, candidiasis and pemphigus (Figure 5) (Lin et al.,
2011; Sweeney et al., 2002). For this reason, a definitive
diagnosis requires some degree of laboratory analysis (Noble
et al., 1998). The diagnosis of tinea pedis is typically
confirmed by direct microscopic examination with KOH
preparations and by a fungal culture of skin scrapings;
however, there are several disadvantages to these methods,
including the false-positive result termed ‘‘mosaic fungus’’
(Padhye & Summerbell, 2005; Robert & Pihet, 2008;
Weitzman & Summerbell, 1995). Histopathological examin-
ation with periodic acid-Schiff (PAS) staining has been
successfully used (Noble et al., 1998) and the improved
sensitivity of molecular tools makes dermatophyte identifi-
cation possible when the fungus fails to grow in culture
(Verrier et al., 2013).
KOH examination is the first screening tool used to identify
fungal hyphae and spores. For an accurate microscopic
diagnosis, the sampling method is important. The lesions
should first be gently cleaned with a 70% alcohol swab to
remove traces of skin products or medications. The skin
scrapings should be made using a blunt scalpel (No. 15). If
multiple lesions are present, the region selected for the
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Figure 5. Differential diagnosis of tinea pedis. Coral-pink color fluoresces under a Wood’s lamp examination (A); maceration between the toes due to
erythrasma (B); plentiful ‘‘tadpole cells’’ without hyphae and bacteria in the Tzanck smear examination (C); a patient with contact dermatitis
mimicking vesicular tinea pedis (D); ‘‘dyskeratotic acantholytic cells’’ and cocci in the Tzanck smear test (E) in a patient with an erosive-
vesiculobullous lesion on the heel due to bullous impetigo (F); plentiful bacilli in a cytologic examination (G) of a maceration with green color between
the toes due to a toe-web infection with a Pseudomonas sp. (H); Tzanck smear examination revealing acantholytic cells (I) in a patient with vesicular
lesions of the feet due to pemphigus herpetiformis (J); Tzanck smear examination reveals acantholytic cells (K); maceration between the toes due to
Hailey-Hailey disease (L); cytology showing a multinucleated giant cell and acantholytic cells (M); a patient with zona zoster (herpes zoster)
mimicking vesicular tinea pedis (N); Tzanck smear test revealing intra- and extracellular Leishmania parasites (O); patient with cutaneous
leishmaniasis resembling infected tinea pedis (P); an erythematous plaque with pustules, vesicles and thickened scaly and brown crusts on the plantar
surface of the foot in a patient with palmoplantar pustulosis (Q); and peeling skin on the plantar surface of the foot in a patient with peeling skin
syndrome (R).

sampling is important because the active advancing border of
the lesion or the roof of the vesicle is preferred to old, loose
scales.
The obtained cellular material should be placed on a
microscopic slide and a 15–20% KOH solution should be
applied. After 15–30 minutes, the specimens can be examined
under a microscope. The presence of septated hyphae and
spores suggests the diagnosis of dermatophytic infections.
A positive result for fungal elements is sufficient to justify
starting treatment because identification of the dermatophytic
species does not typically affect the choice of treatment. The
addition of Parker blue ink, chlorazol black and rapid contrast
stains may facilitate the identification of hyphae and spores
(Lim & Lim, 2008). Although calcofluor white yields fewer
false-negative results compared to KOH, it requires a
fluorescent microscope, which limits its use in clinical
practice in undeveloped or developing countries (Markus
et al., 2001). However, most of the larger microbiology
laboratories (at least in the USA, UK, France, Germany and
Japan) possess such equipment.
Importantly, in macerated or erosive-vesiculobullous
lesions, Gram-negative bacterial co-infections contribute to
decreased culture sensitivity (Field & Adams, 2008) or it may
be difficult to detect fungal elements; therefore, negative
direct microscopic results do not exclude the possibility of
fungal infections. In these cases, a fungal culture is usually
used to detect the causative fungi (Noble et al., 1998).
