More Than Skin Deep: Dermatologic Conditions in Athletes

Abstract

Context:

Athletes are a unique group of patients whose activities, particularly in high-contact sports such as wrestling and football, place them at high risk of developing skin conditions. The correct diagnosis of sports dermatoses requires familiarity with their clinical characteristics. It is critical that primary care physicians recognize the most common skin disorders to provide prompt treatment and prevent transmission.

Evidence Acquisition:

The Mayo Clinic library obtained articles from 2012 onward related to dermatologic conditions in athletes.

Study Design:

Review article.

Level of Evidence:

Level 3.

Results:

Dermatologic diseases in athletes are often infectious and contagious due to close-contact sports environments. Sports-related dermatoses include bacterial infections, such as impetigo, ecthyma, folliculitis, abscesses, furuncles, carbuncles, erysipelas, and cellulitis; fungal infections, such as tinea and intertrigo; viral infections, such as herpes, verrucae, and molluscum contagiosum; and noninfectious conditions, such as acne, blisters, and contact dermatitis.

Conclusion:

This article aims to address the manifestations of the most common cutaneous diseases in athletes on the first primary care visit. It discusses the appropriate tests and most recent evidence-based treatments for each ailment. It also addresses return-to-play recommendations related to the guidelines and regulations of selected sports organizations in the United States.

Strength of Recommendation Taxonomy (SORT):

C.

Primary care physicians are often the first to treat dermatologic diseases. Some dermatologic conditions are unique to specific populations such as athletes. Dermatologic diseases account for 8.5% of high school and 20.9% of college sports-related conditions. Risk factors include shared locker rooms, benches, and buses, as well as skin breakdown and warm moist environments. The risks are higher for contact sport participants. ³⁴ It is important for primary care physicians to recognize these skin conditions, diagnose and treat appropriately, and understand the implications of specific skin conditions that can result from engaging in sports. This review discusses some of the most common dermatologic conditions that occur in athletes.

Bacterial Infectious Disorders

A majority of skin and soft tissue infections are caused by group A Streptococcus and Staphylococcus aureus. Treatment is similar unless community-associated methicillin-resistant Staph aureus (MRSA) is suspected. ²⁵

Impetigo

Impetigo is a primary or secondary superficial bacterial infection resulting from skin breakdown. In athletes, abrasions serve as potential entry sites for pathogenic microorganisms.^2,13,19

Clinical Presentation

Impetigo presents with papules and pustules coalescing into an erythematous plaque with an overlying honey-colored crust, most commonly found on the face or extremities (Figure 1). The palms and soles are spared. A bullous variant with flaccid vesicles that quickly rupture may also be seen, and it often favors the torso.

Figure 1.

Impetigo.

Diagnosis

Diagnosis is based on history and physical examination. Cultures are not needed if the condition is resolved with treatment.

Treatment

A summary of treatments for impetigo can be found in Table 1.

Table 1.

Summary of treatment for impetigo

Type	Treatment	Dosage	Other Recommendations
Nonbullous: first line	Topical mupirocin	Applied TID for 10 days	Overlying crust removed frequently to improve antibiotic absorption
Bullous: first line	Cephalexin	500 mg PO QID for 7 days
	Amoxicillin-clavulanate	500 mg PO BID for 7 days
Bullous: penicillin allergy	Azithromycin	250 mg/tab, 2 tabs PO for 1 day, then 1 tab PO daily for 4 days
MRSA	TMP-SMX	160-800 mg PO TID for 7 days
	Clindamycin	600 mg PO TID for 7 days or 300-450 mg QID PO (risk of GI adverse effects)

BID, twice a day; GI, gastrointestinal; MRSA, methicillin-resistant Staphylococcus aureus; PO, per oral; QID, 4 times a day; TID, 3 times a day; TMP-SMX, trimethoprim-sulfamethoxazole.

