Treatment Principles For Tinea Pedis

Given the common presentation of tinea pedis, this author looks to the literature and his own experience in discussing diagnostic pearls, effective treatment modalities and keys to educating patients on preventing recurrence.

Tinea pedis is by far the most common fungal disease and despite 15 to 25 percent of people having athlete’s foot infections at any one time, both patients and doctors can misdiagnose these infections as simply “dry skin.”^1,2 Even when the infection becomes symptomatic and the patient receives treatment, tinea pedis recurs often and eventually spreads to infect the nail beds. Researchers have also found that the presence of tinea pedis triples the risk of nonpurulent leg cellulitis.³ Most importantly, tinea pedis increases the risk of diabetic foot syndrome.⁴

Tinea pedis is a dermatophyte foot infection that affects the soles and interdigital skin of the toes. The same fungus infects the nails as onychomycosis. Tinea pedis is also called athlete’s foot or ringworm.⁵ Using the term ringworm may help patients adhere to a treatment program. The infection often spreads to other parts of the body, especially the groin and to other people.² Concurrent tinea cruris is so common that physicians recommend patients put on their socks before putting on their underwear to avoid the transfer of infected keratinocytes from one warm, dark, moist site to another.

Historically, the prevalence of dermatophyte infections has climbed the social scale from initially infecting poorer children in the 1930s to infecting mostly adults today.⁶ The principal site of dermatophyte infection has also changed from children’s scalps to the toes of adults.

The advent of “athlete’s foot” infections became one of the most common and talked about diseases in America in the 1930s.⁷ Today, tinea pedis has spread around the globe. The World Health Organization estimates the global prevalence of dermatomycosis is approaching 20 percent.⁸

So is tinea pedis contagious? Dermatophyte infections are weakly contagious to a susceptible host via contaminated floors, towels or clothing. This means tinea pedis more easily spreads to genetically susceptible contacts. Researchers have identified a growing variety of host genetic factors that affect individual susceptibility.⁹ Some people, such as physicians, are resistant to infection even though they are exposed to the pathogen on a daily basis.

There are also variations in site susceptibility within infected individuals. Interestingly, some infected patients never develop a bilateral pattern as one might expect. One hand or foot may be spared while the other limbs are chronically infected. In general, we can think of genetic susceptibility to Trichophyton rubrum infection as an autosomal dominant pattern disease with incomplete penetrance.¹⁰

This variation in susceptibility to tinea pedis helps explain the potential for infection among family members. Dermatophyte infections are weakly contagious to genetically susceptible family members so not every family member will become infected. This is not unlike how the influenza virus may affect a family. Not all members of the family develop the infection even though they certainly exposed to the virus or fungus. Explaining genetically determined susceptibility to patients helps alleviate excessive concern that the cleanliness of the family shower is the culprit.

Although the dark, warm, moist environment of modern foot gear and individual genetic susceptibility are big drivers of tinea pedis, the direct cause of the infection is a variety of dermatophytes. Dermatophytes thrive on only dead keratin and cannot infect deeper tissue that is alive. Rippon has previously divided the Trichophyton dermatophytes into 22 species based upon their colony and structural morphology.¹¹ Today, DNA sequencing recognizes only 16 different species in the genus.¹² The primary cause of tinea pedis is Trichophyton rubrum in 70 percent of the cases.⁵ Trichophyton interdigitale and Epidermophyton floccosum can also cause tinea pedis. Occasionally, Tricholosporum violaceum, first found in Costa Rica, is the infecting fungus.⁵

Although we think of the Trichophytons as growing too slowly to change their antifungal susceptibilities like bacteria do with antibiotics, their worldwide distribution, pathogenicity and resistance to antifungal drugs has slowly and continually increased. Singh and colleagues have reported a high terbinafine resistance in Trichophyton interdigitale isolates in Delhi, India.¹³ These isolates harbor mutations to the squalene epoxidase enzyme, making them resistant to terbinafine.