Antifungal sulfur compounds secreted by some bacteria (such
 DOI: 10.3109/1040841X.2013.856853
as P. aeruginosa) and the displacement of dermatophytes by
Gram-negative bacteria decrease the rate of dermatophyte
isolation from tinea pedis lesions (Abramsom, 1981; Leyden
& Kligman, 1978). In these cases, a scraping smear can be
performed and the specimens can be stained with
Papanicolaou, Giemsa or methylene blue. Alcohol fixation
is required for the Papanicolaou stain (Durdu et al., 2011).
Whereas the staining procedure for the Papanicolaou stain is
longer, smears can be quickly stained by the May-Grünwald-
Giemsa stain (Woods & Walker, 1996). These cytological
staining methods are important for identifying secondary
dermatoses. However, the methylene blue stain shows poor
cytoplasmic and nuclear features (Durdu et al., 2011). In
suspected cases, confirmatory stains such as Gomori
methenamine silver (GMS) and PAS can be used (Powers,
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1998). Fungal hyphae and spores can also be visualized with
confocal microscopy, which is a noninvasive, painless, real-
time, reflectance imaging technique for the skin. Before
imaging, an isotonic sodium chloride solution is typically
applied to the skin for lens immersion and one drop of a 10%
KOH solution is then applied to the skin for easy visualization
of the fungal hyphae. This method is very expensive for the
diagnosis of tinea pedis; however, hand-held confocal micro-
scopes could be improved for routine clinical use in the future
(Markus et al., 2001).
Fungal culture is used extensively in many laboratories for
the routine diagnosis of tinea pedis (in combination with
For personal use only.
direct microscopic examination). In addition, many centers
routinely culture all dermatology specimens as this provides
invaluable epidemiological data concerning changes in
dermatophyte prevalence and the species spectrum. Indeed,
several studies have reported that only a small proportion of
samples are microscopy negative and culture positive
(Arabatzis et al., 2007; Borman et al., 2007; Levitt et al.,
2010; Verrier et al., 2013). Fungal culture is also important in
cases refractory to antifungal treatment. Although a fungal
culture is inexpensive, it is time-consuming and can require 2-
3 weeks to obtain positive results (Noble et al., 1998). Levitt
et al. (2010) showed that the KOH smear and fungal culture
are complementary diagnostic tools: the first test is very
sensitive, whereas the latter is more specific. A negative
culture does not always exclude tinea pedis. Rapidly culturing
dermatophytes from each toe web by hand (Sano et al., 2005)
or using several specific media that minimize the carryover
effect of topical antifungal medications (Adachi & Watanabe,
2007; Nakashima et al., 2002) have improved the diagnosis of
tinea pedis. Our group has also discussed the diagnostic value
of conventional techniques, including physiological tests
(Ates et al., 2008), improved conidia formation using several
laboratory media (Döğen & Ilkit, 2013; Ilkit et al., 2012c),
in vitro hair perforation tests (Gümral et al., 2013) and urease
activity (Ates et al., 2008).
When direct microscopic examination and culture are
negative, a histopathological examination can be performed to
narrow the differential diagnosis; although histopathology can
be adopted in certain cases, it is not standard procedure in
many microbiology laboratories. Three changes in the stratum
corneum can be associated with dermatophyte infections:
(i) the presence of neutrophils, (ii) compact orthokeratosis
and (iii) the presence of the ‘‘sandwich sign.’’ The last
Tinea pedis: common fungal infection 11
sign is characterized by hyphae between the upper normal
basket-weave stratum corneum and the lower layer of the
parakeratotic stratum corneum. The detection of fungal
elements is difficult when the histopathological examination
is performed using hematoxylin and eosin (H&E) stain. In
H&E-stained sections, hyphal elements are detected in only
57% of PAS-positive cases of tinea. Moreover, the number of
fungi observed in the horny layer is typically low and thus
may be easily overlooked, even when they are stained with
PAS or GMS (Weedon, 2010). If these confirmatory stains are
also negative, the histopathological findings may mimic
dyshidrotic dermatitis (Guarner & Brandt, 2011). For this
condition, tissue homogenate cultures and molecular-based
techniques, such as PCR, may be used to detect dermatophytic
fungi (Garg et al., 2009; Kanbe, 2008).