Return-To-Play Recommendations

This section focuses on guidelines for wrestlers because the infections observed in these athletes can be generalized to other types of athletes. A summary of return-to-play recommendations for all infection disorders is found at Table 2. ²¹ Skin-to-skin contact should be limited until the lesions are completely dry. Merely covering the lesions does not clear an athlete to return to play. The National Federation of State High School Associations (NFHS) recommends return to contact practice and competition after 72 hours of treatment, provided that the infection is not actively draining. For college wrestling, the National Collegiate Athletic Association (NCAA) recommends return to play if (1) no new lesions occur within 48 hours, (2) lesions have been treated for at least 72 hours prior to competition, and (3) lesions are not moist or draining. ¹⁶ All organizations recommend covering noninfectious residual lesions with bio-occlusive prewrap and tape during competition.^16,21

Table 2.

Summary of return-to-play recommendations for infectious skin conditions ^a

Condition	NCAA	NFHS
Bacterial infections
CA-MRSA	No new lesion for 48 hours	No new lesion for 48 hours
Impetigo	No moist exudative or draining lesions	No draining or oozing lesions
Folliculitis	Site may be covered once inactive and patient meets participation criteria	All lesions must have scabs
Furuncle	Oral antibiotics for 72 hours	Oral antibiotics for 72 hours
Carbuncle	No moist exudative or draining lesions	No draining or oozing lesions
Cellulitis	Active infections may not be covered	All lesions must have scabs
Fungal infections
Tinea pedis	No restriction	No restriction
Tinea capitis	Oral antifungals at >14 days	Oral or topical antifungals at >14 days
Tinea corporis	Antifungal at >72 hours Lesions must be covered	Oral or topical antifungals at >72 hours Written release from team physician Lesions must be covered by occlusive dressing
Viral infections
Primary HSV (any)	All vesicles crusted No systemic symptoms No new lesion for 72 hours Oral antivirals for 120 hours No active lesions	Oral antivirals for 10-14 days No new lesions during 48-hour antiviral treatment All lesions have scabs
Reactivation of HSV	No active lesions Oral antivirals for 120 hours	Oral antivirals for 120 hours No new lesions during 48-hour antiviral treatment All lesions have scabs
Verrucae vulgaris	Facial: cover with mask Nonfacial: cover or curette	Facial: cover with mask Nonfacial: cover or curette
Molluscum contagiosum	Curetted or removed Site covered	24 hours post-curettage Site covered

CA-MRSA, community-associated methicillin-resistant Staphylococcus aureus; HSV, herpes simplex virus; NCAA, National Collegiate Athletic Association; NFHS, National Federation of State High School Associations.

^aContains data from Likness. ²¹

Ecthyma

Ecthyma, a deep form of impetigo, is caused by group A beta-hemolytic streptococci. ²⁵

Clinical Presentation

Ecthyma is characterized by ulcerative, nonundermined, “punched-out” superficial ulcerations with prominent yellow (serous) crust (Figure 2).

Figure 2.

Ecthyma.

Diagnosis

Diagnosis is based on clinical presentation. Cultures may be ordered if the condition does not resolve with treatment.

Treatment

Treatment of ecthyma is the same as for impetigo (Table 1), except that oral antibiotics are recommended. ¹⁹ Use of acetic 0.025% acid soaks can help chemically debride the overlying crust. Acetic acid is available at some pharmacies or it can be made by mixing 3 tablespoons of white vinegar with 1 quart of water. Soak twice a day for 10 to 15 minutes until significant clinical improvement is noted.

Return-to-Play Recommendations

The recommendations are the same as those for impetigo.

Folliculitis

Folliculitis is the inflammation and infection of hair follicles. Recently shaved follicles and areas of the body with more friction could be predisposing or aggravating factors. ²⁵

Clinical Presentation

Folliculitis presents with erythematous papules and pustules that develop around hair follicles. It can also turn into nonhealing crusted sores anywhere on the skin except the palms and soles. There are 3 common subtypes of folliculitis. Staphylococcal folliculitis is usually pruritic and localized (methicillin-sensitive). It is occasionally painful and may cause systemic symptoms with widespread infection. Pseudomonas folliculitis, or “hot tub folliculitis,” presents with pruritic erythematous urticarial papules or pustules usually caused by inadequately disinfected whirlpool tubs and hot tubs or contaminated soaps and sponges. Pseudofolliculitis barbae, or “razor bumps,” is not a true bacterial infection. It is inflammation around the follicles in shaved areas and is more common in individuals with curly hair, with a high prevalence in African American men.

