Selected skin diseases located on the feet
Tinea pedis (ringworm of the feet, athlete’s foot)
is the most common dermatophyte infection in the developed world. Three main factors
constitute the basis of any tinea pedis infection; warmth, moisture and friction. Tinea
pedis does not affect barefoot people. Shoes, in particular plastic and occluded, create a
milieu for dermatophytes to prosper. Tinea pedis is most often caused by anthropophilic
subspecies of Trichophyton; T. rubrum and T. mentagrophytes (interdigital). These agents
can be transmitted directly from person to person as well as by the scales harbouring the
fungus shed on a carpeted floor or in shared shoes. Tinea pedis may present in
several clinical forms:

Jacyk WK, MD Department of Dermatology, University of Pretoria |
INTRODUCTION
The spectrum of diseases presented in this article covers benign common conditions with
variable aetiology as well as some diseases caused by fungi, viruses, bacteria and
ectoparasites. (SA Fam Pract 2004;46(1): 37-41)
A. FUNGAL INFECTIONS
Tinea pedis (ringworm of the feet, athlete’s foot) is the most common dermatophyte
infection in the developed world. Three main factors constitute the basis of any tinea
pedis infection; warmth, moisture and friction. Tinea pedis does not affect barefoot
people. Shoes, in particular plastic and occluded, create a milieu for dermatophytes to
prosper. Tinea pedis is most often caused by anthropophilic subspecies of Trichophyton; T.
rubrum and T. mentagrophytes (interdigital). These agents can be transmitted directly from
person to person as well as by the scales harbouring the fungus shed on a carpeted floor
or in shared shoes. Tinea pedis may present in several clinical forms:
1. Interdigital, intertriginous form (toe web infection, classic athlete’s
foot) (Figure 1)

Figure 1. Interdigital tinea pedis |

Figure 2. Tinea pedis affecting the dorsal aspects of the feet |
This is the most common and usually the initial presentation of tinea pedis. The third
and fourth interdigital spaces are most frequently involved. Often discrete scaling or
slight maceration are the only signs. In other cases there is more pronounced inflammation
with redness, vesiculation, desquamation and maceration. If the condition is left
untreated it may extend to other interdigital clefts, soles and even to the dorsum of the
feet (Figure 2). Tinea pedis may be complicated by superinfection with bacteria,
lipophilic diphtheroides, staphylococcus aureus and haemolytic streptococci.
2. Squamous, hyperkeratotic form (“moccasin” type) (Figure 3)

Figure 3. Hyperkeratotic form of tinea pedis |
This type is characterised by erythematous and scaly lesions affecting the soles, heels
and sides of the feet. In extensive involvement, prominent hyperkeratosis with fissures
leads to a “moccasin” presentation. Trichophyton rubrum is usually grown in this
dry-type of infection.
3. Vesiculobullous form
It is more inflamed with vesicles and blisters and it extends from the web spaces to the
dorsum of the foot and to the soles. The inducing agent is usually T. mentagrophytes. The
most common complication of ordinary tinea pedis is Gram-negative toe web infection, which
can occasionally be extremely inflammatory to the point of causing disability. A vesicular
eruption (ide reaction) can develop at a distant site from the feet, most often on the
palms and inner aspects of the fingers. It is an allergic reaction and occurs in acute,
exudative forms of tinea pedis.
The differential diagnosis of tinea pedis is vast and includes candidal, mould and
bacterial infections, foot eczema and acral psoriasis.
Management of tinea pedis requires in addition to topical and/or systemic antifungal
therapy the maintenance of a dry local environment and avoidance of occlusive footwear.
Socks, preferably made of cotton should be changed frequently and shoes should be
alternated.
The morphology of the skin lesions dictates the type of the vehicle to be used; sprays,
lotions, creams, or ointments. Both feet have to be treated even if the changes in one are
clinically not apparent.
The list of available effective topical preparations is long, and includes either
imidazoles or terbinafine.
The interdigital and vesiculobullous types of tinea pedis usually respond well to
topical therapy. The medication is usually applied twice daily. The minimum period of
topical treatment has never been clearly determined.
Patients with the hyperkeratotic type of tinea pedis constitute a more difficult group to
treat and an orally active antimycotic is often needed. Intraconazole 100 mg daily is
recommended for four weeks. Other treatment schedules have also been suggested 400 mg
daily for one week or a pulse of 200 mg daily for a week, each month for 3-4 months.
Terbinafine appears particularly useful in infections caused by T. rubrum – 250 mg
once daily for two weeks.
B. CANDIDIASIS OF THE FEET
Candida albicans often affects the intertoe clefts. As in tinea pedis the cleft between
the third and fourth toe is most often affected. Lesions are usually characteristically
white with erosions and fissures (Figure 4). The process is usually more acute than that
due to dermatophytes, there is itch and often pain. The inflammation initially confined to
the clefts can later spread beyond this area. Treatment of candidal infection of the feet
is the same as for acute or subacute forms of tinea pedis. Imidazoles and nystatine are
the most useful agents, terbinafine is much less effective.

