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Fungal Infections and Parasitic Infestations in Sports

Expedient Identification and Treatment

Rebecca C. Winokur, MD; William W. Dexter, MD

Sports Dermatology Series Editor:
William W. Dexter, MD


In Brief: Common fungal infections include tinea corporis, capitis, cruris, versicolor, and pedis, as well as onychomycosis. Prevention of spread is important and involves frequent skin surveillance, avoidance of shared equipment, and regular equipment cleaning. The NCAA recommends treatment of tinea corporis and capitis infections and covering any exposed infection before return to play. Parasitic infestations occur because of the close physical contact of team members and athletes in contact sports. Both scabies and pediculosis should be treated before return to play, according to NCAA guidelines. Cutaneous larva migrans, a chronic parasitic infection caused by a hookworm, may be seen in beach volleyball players.

Fungal infections, such as the various forms of tinea (table 1) and onychomycosis, are common among athletes; parasitic infestations less so. Both, however, require diligent diagnosis and expedient treatment. The warm, moist environment of the skin, occlusive equipment, and towel sharing predispose athletes to fungal infections, and close contact and various environments can raise the risk of parasitic infestation. Proper hygiene and other prevention steps are also integral to disease management.

TABLE 1. Tinea Infections: Characteristics, Treatment, and Return-to-Play Issues

TreatmentNCAA Guidelines
Head and
hair shafts
Ketoconazole, 200-400 mg
QD for 2-4 wk, itraconazole
200 mg QD for 1-2 wk, or
fluconazole 150 mg once
weekly for 3-5 wk
Minimum 2 wk oral
therapy for scalp lesions and
disqualification of wrestlers
who have extensive and
active lesions
Trichophyton sppTopical: terbinafine 1%,
clotrimazole 1% or naftifine cream
BID for 2 wk after disappearance
of lesions
Oral: ketoconazole, 200-400 mg
daily for 2-4 wk, itraconazole 200 mg
QD for 1-2 wk, or fluconazole 150 mg
for 3-5 wk once weekly
Minimum 72 hr topical
therapy for skin lesions and
disqualification of wrestlers
who have extensive and
active lesions
FeetT rubrum,
T mentagrophytes
Mild: antifungal powder
Moderate: terbinafine or naftifine
BID for 2-4 wk
Severe: terbinafine 250 mg PO QD
or itraconazole 100 mg PO QD
for 10 dy with an antifungal cream
No specific guidelines
GroinT rubrum,
T mentagrophytes
Topical imidazole or terbinafine
1% cream QD or BID for 14 dy
No specific guidelines
YeastTopical selenium sulfide shampoo
QD for 7 dy or 2% ketoconazole cream
for 1-2 wk
No specific guidelines

*All are diagnosed with a clinical exam and confirmed by microscopic visualization of branching hyphae in potassium hydroxide preparations. In tinea versicolor, the microscopic visualization has a "spaghetti and meatballs" appearance.

NCAA = National Collegiate Athletic Association; QD = once daily; BID = twice a day; PO = orally

Tinea Corporis and Tinea Capitis

Tinea is described by its area of eruption on the body. Tinea corporis (body) and tinea capitis (head) are typically caused by dermatophytes of the genus Trichophyton.1,2 Tinea corporis is especially common among wrestlers and is referred to in this setting as tinea gladiatorum (see "Herpes and Tinea in Wrestling: Managing Outbreaks, Knowing When to Disqualify"). Trichophyton tonsurans is the leading cause of tinea capitis in the United States, and wrestlers with asymptomatic tinea capitis may be the reservoir for transmission of tinea gladiatorum.1

Dermatophytes infect the dead keratin layer in skin and are not present on mucosal surfaces.2 Factors inherent to wrestling that facilitate transmission are skin-to-skin contact, occlusive equipment, and macerated skin.1