How To Recognize The Clinical Types Of Tinea Pedis

There are three clinical subtypes of tinea pedis: interdigital, moccasin and vesiculobullous.¹⁴ The most common form is interdigital tinea. It typically occurs in the fourth and fifth toe web spaces but can spread to all the toe webs. Interdigital tinea pedis is characterized clinically by maceration, scaling and itching of the skin.¹⁵ Interdigital tinea pedis is caused primarily by Trichophyton interdigitale. It is often the clinical model chosen to investigate the efficacy of topical therapies in part because the thinnest skin on the foot makes the shortest treatment duration. Published efficacy rates and recommended durations of therapy for interdigital tinea pedis may not necessarily apply to other clinical forms of tinea pedis.

A variant of interdigital tinea pedis caused by T. mentagrophytes has a more aggressive clinical presentation.¹⁴ This ulcerative form of tinea pedis is secondarily infected with Gram negative bacteria and is also known as dermatophytosis complex.¹⁶ It is characterized by maceration, denuded tissue, desquamation and foul odor arising from the process of tissue breakdown.^14,15 Initial management via systemic antibiotics with Gram negative coverage, astringent foot soaks, rest, elevation and even hospitalization may be necessary.

The moccasin or chronic dry form of tinea pedis is typically the result of Trichophyton rubrum, a keratophilic fungus. This form presents as a non-inflammatory infection manifesting as mild erythema and dry silvery scales that favors the thicker keratin of the plantar aspect of the feet. Interestingly, Trichophyton rubrum actually produces penicillin in vitro and in vivo to help the infection compete with bacteria on the skin.¹⁷ The dry hyperkeratotic form of tinea pedis is concentrated within the callused areas of the sole and extends laterally to Wallace’s line, where thin dorsal skin meets the thick skin of the sole.

When the infection encompasses the entire sole, it can be called a moccasin pattern.¹ The body responds to the infection with accelerated keratinization in an attempt to shed the infected keratinocytes.
This hyperkeratosis may simply appear as dry skin and cracked heels. Many patients attempt to reduce this scale by using abrasive files to scrape the dead skin away, not realizing they may be spreading a fungal infection. Aggressive scraping can trigger lichen simplex chronicus and neurodermatitis.

Trichophyton mentagrophytes is the most frequent cause of vesiculobullous or acute inflammatory tinea pedis. Researchers have shown that younger active patients are more prone to infection with Trichophyton mentagrophytes.¹⁴ This species is more capable of attaching to moist abraded keratin and penetrating deeper than Trichophyton rubrum, triggering a greater inflammatory host response. T. mentagrophytes is zoonotic, meaning it can spread from animals to humans through direct contact and is typically present with ringworm infections spread from companion animals.¹⁸

Vesiculobullous tinea pedis presents with tiny pruritic vesicles, pustules and multilocular bullae. They develop with erythematous bases on the arch, interdigital spaces and other non-weightbearing surfaces.¹⁵ This infection may start as a superficial dry scaling of the sole that subsequently drives deeper into the skin, stimulating acute inflammation and vesicle formation. Many polymorphonuclear cells accumulate, creating pustules and blisters. Symptoms of severe itching and excoriation are typical. These lesions can also become secondarily infected with Staphylococcus aureus or Streptococcus pyogenes.¹⁴

Interestingly, we have applied the term ringworm to cases of tinea corporis, tinea capitis, tinea pedis and tinea cruris. It is a common descriptive term for a raised, scaly border that snakes its way around the edge of the lesion like a worm forming a circular plaque with central clearing. The raised periphery represents the active infection front. As the scales are desquamated, the center of the lesion clears, resembling fungal fairy rings in a lawn.