Figure 4. Interdigital changes caused by Candida |
C. NON-DERMATOPHYTIC INFECTIONS OF THE FEET
Scytalidium hyalinum and Scytalidium dimidiatum (Hendersonula toruloidea),
non-dermatophytic moulds, can produce pictures very similar to dermatophyte-induced tinea
pedis (and tinea unguium). These agents may imitate in particular infections attributed to
T. rubrum. The frequency of infections with these agents appears to grow worldwide, as
well as in Africa.
Kambila et al.1 found Scytalidium dimidiatum responsible for 34% of cases of
tinea pedis in Gabon and Gugnani and Oyeka for 10% in Nigeria. 2 There are no
data from South Africa.
It is quite likely that an apparent lack of success in the treatment of tinea pedis (and
unguium) in some cases in South Africa can be explained by the fact that the infection is
due to these non-dermatophytic moulds. These agents are generally considered resistant to
itraconazole and terbinafine. Culture is therefore indispensable and should be performed
on media with and also without cycloheximide (actidion), since this agent inhibits the
growth of Scytalidium species. It is important to remember this and to advise the
mycologist when sending the material.
D.SKIN CHANGES ON THE FEET CAUSED BY ECTOPARASITES
Larva migrans
Cutaneous larva migrans is a selflimiting skin eruption caused most often by larvae of
dog and cat hookworms (Ancylostoma caninum and Ancylostoma braziliense, respectively).
These hookworms reside in the intestines of these domestic animals and their ova are shed
with faeces. Under favourable conditions of humidity and temperature the ova hatch into
infectious larvae, which may penetrate human skin. Cutaneous larva migrans is most
frequent in warmer climates in shady areas and beaches. In humans, larvae are not able to
complete their natural cycle and remain confined to the skin. When they migrate through
the skin, release of larval secretions produces a local inflammatory reaction. The route
of larvae migration is manifested by a wandering threadlike line (creeping eruption),
which is severely pruritic (Figure 5).

Figure 5. Larva migrans |
The feet are often affected. The process ends with the death of the larvae, which takes
place between 1 and 3 months in the majority of cases.
The treatment of choice is oral administration of albendazole.3 The dose of
400 mg once or twice daily for 3 days is effective. Cryotherapy with liquid nitrogen
seldom kills the larvae. The larval tract reflects an allergic reaction to the larva and
does not indicate its actual location.
Tungiasis
Tungiasis is caused by the sand flea (Tunga penetrans). It occurs in tropical regions,
including South Africa.
Only the impregnated female of that flea is a menace to humans. She burrows into the
skin of a man or other mammal and deposits the eggs. Lesions are found most often on the
feet, under the toenails, between the toes and on the heels (Figure 6).

Figure 6. Tungiasis |
The uncomplicated lesion is a small nodule with a dark central point, which often still
contains the distended egg-filled abdomen of the flea. Often there is an erythematous halo
and swelling. The itch is often severe. The numbers of lesions vary. This clear picture
is, however, seldom seen. Secondary infection usually ensues with development of pustules
and suppurative ulcers. When the lesions are multiple, crusting gives the area a honeycomb
appearance. Lymphangitis, cellulitis, regional lymphadenitis are common.
In uncomplicated cases treatment consists of removing the flea. In cases with secondary
infection the parasite can be killed by application of chloroform. Pyoderma is treated in
the standard way.
E. VIRAL WARTS (Figures 7, 8, 9)
Viral warts, or infection with human papilloma viruses, are often located on the feet.
Those on the dorsal aspect are usually common warts and much less often juvenile plane
warts.

Figure 7. Mosaic plantar warts |

Figure 8. Plantar warts, deep, myrmecia type |
Their biology and management do not differ from that of warts in other locations. Warts
situated on the volar (plantar) aspect of the feet constitute a separate subgroup, caused
by specific strains of human papilloma virus and require often a different therapeutic
approach. The details are contained in my recent review on warts.4

Figure 9. Multiple common warts on the dorsal aspects of the feet |
F. PITTED KERATOLYSIS
Pitted keratolysis or keratosis plantare sulcatum is infection of the horny layer of the
sole and volar aspect of the toes.
It is caused by a species of Corynebacterium. The lesions consist of shallow,
punched-out circular pits ranging from 1-6 mm in diameter, often coalescing to form larger
depressed areas of a few cm (Figure 10).

Figure 10. Pitted keratolysis |
Pitted keratolysis is often asymptomatic but may cause pain and have an offensive
odour. Hyperhidrosis is usually present. Pitted keratolysis occurs most often in a
tropical environment with high humidity in people wearing occluded shoes. Management
consists of removing the patient from a chronically wet environment and application of a
variety of topical preparations – topical antibiotics (2% Fucidin ointment or cream,
2% Erythromycin topical solution). Control of associated hyperhidrosis with 5% formalin
solution or 40% formalin ointment also helps.
G. FOOT ECZEMA
Various types of eczema occur on the feet. Contact forms, irritant or allergic, occur
more often than atopic.
1. Contact foot eczema
In contact eczema the dorsal aspects of the feet are mainly affected but plantar
surface, heels and toes can also be involved. The involvement of the dorsum of the foot
points to allergens in shoe uppers or lining – shoe dermatitis (Figure 11).