Diagnosis

Clinical presentation is sufficient for diagnosis; however, a culture may be helpful if the condition does not resolve with treatment.

Treatment

A summary of treatments for folliculitis can be found in Table 3.^16,30 For prevention, it is important that hot tubs and whirlpool tubs be disinfected regularly. Athletes should not share towels, and frequent shaving of high-friction areas should be avoided.

Table 3.

Summary of treatment for folliculitis ^a

Type	Treatment	Dosage	Other Recommendations
Staphylococcal folliculitis: first line	Cephalexin	500 mg PO QID for 7 days	No shaving over infectious area Small lesions: warm compresses 4 times daily Large lesions: incision and drainage, with wound culture preferred
Staphylococcal folliculitis: penicillin allergy	Azithromycin	250 mg/tab, 2 tabs PO for 1 day, then 1 tab PO daily for 4 days
Staphylococcal folliculitis: MRSA suspected	TMP-SMX	160-800 mg PO BID for 10 days
Pseudomonas folliculitis	Without treatment, resolves in 5-7 days without systemic spread	N/A	Fluoroquinolone for recalcitrant cases
Pseudofolliculitis barbae	Clindamycin phosphate and benzoyl peroxide gel 1.2%/5%	Applied at bedtime	Condition tends to be chronic, use of specialized straight razor can help to minimize inflammation

BID, twice a day; MRSA, methicillin-resistant Staphylococcus aureus; N/A, not applicable; PO, per oral; QID, 4 times a day; TMP-SMX, trimethoprim-sulfamethoxazole.

^aContains data from Klossner ¹⁶ and Stevens et al. ³⁰

Return-to-Play Recommendations

For staphylococcal folliculitis or pseudomonas folliculitis, playing is permitted after 48 hours of no new lesions and 72 hours of antibiotic therapy, a “48-hour/72-hour” rule. For medium- and low-risk contact sports, the lesions should be dry, not oozing, and may be covered with prewrap. There are no restrictions for athletes with pseudofolliculitis barbae, except in cases of secondary infection with bacteria or fungi. Secondary infection would be suspected with increasing erythema, edema and pain, skin induration, and active drainage. ³⁰

Abscesses, Furuncles, and Carbuncles

An abscess is a painful collection of pus under the skin. A furuncle, or boil, is an abscess formed within the hair follicle. A carbuncle is a cluster of furuncles connected to each other under the skin, usually caused by Staph aureus.

Clinical Presentation

Abscesses, furuncles, and carbuncles are painful, indurated, tender, fluctuant erythematous nodules, often with central pustules.

Diagnosis

Diagnosis is based on clinical presentation; however, wound cultures can be taken if necessary.

Treatment

A summary of treatments for abscesses, furuncles, and carbuncles can be found in Table 4. ³⁰

Table 4.

Summary of treatment for abscesses, furuncles, and carbuncles ^a

Type	Treatment	Dosage	Other Recommendations
Immunocompetent patient	Incision and drainage If the abscess is loculated, the drained cavity is packed with a wick	N/A	Small lesions: warm compresses QID; incision and drainage with wound culture Large lesions: incision and drainage with wound culture preferred
Immunocompromised patient	TMP-SMX	160-800 mg PO BID for 10 days

BID, twice a day; N/A, not applicable; PO, per oral; QID, 4 times a day; TMP-SMX, trimethoprim-sulfamethoxazole.

^aContains data from Stevens et al. ³⁰

Return-to-Play Recommendations

Athletes can typically return to play once the lesions are dry. If lesions are still moist or draining, they cannot return, even if the site is covered. For non-MRSA infections, the NFHS recommends return to contact practice, and competition may occur after 72 hours of treatment, provided the infection is not actively draining. Abscess incision and drainage should be performed for MRSA infection. Consider return to practice after treating for 72 hours without further drainage or new abscess formation. An appropriate covering is needed after incision and drainage if the lesion is dry. Abscesses complicated by cellulitis are governed by the 48-hour/72-hour rule.