Diagnosis. Typically, the athlete has scaly, red, pruritic plaques with well-defined, raised borders that are ring-shaped.2,3 (See figure 4 of the herpes and tinea article.) Diagnosis can be made clinically and is confirmed by direct microscopic visualization of branching hyphae in potassium hydroxide (KOH) preparations of skin scrapings from the scaling borders (figure 1).2 Recent use of over-the-counter (OTC) topical antifungal medication can result in a false-negative KOH test.3 When the history and clinical exam are highly suggestive of tinea but the KOH preparation is negative, fungal culture or skin biopsy is indicated.1,4 Of note, a skin biopsy specimen should be examined by a dermatopathologist (a physician with training in dermatology and pathology). The differential diagnosis comprises many dermatoses, including atopic dermatitis, impetigo, and psoriasis.4

Treatment. Management can be difficult, because optimal therapy has not yet been defined, and responses vary, depending on host factors such as the host's level of cellular-based immune response and the extent and severity of the infection.1 The long incubation period and unknown treatment time to become noninfectious compound the problem.

Topical regimens should be tried before oral regimens for any acute, superficial, localized, noninflammatory fungal infections in athletes who are not immunosuppressed.4 There are many topical antifungal creams and lotions available, such as OTC terbinafine hydrochloride 1% cream, OTC clotrimazole 1% cream, or prescription naftifine hydrochloride 1% cream, which all can be used twice daily.

Clotrimazole is also available in combination with a corticosteroid. Because the combination products typically contain midpotency corticosteroids, use in intertriginous areas should be discouraged, while use in other areas should be limited to less than 1 week. After treatment with a combination product, clotrimazole alone should be used. Treatment typically continues for 2 weeks after lesions disappear.3

Oral treatment can be used when either topical treatment fails, the athlete is immunosuppressed, or the infection is inflammatory or widespread.1 Oral treatment with griseofulvin is no longer favored, given its low success rate.3 Ketoconazole (200 to 400 mg daily for 2 to 4 weeks), itraconazole (200 mg daily for 1 to 2 weeks), and fluconazole (150 mg once weekly for 3 to 5 weeks) are considered more effective but may cause liver toxicity with extended use. They also are relatively expensive.2-5 In addition, terbinafine hydrochloride is being investigated as an alternative for chemoprophylaxis and therapy for tinea corporis gladiatorum (Brian B. Adams, MD, written communication, September 9, 2021).

Pulse therapy can be considered if there are multiple areas of infection or chronic lesions.3 After 72 hours to 2 weeks of treatment, any lesions should then be cleaned and covered with a gas-permeable dressing before participation.2

Prevention. Preventing transmission is important and includes not sharing equipment or towels, sanitizing headgear on a regular basis, cleaning mats frequently, and following basic principles of good hygiene, including hand washing and daily laundering of all sports clothing.2,5 Commercial skin protectants for wrestlers are available, but evidence is lacking on their efficacy. Prophylaxis with itraconazole or fluconazole has been proposed.

Kohl et al6 published a double-blind placebo-controlled trial that showed that wrestlers treated with 100 mg of fluconazole weekly during wrestling season had a significantly lower incidence of tinea gladiatorum as compared with the placebo group. The risk of liver toxicity and potentially resistant fungi versus the uncertain benefit of such therapy should be weighed and requires further study.6

Return to play. The National Collegiate Athletic Association (NCAA) recommends examination of the KOH preparation to determine the activity level of the infection, although specific recommendations regarding the number of hyphae seen per high-powered field have not been established. An alternative to examining the KOH preparation is to determine the quantity and location of lesions on the body. The NCAA 2021 wrestling guidelines7 state that wrestlers with "solitary, or closely clustered, localized lesions . . . in a body location that cannot be adequately covered" should be disqualified. For return to play, the NCAA guidelines7 recommend:

*A minimum of 72 hours of topical therapy for skin lesions,

*A minimum 2 weeks of oral therapy for scalp lesions, and

*Disqualification of wrestlers with extensive and active lesions.