Nested PCR is not only rapid but also simple and
inexpensive in comparison to other molecular methods for
the detection of dermatophytes (Garg et al., 2009; Verrier et al.,
2013). The fungal pathogen can be identified within 48 hours
using a nested PCR/sequencing assay, whereas the results
from a culture require at least 2 weeks (Verrier et al., 2013).
Real-time PCR has also been successfully used to identify
dermatophytic fungi from clinical samples and from cultures
(Arabatzis et al., 2007; Bergmans et al., 2010), including
rare macroconidia-producing dermatophyte species (Yüksel &
Ilkit, 2012). Recently, a Matrix-Assisted Laser Desorption/
Ionization-Time-of-Flight Mass Spectroscopy (MALDI-TOF
MS) procedure was also successfully used for the identification
of clinical dermatophyte species (L’Ollivier et al., 2013).
Treatment
Tinea pedis can be treated with topical or oral antifungals or a
combination of both. Topical agents are used for 1–6 weeks,
according to the content of the antifungal medication. A
recent meta-analysis, which included a total of 135 rando-
mized controlled trials, showed no differences in antifungal
effects, safety or tolerability among antifungal classes (Rotta
et al., 2012). Terbinafine has been shown to be effective in
patients with interdigital tinea pedis after only 1 week of
treatment (Schäfer-Korting et al., 2008); however, patients
with hyperkeratotic tinea pedis should be treated for 4 weeks.
Topical ciclopirox has antidermatophytic, antibacterial and
anticandidal activities and is therefore particularly effective
against dermatophytosis complex (Gupta et al., 2005).
In patients with hyperkeratotic tinea pedis, antifungal
medications should be applied to the bottoms and sides of the
feet. Although interdigital tinea pedis may be asymptomatic,
patients should apply topical drugs to the interdigital areas
and to the soles of the feet because of the likelihood of
plantar-surface infection. Patients tend to stop using medica-
tions after the symptoms resolve, which leads to disease
recurrence. Patients may also be motivated to apply an
excessive quantity of topical medications (Friedrich, 2013).
Drying agents such as potassium permanganate or Burow’s
solution can be used for vesicular tinea pedis. Topical urea or
other keratolytic medications can be added for moccasin-type
tinea pedis (Shemer et al., 2010). If the lesions are inflamed,
topical antifungal and corticosteroid combination medications
can be used for a short period of time (Friedrich, 2013).
 12 M. Ilkit & M. Durdu
These combination drugs are more often chosen by non-
dermatologist physicians than by dermatologists (Smith et al.,
1998). However, patients with extensive chronic hyperker-
atotic tinea pedis or inflammatory and vesicular tinea pedis
typically require oral therapy, as do patients with concomitant
onychomycosis, diabetes, peripheral vascular disease or
immunocompromised conditions. A recent study of oral
treatments for tinea pedis revealed that terbinafine was more
effective than itraconazole and griseofulvin (Bell-Syer et al.,
2012). Itraconazole showed interactions with other medica-
tions, including HMG-CoA reductase inhibitors, calcium-
channel blockers, warfarin, cyclosporine, benzodiazepines
and certain anti-arrhythmic medications. In diabetic patients,
itraconazole interacted with oral hypoglycemic drugs and
increased the risk of hypoglycemia. Terbinafine, however,
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may be a safe choice for diabetic patients (Matricciani et al.,
2011). Furthermore, Ozcan et al. (2010) investigated the
dermatophyte species that cause tinea pedis and onychomy-
cosis as well as the in vitro susceptibility of these dermato-
phytes to terbinafine, itraconazole and fluconazole in patients
with non-insulin-dependent diabetes mellitus. They reported
that terbinafine was the most effective antifungal drug,
whereas fluconazole was the least effective antifungal drug.