Erysipelas and Cellulitis

Erysipelas and cellulitis are bacterial infections that affect the superficial and deeper dermis and subcutaneous tissue, respectively. Predisposing factors in athletes include untreated skin abrasions, impetigo, and abscesses.

Clinical Presentation

The hallmarks of both conditions are erythema, edema, and warmth, often associated with acute fever and chills. Erysipelas presents with raised, well-demarcated, smooth, vividly red plaque (Figure 3). Cellulitis is a deeper, fainter, ill-defined, red edematous patch or minimally raised plaque.

Figure 3.

Erysipelas.

Diagnosis

No studies are needed initially for diagnosis. Laboratory tests, including complete blood count, kidney function tests, blood cultures, and wound cultures (not as sensitive, except with a coexisting abscess), can be ordered for manifestations, such as fever, chills, and worsening rash.

Treatment

A summary of treatments for erysipelas and cellulitis can be found in Table 5. ¹¹

Table 5.

Summary of treatment for erysipelas and cellulitis ^a

Type	Treatment	Dosage	Other Recommendations
Non–CA MRSA: first line	Cephalexin	500 mg PO QID for 10 days	Elevation of extremity to decrease edema
Non–CA MRSA: penicillin allergy	Azithromycin	250 mg/tab, 2 tabs PO for 1 day, then 1 tab PO daily for 4 days
CA-MRSA: first line	TMP-SMX	160-800 mg PO BID for 10 days	Incision and drainage of abscess helpful
	Clindamycin	300 mg PO TID for 10 days (potential for GI adverse effects)	If no improvement within 72 hours, blood cultures should be taken
CA-MRSA: if no improvement with PO therapy	Vancomycin	1 g intravenous every 24 hours	After improvement on intravenous antibiotics, conversion to PO

BID, twice a day; CA-MRSA, community-associated methicillin-resistant Staphylococcus aureus; GI, gastrointestinal; PO, per oral; QID, 4 times a day; TMP-SMX, trimethoprim-sulfamethoxazole.

^aContains data from Gunderson and Martinello. ¹¹

Return-to-Play Recommendations

Playing is allowed after completion of the appropriate antibiotic course. Lesions should be covered. Athletes should wash after practice, towels should not be shared, and contact with infected individuals should be limited.

Other Infectious Disorders

Tinea

Tinea, or ringworm, refers to superficial dermatophyte infections spread by person-to-person or animal contact or by touching contaminated surfaces. The fungus can live outside the host for an indeterminate time. Warm moist environments increase the survival of this pathogen.

Clinical Presentation

Tinea infections classically present as an annular plaque with central clearing and elevated scaly active edge (Figure 4). They occur most often on the feet, where vesicular presentations are most common, on the groin, and under skinfolds; however, the infection may occur anywhere on the body. They are classified by anatomic location. Tinea pedis involves the feet; tinea cruris, the groin; tinea capitis, the scalp; tinea barbae, the bearded face; tinea unguium, the nails; and tinea corporis, other body surfaces not previously mentioned.

Figure 4.

Tinea corporis.

Tinea versicolor, caused by several species of fungi (Malassezia [nondermatophyte]), is characterized by abundant, asymptomatic, hypopigmented or hyperpigmented oval skin patches. Individual lesions are often 1 to 3 cm in diameter, but dozens of lesions may coalesce to form a maplike appearance on the upper chest and back. The skin surface typically has a dry or dusty surface. The lesions may be skin colored, slightly hypopigmented, or slightly hyperpigmented, but all lesions on a person have a uniform color. ¹²

Diagnosis

Clinicians can make this diagnosis in various ways. The leading edge of the lesion can be scraped with a 15-blade scalpel. Direct examination is performed with a 10% or 20% potassium hydroxide preparation; skin cells lyse, allowing for visualization of the septated fungal hyphae. Heating the preparation and allowing it to sit for 3 minutes improves diagnostic yield. All classifications are diagnosed in the same manner. When diagnosis is uncertain or potassium hydroxide preparation test results are negative, a culture can be taken. Skin biopsies with special stains are also diagnostic.