Tinea Pedis

Tinea pedis, or athlete's foot, is a common affliction usually caused by the ubiquitous fungi T rubrum or T mentagrophytes. The moist environment in footwear creates a favorable environment for invasion.8

Tinea pedis comes in three forms. The most common is found in the intertriginous web spaces (figure 2).4 This is a scaly peeling eruption with or without erythema, maceration, or fissuring.8 Extension from the web space to the plantar or dorsal surface is common.1,2,8 The second form includes an eruption of vesicles and bullae on the midfoot, and the third form occurs as hyperkeratotic scale with minimal erythema on the plantar surface.8 All three types cause itching, which worsens after the removal of socks.

Diagnosis. The diagnosis is clinical and confirmed by direct microscopic visualization of branching hyphae in KOH preparations of skin scrapings. Other conditions of the feet that should be considered in the differential diagnosis are contact dermatitis, atopic dermatitis, erythrasma, psoriasis, dry skin, pitted keratolysis, and bacterial or viral infections.1,4

Treatment. Mild cases of tinea pedis can be treated with an antifungal powder. Moderate cases are best treated with an antifungal cream such as terbinafine or naftifine twice daily for 2 to 4 weeks.1,2,8 Oral therapy—with terbinafine 250 mg once daily for 10 days or itraconazole 100 mg twice daily for 10 days—combined with an antifungal cream is recommended for severe cases and hyperkeratotic tinea pedis.8 Wet dressings using Burow's solution applied three times a day are helpful for symptom relief if maceration or vesicles are present.

Prevention. Though further studies are needed, prevention may be maximized by keeping the feet clean and dry by wearing moisture-wicking socks with frequent changing and wearing sandals in locker rooms and showers.1,2,8 The incidence of asymptomatic tinea pedis may be high among swimmers; therefore, these prevention measures should be closely observed on swimming and diving teams.9

Return to play. The NCAA guidelines do not specifically make recommendations regarding return to play with tinea pedis. The guidelines recommend that any "infectious skin conditions that cannot be adequately protected should be considered cause for medical disqualification from practice or competition." "Adequately protected" is defined as a "wound or skin condition (that) has been deemed noninfectious and adequately medicated . . .and is able to be covered by a securely attached bandage made of nonpermeable material that will withstand the rigors of competition."7

Tinea Cruris

Tinea cruris or tinea of the groin, also known as "jock itch," is seen frequently in athletes and is caused by T rubrum or T mentagrophytes. These infections begin in the crural folds and develop into half-moon-shaped plaques that often have a well-defined scaly border. The advancing border is usually erythematous and appears brown in light-skinned athletes, and small vesicles may be present.4 Itching is a common symptom and, unlike with candidiasis, the scrotum is usually not involved. The differential diagnosis in these cases includes candidal infections, psoriasis, erythrasma, eczematous dermatoses (including contact and seborrheic dermatitis), and extramammary Paget's disease.

Treatment with a topical imidazole, (eg, clotrimazole 1%) or a topical allylamine cream (eg, terbinafine 1%) once daily to twice daily for 14 days can be used. Keeping the area dry, avoiding tight clothing, and applying OTC anti-itch powders or low-potency topical corticosteroid cream for several days will help to alleviate symptoms. There are no standards for return to play with tinea cruris infections, but those affected should practice good hygiene as noted above, avoid towel sharing, and cover any active eruptions.

Tinea Versicolor

Tinea versicolor is caused by a yeast—Malassezia furfur—that is a normal part of the skin flora. Excessive heat, humidity, and oily skin promote the growth of this organism in the stratum corneum.

Tinea versicolor is seen most commonly in adolescence when sebaceous activity is high, and it manifests as asymptomatic multiple, small, circular macules of varying colors, from hypopigmented to brown (figure 3). Lesions appear hypopigmented on sun-exposed skin. The upper extremities and trunk are affected more often than the lower extremities.