They therefore suggested that terbinafine should be used for
dermatophytosis in patients with diabetes mellitus.
The early diagnosis and treatment of tinea pedis would
reduce the incidence of tinea unguium. Typically, this
For personal use only.
infection requires 3–12 months of treatment, rendering it
more cumbersome, difficult and expensive to treat than tinea
pedis (Perea et al., 2000).
Prevention and control
Although not life threatening, tinea pedis constitutes an
important public health problem because of its high preva-
lence in risk groups and its associated morbidity. The disease
can have certain negative consequences for patients, such as
itching and can potentially undermine work and social lives,
particularly in the aging population (Padhye & Summerbell,
2005; Weitzman & Summerbell, 1995). Tinea pedis is
transferred via infected skin scales and control may be
accomplished by educating infected individuals to avoid
contaminating surfaces by not walking barefoot on the floors
of homes or near swimming pools, public locker rooms and
public showers (Gentles, 1957; Gip, 1967; Weitzman &
Summerbell, 1995). Anthropophilic dermatophytes can sur-
vive at least 123 days in a chlorinated swimming pool at
temperatures of 28–31  C (Fisher, 1982). Measures that can
be taken to prevent tinea pedis include practicing good
personal hygiene (regular washing of the feet, thorough
drying and application of foot powder) and keeping the skin
dry and cool at all times. The sharing of socks, slippers, shoes
and towels with infected individuals should be avoided (Ilkit
et al., 2005; Padhye & Summerbell, 2005; Weitzman &
Summerbell, 1995). Excessive moisture and occlusion of the
feet can also be reduced by wearing sandals or ventilated
footwear (Padhye & Summerbell, 2005). In addition, ultra-
violet treatment using an ultraviolet C sanitizing device and
ozone gas reduce the fungal burden in shoes (Ghannoum
et al., 2012; Gupta & Britnell, 2013).
Crit Rev Microbiol, Early Online: 1–15
Textiles (e.g. socks, towels and bed linens) in contact with
infected skin can serve as carriers of a fungus (Bonifaz et al.,
2013; Hammer et al., 2012); conversely, antimicrobial fabrics
may contribute to controlling dermatophytes (Hammer et al.,
2012). Trichophyton rubrum can be transferred from con-
taminated to non-contaminated textiles during storage in a
laundry basket and during the domestic washing procedure at
30  C; however, washing at 60  C eliminates T. rubrum
(Hammer et al., 2011). The high prevalence of occult tinea
pedis (up to 55.1%) warrants antifungal treatment strategies
for the prevention of tinea pedis in the community
(Perea et al., 2000).
Conclusion
In the last five decades, tinea pedis has become a worldwide
epidemiological and economic problem with the predomin-
ance of T. rubrum. The chronic and contagious nature of tinea
pedis means that it will continue to be a medical concern in
the twenty-first century. This review highlights the discovery,
evolution, causes of spread and reproduction of the two major
etiological agents of tinea pedis, T. rubrum and T.
mentagrophytes sensu lato. Accurate clinical data, including
the appropriate diagnosis of the clinical forms of tinea pedis
and the reliable identification of the causative fungus, will
improve the education and knowledge of medical practitioners
in the field. Molecular tools, such as nested PCR, improve the
consistency and quality of diagnoses and patient care and are
required to obtain clues regarding the source of infection.
Treatment not only improves the symptoms of tinea pedis but
also prevents the risk of spread to other regions of the body,
thus reducing local and systemic complications. Although
tinea pedis constitutes one of the most frequent infectious
diseases in man, specific measures for its control have been
exercised only sporadically until now. Further studies with
emphasis on applying modern taxonomic concepts in a
clinical context will enhance our current understanding of the
field.
Acknowledgements
We appreciate and give our sincere thanks to the anonymous
reviewers for their critical comments on earlier drafts of this
paper. We also apologize to those whose studies could not be
included herein, as citation of the published literature was
selective due to space limitations.
Declaration of interest
The authors report no conflicts of interest. The authors alone
are responsible for the content and the writing of the paper.
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