For the diagnosis of tinea versicolor, the fungus can be identified under the light of a Wood ultraviolet lamp; Malassezia infections produce a subtle yellowish-orange hue. Examination under a microscope can also identify tinea versicolor. ⁹

Treatment

A summary of treatments for tinea can be found in Table 6.^3,15,26,32 Hepatic injury related to long-term use of oral antifungals is generally not a prohibitive factor. The safety profile of terbinafine makes this the preferred agent in most circumstances. Ketoconazole has a hepatoxicity rate of approximately 1 in 2000 and should be used cautiously. ³³ Patients should be monitored with liver function testing for treatment lasting longer than 6 weeks.

Table 6.

Summary of treatment for tinea

Type	Treatment	Dosage	Other Recommendations
All types of superficial tinea infections (except on scalp)	Topical imidazoles (clotrimazole, ketoconazole, miconazole) or allylamines (terbinafine, naftifine)	Applied TID for 7 days (treatment could last 3-30 days)	Treatment with allylamines reported to have better efficacy and shorter duration 32
Widespread infection, failed topical treatment, or immunocompromised patient	Systemic treatment with imidazoles or terbinafine	Fluconazole: 150 mg tab PO weekly for 3 weeks. Itraconazole: 200 mg tab PO daily for 2 weeks Terbinafine: 250 mg tab PO daily for 2 weeks	Systemic treatment with terbinafine is more effective than with griseofulvin and equally effective as with any imidazole
Tinea capitis	Systemic treatment with griseofulvin (first line), imidazoles, or terbinafine	Griseofulvin: 20-25 mg/kg PO daily Terbinafine: 250 mg tab PO daily Itraconazole: 5 mg/kg PO daily Fluconazole: 8 mg/kg PO weekly Duration: 6-12 weeks or longer until fungal cultures are negative 3	Selenium sulfide 2.5% shampoo is effective against fungal spores, could be used as adjunctive therapy 15
Tinea unguium 26	Systemic terbinafine or imidazoles Option for mild to moderate onychomycosis without involvement of the lunula: topical ciclopirox nail lacquer therapy	Terbinafine: 250 mg tab PO daily for 6-12 weeks Itraconazole: 200 mg tab PO daily for 6-12 weeks Fluconazole: 150 mg tab PO weekly until nail is normal or acceptably improved	100% cotton socks should be worn and changed often Breathable footwear should be worn In shaded bathing areas, feet should be protected and kept dry throughout the day Tinea pedis should be recognized and treated Chronic health conditions (eg, diabetes, smoking) should be managed and healing promoted

PO, per oral; TID, 3 times a day.

Return-to-Play Recommendations

The NCAA and NFHS recommendations include 72 hours of topical treatment for nonscalp infections and 2 weeks of systemic antifungal medication for scalp infections.^16,23 Tinea epidemics can be prevented by the recognition and treatment of infected individuals and the restriction of participation while lesions are being treated.

Herpes Simplex

Herpes simplex virus (HSV) type 1 (HSV-1) is a common infection that can involve the oral mucosa or lips (herpes labialis), eye (herpetic keratitis), hands or fingers (herpetic whitlow), or bearded area (herpetic sycosis). ²⁹ Herpes gladiatorum, with skin-to-skin involution involving the torso, is the most common infection site in wrestlers. ³¹ It is estimated that 40% to 63% of the US population has HSV-1. ³¹

Genital herpes is a sexually transmitted disease that is most commonly caused by HSV type 2 (HSV-2); however, the incidence of genital herpes caused by HSV-1 is increasing. In the United States, nearly 1 in 5 adults, approximately 50 million people, have HSV-2 infections. ¹⁰ HSV has been found to survive on plastic-coated seats in spa facilities for up to 4.5 hours.^1,18