In general, tinea pedis is histologically characterized by acanthosis and hyperkeratosis with a sparse, superficial, perivascular infiltrate in the dermis. The vesiculobullous forms shows spongiosis and parakeratosis. Staining with periodic acid Schiff or methenamine silver stain can help to demonstrate characteristic fungal filaments.⁵

Pertinent Pearls On Diagnosing Tinea Pedis

One can mistake the clinical subtypes of tinea pedis infections for candidiasis, atopic eczema, contact dermatitis, psoriasis and erythrasma.¹⁴ The physical examination coupled with a degree of diagnostic acumen is generally sufficient to diagnose tinea pedis. However, if a cutaneous dermatophyte infection goes misdiagnosed and the initial treatment is with a topical corticosteroid, the appearance of the infection may be altered, making diagnosis more difficult (i.e. tinea incognito).¹⁶ The corticosteroids obscure the clinical clues of erythema, scale and a well-defined border, and may lead to a deep-seated folliculitis called Majocchi granuloma.¹⁹

Demonstration of the fungus by microscopic examination of the scrapings taken from the involved site is the gold standard for diagnosis.¹⁴ One can gather dry scales from the instep, heel and sides of the foot by scraping with the edge of a glass microscope slide onto a collection slide. Clinicians should unroof the bullae and either mount the entire roof intact or obtain scrapings from the underside of the roof that have the highest concentration of fungus. Add a few drops of a 10% to 20% solution of potassium hydroxide with Chlorazol (Delasco) to the material on the glass slide. Place a coverslip over the specimen and examine this under the microscope. The addition of one or two drops of Chlorazol black E, potassium hydroxide and dimethyl sulfoxide solution speeds clearing of keratin without the need for heating.²⁰ The mycelia are easily visible under low power (100X) while the dermatophyte specific segmented branching hyphae are best to appreciate under medium power (400X).

When speciation or laboratory confirmation of the diagnosis is necessary, the fungal culture has traditionally been the gold standard. However, histopathological diagnosis with periodic acid Schiff stains adds a degree of sensitivity. With the advent of polymerase chain reaction (PCR), fungal testing has become more rapid, sensitive and specific than cultures. Polymerase chain reaction with enzyme-linked immunosorbent assay (ELISA), an immunological method, allows identification of the involved species within 24 (maximum 48) hours.²¹

What Are The Best Treatment Options For Tinea Pedis?

One can treat about 90 percent of patients with tinea pedis with topical antifungal medications only.²² Topical therapies are most effective when the amount and duration of the prescription match the clinical type of tinea pedis. Depending on the type of clinical infection, I have found the recommended duration of therapy can vary from one week for interdigital tinea pedis to more than two months for chronic plantar tinea pedis. The duration application is primarily driven by the turnover time of the site of infection. The interdigital skin model may turn over quicker with symptoms clearing in just two weeks while thick plantar skin often takes two months to completely renew itself.  

Patients often underestimate the parts of the feet that need treatment, focusing only the symptomatic areas. The best method to teach patients adequate antifungal coverage is for the physician to actually apply a sample cream during the diagnostic visit that covers all the areas of the foot that need treatment, extending beyond the symptomatic sites. A patient who understands a proper application technique is more likely to be adherent to the treatment plan. Teach patients to continue applications for at least one week beyond the complete clearance of symptoms and emphasize the importance of weekly prophylactic applications in the long term.

Ensuring that patient have sufficient antifungal cream on hand may be even more important for successful clearing of the chronic infection. Initial antifungal cream prescriptions generally undertreat chronic tinea pedis. A good rule is 1 gram of cream per foot per application. A single physician sample size tube contains 2 grams, enough for one application of both feet. Treating both feet daily for two months may require 120 grams with the the first prescription and one copay. Thin interdigital skin turns over every month so one can manage it with a single 30 gram tube of cream. Over-the-counter antifungal creams come in 15 gram tubes so they are insufficient to clear plantar tinea and, on a per gram basis, are less economical for patients than a covered prescription’s copay.

Which Topical Antifungal Works Best?