The diagnosis is made clinically but can be confirmed with direct microscopic visualization of branching hyphae and spores (sometimes said to have a "spaghetti and meatballs" appearance) in KOH preparations of skin scrapings.10,11 The differential diagnosis includes pityriasis rosea, secondary syphilis, seborrheic dermatitis, dermatophytosis, other annular lesions, and hypopigmented lesions, including vitiligo.10

Treatment includes topical selenium sulfide shampoo once daily for 7 days or 2% ketoconazole cream for 1 to 2 weeks. It is uncertain whether tinea versicolor can be spread by skin-to-skin contact; therefore, there are no established rules regarding return to play. Athletes should practice good hygiene and avoid sharing towels and equipment.


Onychomycosis, typically caused by T rubrum or T mentagrophytes, is common among athletes, particularly those who swim in pools, use communal showers, or have chronic tinea pedis and wear occlusive footwear.12 The infection results from migration of the fungus under the distal nail plate, leading to a nail bed infection that results in the discoloration of the nail plate (figure 4). Subungual debris then forms, and the nail plate becomes distorted, thickened, and separated from the nail bed. Over time, the nail plate becomes brittle and crumbles. Symptoms include pain with activity and, more commonly, aesthetic concerns.12

Diagnosis. There are four clinical forms, and the two most common are distal onychomycosis and superficial onychomycosis. Candida is also a causative organism in onychomycosis, especially the proximal subungual form.

The diagnosis of both is made clinically and confirmed by KOH test, fungal culture, and nail biopsy for microscopic evaluation with periodic acid-Schiff (PAS) stain. Nail biopsy with PAS stain is the superior method of detection.13 There are many technical problems with performing KOH tests on nail scrapings, with false-negative results. Candida spores are seen on KOH and PAS preparations. The differential diagnosis of onychomycosis includes inflammatory, traumatic, allergic, hereditary, and infectious nail dystrophies.

Treatment. First-line treatment is no longer with griseofulvin or ketoconazole, given the need for 10 to 18 months of therapy and success rates as low as 15% to 30%.12 Newer therapies include itraconazole (200 mg daily for 3 to 4 months), terbinafine (250 mg daily for 2 to 4 months), and fluconazole (150 mg once weekly for 10 to 18 months). Potential side effects of all these medications include liver toxicity and gastrointestinal disturbances. In addition, fluconazole inhibits cytochrome-P450-dependent enzymes; therefore, it has many potential medication interactions.

A newer topical nail lacquer is indicated for a single-nail-plate infection but requires daily topical application for 6 to 12 months. In addition to daily application, the nail is cleaned once weekly with alcohol, and then, periodically, any unattached infected nail is removed. In two simultaneous double-blind vehicle controlled studies, Gupta et al14 showed that ciclopirox 8% nail lacquer solution is significantly more effective than placebo in the treatment of mild-to-moderate onychomycosis. In these two studies, side effects included localized erythema and mild application-site reactions.

Prevention. Preventing recurrence is important. Seraly and Fuerst12 suggest that patients with a history of tinea pedis or onychomycosis use a weekly topical antifungal cream alone or in a premixed combination with an absorbent powder. It may also help to keep the feet dry with moisture-wicking socks and to wear sandals in all shared bathing and showering facilities, although evidence about the efficacy of these measures is lacking.

Return to play. There are no specific return-to-play restrictions for onychomycosis, but wearing sandals in the locker room and showers may be important, particularly until the athlete is successfully treated, which can be difficult.


Scabies mites—Sarcoptes scabiei—are easily transmitted through skin-to-skin contact. Once on the skin surface, the mite burrows in to the epidermis, but symptoms may not arise until 3 to 4 weeks after exposure.2

Infestation manifests as small linear burrows and/or vesicles characteristically in axillary skinfolds, finger and toe web spaces, the flexor surface of the wrists, the extensor surface of the elbows and knees, periumbilicus, genitalia, buttocks, and lateral foot. The head and back are often spared. The most prominent symptom is moderate-to-severe pruritus.11 In first-time infections, pruritus may not develop for several weeks, whereas subsequent infections in a sensitized individual may cause symptoms within 24 hours.1

Diagnosis. The diagnosis can be made by symptoms and a history of exposure. Confirmation of the diagnosis is done with the scabies test. In this test, the female adult mite is identified by direct microscopic visualization from an ink-and-mineral-oil preparation of skin scrapings from an infected papule.