HSV-1 and HSV-2 travel to the sensory dorsal root ganglion, where latency is established. Reactivation episodes can occur, and these viruses are incurable. From 1991 to 2003, the NCAA’s Injury Surveillance Program estimated that 39% of skin infections were HSV. ²⁴

Reactivation Triggers

Stress, cold, fever, and corticosteroids can trigger reactivation. Respiratory droplets or exposure to mucocutaneous secretions of an asymptomatic shedder are also factors. Most individuals with herpes simplex labialis carry HSV-1 on their hands. HSV collected from genital lesions can survive up to several hours on fomites and hard surfaces and 72 hours on dry cotton gauze. There is no difference between HSV-1 and HSV-2 regarding reactivation triggers. ¹⁸

Clinical Presentation

Within 1 to 2 days, vesicles on a red base appear and rupture, then small painful erosions develop. Recovery with complete skin reepithelization occurs within 2 weeks. The antibodies formed against HSV-1 do not protect against reactivation. Viral shedding lasts several weeks, even after all skin manifestations resolve. Recurrence often occurs at sites of prior involvement. ²⁴

Herpes simplex labialis

Recurrent orofacial herpes has a shorter prodrome that includes focal tingling or pain. Within 24 hours, vesicles appear, coalesce, rupture, and rapidly crust over. The lesions heal without scarring within 10 days. Shedding occurs for 3 to 5 days after the lesions crust over, with shorter and milder recurrent episodes. Eruptions close to the eye can involve the trigeminal nerve and result in blindness.

Herpes gladiatorum

The incubation period is 2 to 20 days. Vesicles appear within 3 to 5 days of direct skin-to-skin contact and are usually located in the head but can occur in the extremities and trunk. The primary infection presents with burning, tingling, or stinging at the site. Vesicles rupture and if confluent, can form erosive patches. Recurrent herpes gladiatorum has been identified in 29% of high school wrestlers and 20% to 40% of collegiate wrestlers. ¹

Herpetic whitlow

This occurs on the pulp of the distal phalanx. It is self-limiting; thus, no treatment is needed unless the condition is extensive. Self-infection can occur over the face, nose, ocular or genital mucosa, or digits.

Diagnosis

Physical examination is usually sufficient for diagnosis. Confirmation can be made by detecting herpetic DNA via polymerase chain reaction in the fluid from the blisters or a swab of the erosion.

Treatment

A summary of treatments for HSV can be found in Table 7.^1,4 Oral therapy may reduce duration and limit transmission; however, it is most effective during the prodromal phase, within the first 48 hours of recurrence.

Table 7.

Summary of treatment for HSV

Type	Treatment	Dosage	Other Recommendations
Initial infection (HSV-1 or HSV-2)	Acyclovir, valacyclovir, or famciclovir	Acyclovir: 200 mg/tab, 1 tab PO 5 times a day or 2 tabs PO TID for 7-10 days Valacyclovir: 1 g tab PO BID for 7-10 days Famciclovir: 500 mg tab PO BID for 7-10 days 4	Active orofacial or labial infections: avoid kissing and utensil sharing Genital infections: avoid contact, sexual intercourse, sharing of towels and clothing
Recurrent infections	Acyclovir, valacyclovir, or famciclovir	Identical to initial infection, but for 5 days
Recurrence prevention	Valacyclovir	500 mg or 1 g tab PO daily or TID throughout wrestling season
Long-term suppressive therapy (history of severe facial outbreaks or more than 6 outbreaks of genital herpes/year) 1	Valacyclovir	500 mg or 1 g tab PO daily

BID, twice a day; HSV, herpes simplex virus; HSV-1, HSV type 1; HSV-2, HSV type 2; PO, per oral; TID, 3 times a day.

Prophylactic therapy in wrestling camps has been found to reduce recurrent outbreaks of recurrent herpes gladiatorum by 87%. The efficacy of prophylactic valacyclovir for primary HSV infections is unknown. ¹

Return-to-Play Recommendations

Suppressive therapy is recommended for HSV-1 seropositive individuals for the duration of the season. According to the NCAA and NFHS, merely covering active herpetic lesions is insufficient.^16,23 Athletes must not have moist lesions, systemic symptoms, or new blisters for 72 hours. All lesions must be dry, with a firm adherent crust. The NCAA and NFHS recommend antiviral therapy for at least 120 hours^16,23; however, there is scant evidence to support this recommendation.