Perhaps the best topical antifungal cream prescription is simply the one that provides the most cream for the longest duration. Randomized controlled studies have proven the superiority of allylamines and azoles over their vehicles.^13–14,23

Research has demonstrated the most effective topical agent to be terbinafine but other topical agents such as the azoles, ciclopirox olamine, butenafine and tolnaftate are also effective in curing athlete’s foot if one prescribes sufficient quantities.^2,24–25 In reality, the prescriber’s choice of topical antifungal is based primarily on the patient’s formulary, which reflects economic choices of the insurer rather than the judgment of the prescriber. Patients with hyperkeratotic tinea pedis can benefit from combining antifungal treatment with medications such as salicylic acid, lactic acid and urea to help increase the penetration of the antifungal preparation.^14,16

When Is Systemic Therapy Appropriate For Tinea Pedis?

Systemic therapy is indicated in the treatment of chronic tinea pedis when repeated attempts to clear an infection with topicals have failed. Physicians have prescribed systemic antifungals like fluconazole (Diflucan, Pfizer), terbinafine and griseofulvin for chronic recalcitrant hyperkeratotic tinea as well as the initial treatment of acute vesicular tinea pedis.

The recommended adult dosing for terbinafine is 250 mg daily for seven to 14 days. Fluconazole dosage is typically 150 mg daily for a month.¹ Laboratory confirmation of the diagnosis is appropriate before systemic therapy begins. A careful review of both the medical and allergy history is important. If you suspect hepatic dysfunction, order appropriate laboratory tests. Short courses of systemic antifungal medication, like short courses of systemic antibiotics, generally do not require baseline hepatic function testing as long as the patient does not have a history of hepatitis or cirrhosis.

Griseofulvin, which reaches the site of infection through the eccrine ducts, can also treat tinea pedis but is less effective than terbinafine or itraconazole, which are keratophilic medications. Griseofulvin requires eight weeks of therapy for tine pedis.¹⁶ Oral itraconazole has a greater potential for drug interactions. Interestingly, Trichophyton interdigitale resistance to terbinafine is reportedly as high as 32 percent in India.¹³

Autoeczematization reactions or infectious disease reactions are secondary cutaneous eruptions that potentially occur in association with any inflammatory skin disorder. The term dermatophytid reaction describes this occurrence in relation to a dermatophyte infection. The pathogenesis may involve an immunologic reaction to fungal antigens similar to a delayed-type hypersensitivity response.²⁶ Patients typically present with pruritic, papulovesicular eruptions that can be quite distant from the site of infection. In one series of 213 patients with tinea pedis, 17 percent of the patients were diagnosed with dermatophytid reactions characterized by vesicular eruptions on the hands.²⁷ Topical corticosteroids and antipruritic agents are typically in use for acute management of symptomatic dermatophytid reactions.

How To Prevent Recurring Fungal Infections

Most dermatophyte infections recur because of a combination of genetic susceptibility and failure of patient behavioral changes that would reduce reinfection. Given that tinea pedis spreads through direct contact or fomites, the Centers for Disease Control and Prevention (CDC) recommend people with an active tinea pedis infection should keep feet clean, dry and cool, and avoid using swimming pools, public showers or foot baths.^14,18 Preventive measures such as wearing sandals in public showers, drying between toes, application of absorbent powder like miconazole (Zeasorb-AF, Stiefel Laboratories) and changing cotton socks daily will also help. Wearing socks is more hygienic than going barefoot in shoes. Elastic hose not only is non-absorbent but constricts the toes and occludes the web spaces, increasing the risk of interdigital tinea pedis. Research has shown that at least 10 percent of patients with tinea pedis and onychomycosis are at risk of reinfection by contact with their socks.²⁸

Patients should also try to avoid activities known to risk the spread of disease such as swimming and washing clothes (especially socks) in cold water.²⁸ Washing clothes with 60°C hot water eliminates both T. rubrum and C. albicans while cold water washing at 30°C allows 17 percent of viable T. rubrum spores to persist.²⁹

In patients with extensive fungal infections, shampooing their legs, feet and toes with 2% ketoconazole will improve hygiene and reduce infections. Obese patients may not be able to reach their limbs so nursing care may be necessary. It is controversial whether spraying shoes with antiseptics actually helps to control fungal infections although studies have shown Lysol and Mr. Clean sprays kill pathogenic bacteria and fungus on surfaces after five minutes of contact, and that antifungals, ultraviolet light, or ozone can decontaminate shoes.^30,31 However, it remains to be seen if these measures actually reduce fungal infections.