Treatment. Topical therapy is nearly 100% effective. Permethrin 5% cream is massaged into the skin over the entire body. Eight to 12 hours later, the cream is washed off. Alternative topical therapies include lindane 1% lotion applied to all areas of the body for 8 hours or sulfur 6% precipitated ointment applied thinly to all areas of the body for three consecutive nights. The Centers for Disease Control and Prevention's 192021 guideline15 for treating sexually transmitted diseases suggests oral ivermectin at 200 µg/kg in a single dose with a repeat dose 2 weeks later as a potential alternative treatment, although studies that compare this regimen with first-line treatments are lacking.1,15

Prevention and return to play. Once an infection is identified in an athlete, all family members and close contacts should be treated so that reinfection is prevented. According to the 2021 NCAA guidelines,7 wrestlers must have a negative scabies test at meet or tournament time to return to play. However, asymptomatic or presymptomatic athletes may slip through the cracks.


Pediculus corporis (body lice), pediculus capitis (head lice), and pediculus pubis (genital lice) affect 6 million to 12 million people per year and are spread by close physical contact, which makes outbreaks among athletes potentially problematic.16 In overcrowded areas and some regions of the world, the louse is a vector for typhus and other more serious infectious diseases. Female patients are more often affected than males, and pediculus capitis is more common in children, whereas pediculus pubis is more common in sexually active adults.

Once a person is infested, it can take up to 10 days for the nit (louse egg) to hatch. Patients may describe nighttime itching and may develop an inflammatory reaction to scratching. As bites emerge, they appear as 2- to 4-mm red papules on an erythematous base. Body lice are often found in the seams of clothing. Head lice are seen behind the ears, on the back of the neck, and on the head. Genital lice may be found around the anus, abdomen, axillae, and chest.

The diagnosis can be made clinically and confirmed by either direct microscopic visualization of the nits or slit-lamp examination of the eyelashes or pubis for visualization of the nits.16

Treatment includes a 7-day course of permethrin lotion, either 1% or 5%, lindane 1% shampoo, petrolatum for eyelashes, and/or shampoo containing pyrethrin and piperonyl butoxide. In addition, a fine comb should be used to remove nits, and all clothing, bed linens, and sporting equipment should be washed and dried in a hot dryer or discarded.16

Prevention of spread includes treating all family members and, in some cases, team members; laundering all clothing; and observing safer-sex practices. According to the NCAA guidelines,7 an athlete may return to play after a full course of treatment if a complete examination of the skin shows no evidence of lice. Noninfectious nodules can persist for several weeks and should not preclude an athlete from participation.

Cutaneous Larva Migrans

Although most chronic parasitic infestations are uncommon in athletes, beach volleyball players are at risk for infestation with cutaneous larva migrans. This hookworm forms red burrows in the lower extremities of the athlete. The burrows elongate by millimeters each day. The infestation is treated with topical thiabendazole with nighttime occlusive dressings or with oral ivermectin. The infestation can be prevented by wearing shoes during beach volleyball.1


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Dr Winokur is a primary care sports medicine physician with Associates in Orthopaedic Surgery in South Burlington, Vermont. Dr Dexter is the director of the sports medicine fellowship and the assistant program director of the family practice residency program at the Maine Medical Center in Portland, Maine. Address correspondence to Rebecca C. Winokur, MD, 6 San Remo Dr, Suite 101, South Burlington, VT 05403.

Disclosure information: Drs Winokur and Dexter disclose no significant relationship with any manufacturer of any commercial product mentioned in this article. Terbinafine hydrochloride is mentioned in this article for an unlabeled use.