Figure 11. Contact dermatitis |
The process usually starts at the dorsal surface of the big toes and spreads to the
dorsa of the feet and the other toes. The most common allergens provoking allergic contact
eczema of the feet are tanning agents, such as chromates, glutaraldehyde, rubber chemicals
and adhesives. Nickel trimming on shoes can also be the cause of eczematous reaction.
Identification and subsequent avoidance of allergens is essential for the management of
contact allergic form.
Symptomatic treatment consists of usage of topical corticosteroids and emollients. In
severe cases a short course of systemic corticosteroids is effective. For details of the
management see the article on contact eczema in the August 2002 issue of Geneeskunde.5
2. Atopic eczema (Figure 12)

Figure 12. Lesions on the feet and lower legs in atopic dermatitis |
Eczematous changes on the feet are not uncommon in widespread atopic dermatitis. They
present usually as chronic lesions with thickening of the skin and lichenification
(increased skin marking). Hyperlinearity of the soles is considered one of the stigmata of
atopic diathesis. Irritant contact eczema is common in atopic patients due to their
defective barrier skin function. Isolated involvement of feet in atopic eczema without
lesions elsewhere is rare.
3. Juvenile plantar dermatosis (forefoot eczema)
It is a dry fissured dermatitis of the plantar surface of the peridigital areas of the
feet. The plantar surface of the toes and the forefoot is dry, red with a glazed and
fissured appearance (Figure 13).

Figure 13. Juvenile plantar dermatosis |
The process affects both feet symmetrically. This condition is seen mainly in children
from 7 to 16 years old. External factors – hyperhidrosis and friction, exacerbated by
occlusive socks made of synthetic fibres and tight rubber shoes – seem to play the
main role. Most cases improve spontaneously at the age when the patients change to leather
shoes.
4. Infective eczema
It represents an eczema in which bacteria, especially staphylococcus aureus and
haemolytic streptococci, provoke an eczematous reaction. This form of eczema occurs mainly
in patients with poor hygiene, pedal hyperhidrosis and tight heavy footwear. Infective
eczema often imitates clinically an acute vesiculobullous form of tinea pedis.
5. Hypostatic eczema (Stasis dermatitis)
This form occurs most often in middle-aged or elderly women with a previous deep
thrombophlebitis or insufficient deep or communicating veins. The clinical picture is
characteristic (Figure 14). Oedema, erythema, hyperpigmentation, due to haemosiderosis and
scaling are seen on the distal part of the lower leg, around the medial ankle and often
the dorsum of the foot. In longstanding cases hard thickening of the skin occurs –
lipodermatosclerosis. Ulcers, particularly in the proximity of the medial ankle are
common. Secondary allergic or irritant contact eczema develops frequently as these
patients are treated with various potentially sensitizing preparations.

Figure 14. Stasis dermatitis |
6. Nummular eczema
Circumscribed, coin-shaped, often severally pruritic lesions are located on the lower
legs and dorsal aspects of the feet. The degree of inflammation may vary. In acute lesions
erythema and vesiculopustules predominate while chronic lesions are dry and scaly.
7. Hyperkeratotic plantar eczema
The term eczema implying vesiculation may be misleading for this affliction. There are
no vesicles. Scaly, fissured hyperkeratotic patches appear symmetrically on the soles
(Figure 15).

Figure 15. Hyperkeratotic dermatitis |
Itching is mild if any. The aetiology is unknown, mechanical trauma seems to aggravate
the process. It is most frequent in the elderly and affects both sexes. Topical therapy is
often not effective and an oral retinoid (Neotigasone) should be considered.
H. Psoriasis of the feet
Psoriasis vulgaris, a very common inflammatory skin disease, is characterised by
well-defined, red, scaly plaques. The lesions van be confined to certain areas or be
widely disseminated. Stable plaque psoriasis located only on the feet is rare (Figure 16).

Figure 16. Lesions of psoriasis vulgaris on the feet |
So-called acral psoriasis is usually pustular psoriasis characterised by fiercely
erythematous plaques with scattered sterile pustules. The toe nails are very often
affected and association with psoriatic arthropathy result in deformities (Figure 17).

Figure 17. Acral pustular psoriasis in a patient with psoriatic arhtopathy |
Most patients with acral psoriasis require systemic therapy (methotrexate, retinoids,
PUVA).
References
- Kombila M, Martz M, Gomez de Diaz M. Hendersonula toruloidea as an agent of mycotic foot
infection in Gabon. J Med Vet Mycol 1990; 28: 215-223.
- Gugnani HC, Oykea C. Foot infections caused by Hendersonula toruloidea and Scytalidium
hyalinum in coal miners. J Med Vet Mycol 1989: 27: 169-179.
- Jones SK, Reynolds NJ, Oliwieski S. Oral albendazole for the treatment of cutaneous
larva migrans. Brit J Dermatol 1990; 122: 99-101.
- Jacyk WK. Warts: Clinical types and treatment. SA Fam Pract 2003: 45: 36-39.
- Jacyk WK. Contact eczema. Geneeskunde 2002; 44: 5-8.