Hyperhidrosis and tinea pedis appear to go hand in hand. Dry, intact epidermis is amazingly resistant to infection but is compromised by any moisture. The typical humidity of the dorsal foot skin is 30 percent while the typical humidity of the fourth toe web is 50 percent. The humidity of a macerated toe web with tinea pedis can reach 70 percent.³² To help reduce toe web humidity, patients can insert cotton between fat toes that anatomically occlude web spaces. Dispensing a roll of cast padding (Webril, Covidien) to patients and demonstrating how to tear and insert the folded pledgets of cotton cast padding between juxtaposed toes helps to lower interdigital humidity.

Absorbent powders with microporous cellulose absorb three times more moisture than plain talcum powder.³³ Some powders also contain antifungal-like miconazole 2% or tolnaftate 1% to help reduce recurrence of the tinea pedis while reducing the effects of hyperhidrosis. In addition, doctors often recommend patients with hyperhidrosis not wear the same pair of shoes every day in order to allow the shoes to dry out thoroughly.

In Conclusion

It is important to remember that patients with diabetes are particularly at risk for postoperative infections and wound breakdown if tinea pedis is untreated.¹³ Recognizing occult tinea pedis in all patients, especially patients with diabetes, and tailoring patient treatments and prevention plans should reduce the risk of secondary bacterial cellulitis as well as onychomycosis.

Dr. Bodman is a retired Associate Professor at the Kent State University College of Podiatric Medicine. He is board-certified by the American Board of Podiatric Medicine.

References

1.     James WD, Elston DM, Berger TG, Andrews GC. Andrews’ Diseases of the Skin: Clinical Dermatology. Saunders/Elsevier, London, 2011, pp. 293-294.
2.     Crawford F, Hollis S. Topical treatments for fungal infections of the skin and nails of the foot. Cochrane Database Syst Rev. 2007; 3:CD001434.
3.     Quirke M, Ayoub F, McCabe A, et al. Risk factors for nonpurulent leg cellulitis: a systematic review and meta-analysis. Br J Dermatol. 2017;177(2):382-394.
4.     Eckhard M, Lengler A, Liersch J, et al. Fungal foot infections in patients with diabetes mellitus--results of two independent investigations. Mycoses. 2007;50(Suppl 2):14-9.
5.     Nigam PK, Boktor SW. Tinea pedis. StatPearls [Internet]. Available at https://www.ncbi.nlm.nih.gov/books/NBK470421/ . Published Dec. 12, 2017.
6.     Homei A, Worboys M. Fungal Disease in Britain and the United States 1850–2000: Mycoses and Modernity. Chapter 2, Athlete’s Foot: A Disease of Fitness and Hygiene. Palgrave Macmillan, Basingstoke (UK), 2013. Available at https://www.ncbi.nlm.nih.gov/books/NBK169220 .
7.     Majima A. The invention of “athlete’s foot”: Lifestyle, cleanliness, and American leisure classes in the early twentieth century. Seikatsugaku rons. 2010; 17:3–13.
8.     Marques SA, Robles AM, Tortorano AM, et al. Mycoses associated with AIDS in the third world. Medical Mycology. 2000;38(1):269–279.
9.     Abdel-Rahman SM. Genetic predictors of susceptibility to dermatophytoses. Mycopathologia. 2017;182(1-2):67-76.
10.     Zaias N, Tosti A, Rebell G, et al. Autosomal dominant pattern of distal subungual onychomycosis caused by Trichophyton rubrum. Am Acad Dermatol. 1996;34(2 Pt 1):302-4.
11.     Rippon JW. The changing epidemiology and emerging patterns of dermatophyte species. Curr Top Med Mycol. 1985;1:208-34.
12.     De Hoog GS, Dukik K, Monod M, et al. Toward a novel multilocus phylogenetic taxonomy for the dermatophytes. Mycopathologia. 2017;182(1-2):5-31.
13.     Singh A, Masih A, Khurana A, et al. High terbinafine resistance in Trichophyton interdigitale isolates in Delhi, India harboring mutations in the Squalene epoxidase (SQLE) gene. Mycoses. 2018; epub Mar 25.
14.     Hsu AR, Hsu JW. Topical review: skin infections in the foot and ankle patient. Foot Ankle Int. 2012 Jul;33(7):612-9.
15.     Joseph WS. A closer look at topicals for tinea pedis. Podiatry Today. 2009; 22(9):48–56.
16.     Goldstein AO, Goldstein BG. Dermatophyte (tinea) infections. UpToDate. Available at https://www.uptodate.com/contents/dermatophyte-tinea-infections  Accessed April 2018.
17.     Youssef N, Wyborn CH, Holt G. Antibiotic production by dermatophyte fungi. J General Microbiol. 1978; 105(1):105–111.
18.     Athlete’s Foot (tinea pedis). Hygiene-related Diseases – CDC. Available at https://www.cdc.gov/healthywater/hygiene/disease/athletes_foot.html .  Accessed April 3, 2018.
19.     Su H, Li L, Cheng B, et al. Trichophyton rubrum infection characterized by majocchi’s granuloma and deeper dermatophytosis: case report and review of published literature. Mycopathologia. 2017;182(5-6):549-554.
20.     Available at https://www.delasco.com/pcat/1/Chemicals/Chlorazol/dlmic020/ .
21.     Miyajima Y, Satoh K, Uchida T, et al. Rapid real-time diagnostic PCR for Trichophyton rubrum and Trichophyton mentagrophytes in patients with tinea unguium and tinea pedis using specific fluorescent probes. J Dermatol Sci. 2013;69(3):229-35.
22.     Otani M. Treatment of tinea pedis in elderly patients using external preparations. Med Mycol J. 2017;58(2):J35-J41.
23.     Crawford F, Harris R, Williams HC. Are placebo-controlled trials of creams for athlete’s foot still justified? Br J Dermatol. 2008;159(4):773-9.
24.     Gupta AK, Chow M, Daniel CR, Aly R. Treatments of tinea pedis. Dermatol Clin. 2003;21(3):431-62.
25.     Rotta I, Sanchez A, Gonçalves PR, Otuki MF, Correr CJ. Efficacy and safety of topical antifungals in the treatment of dermatomycosis: a systematic review. Br J Dermatol. 2012;166(5):927-33.
26.     Cheng N, Rucker Wright D, Cohen BA. Dermatophytid in tinea capitis: rarely reported common phenomenon with clinical implications. Pediatrics. 2011;128(2):e453-7.
27.     Veien NK, Hattel T, Laurberg G. Plantar Trichophyton rubrum infections may cause dermatophytids on the hands. Acta Derm Venereol. 1994;74(5):403.
28.     Vlahovic TC. Onychomycosis: evaluation, treatment options, managing recurrence, and patient outcomes. Clin Podiatr Med Surg. 2016;33(3):305-18.
29.     Hammer TR, Mucha H, Hoefer D. Infection risk by dermatophytes during storage and after domestic laundry and their temperature-dependent inactivation. Mycopathologia. 2011;171(1):43-9.
30.     Rutala W, Barbee S, Aguiar N, et al. Antimicrobial activity of home disinfectants and natural products against potential human pathogens. Infection Control Hospital Epidemiology. 2000; 21(1):33-38. 2000.
31.     Gupta AK, Brintnell W. Ozone gas effectively kills laboratory strains of Trichophyton rubrum and Trichophyton mentagrophytes using an in vitro test system. J Dermatolog Treat. 2014;25(3):251–5.
32.     Bodman MA. Moisture content of pedal skin. Unpublished raw data, 2016.
33.    Available at https://www.zeasorb.com/products/prevention.html .

Editor’s note: For related articles, see “Treating Tinea Pedis In Patients With Diabetes” in the June 2012 issue of Podiatry Today or “A Closer Look At Topicals For Tinea Pedis” in the September 2009 issue.