HSV detected by polymerase chain reaction can persist even after 5 days of antiviral treatment. ¹ The relationship to infectivity is unknown.USA Wrestling requires that the team physician and medical coordinator give final clearance. With USA Wrestling also, merely covering the lesions is not sufficient. Oral medications must also be taken for more than 72 hours.^1,6

Intertrigo

Intertrigo is caused by inflammation of the skin folds and results from rubbing, heat, moisture, and hyperhidrosis. ¹⁴ Skin manifestations are attributed to skin-on-skin friction; however, there can also be secondary fungal or bacterial infection. Gram-positive and gram-negative bacteria can be seen, but Candida superinfection is most common. In rare cases, intertrigo can be complicated by concomitant dermatophyte infections.

Clinical Presentation

Intertrigo presents as a bright red variably eroded patch that affects warm moist areas, such as the groin, axillae, buttocks, interdigit, inframammary folds, and antecubital fossae. Other risk factors include hyperhidrosis, poor hygiene, closed-toed or ill-fitting shoes, and tight-fitting clothes that retain moisture. ¹⁴

Diagnosis

Clinical history and presentation are often characteristic but may appear similar to inverse psoriasis. The presence of pustules at the edges of the patch favors candidal intertrigo.

Treatment

Topical or oral antibiotic or antifungal coverage or topical anti-inflammatories (ie, corticosteroid creams or calcineurin inhibitors) are recommended in the absence of secondary infections.

Other recommendations include minimizing moisture and friction. The wearing of light, nonconstricting, absorbent cotton or polyester clothing is recommended. Nylon and synthetic fibers can exacerbate the condition. Skinfolds need to be kept clean and dry. Miconazole powder can be used on flare prone areas, but it is not effective with active disease. Showering immediately after training, drying off completely, and wearing clean dry clothing are recommended. Open-toed shoes are an option.

Return-to-Play Recommendations

There are no clear guidelines for return to play. Secondary fungal or bacterial skin infections should be treated in accordance with NCAA guidelines. ¹⁶ Dry unresolved lesions should be covered with bio-occlusive dressings and prewrap during competition.

Verrucae Vulgaris

Verrucae vulgaris (warts) are skin lesions caused by human papilloma virus infections acquired from direct contact (eg, person-to-person) or from the environment (eg, showers and swimming pools). Wet or broken skin increases the chance of penetration.

Clinical Presentation

Warts are usually rough hyperkeratotic papules with papillomatous (cauliflower-like) projections. Palmar and plantar warts present as endophytic hyperkeratotic papules or small plaques with interrupted skin lines. Small black dots representing thrombosed capillaries are commonly seen (Figure 5).

Figure 5.

Verruca vulgaris.

Diagnosis

Clinical presentation is usually sufficient, and skin biopsy is rarely necessary.

Treatment

There are several treatment options, such as liquid nitrogen, laser, curettage, salicylic acid, cantharidin, trichloroacetic acid, and duct tape. Topical medications include imiquimod, 5-fluorouracil, and squaric acid diphenylcyclopropenone. ²⁰ Oral medications include cimetidine and zinc sulfate for generalized lesions. ²⁷

Return-to-Play Recommendations

Playing with covered lesions or after curettage is permitted. ²¹

Molluscum Contagiosum

Also known as “itch of the bath,” molluscum contagiosum is a skin condition caused by poxvirus infection acquired from skin-to-skin contact. ⁵ The prevalence is 7.5% in swimmers and 3.6% in nonswimmers.

Clinical Presentation

Molluscum contagiosum presents with small, firm, raised, round, flesh-colored, nonfollicular, centric smooth papules that can appear anywhere on the body. The lesions are often pruritic with a central dell or umbilication (Figure 6).

Figure 6.

Molluscum contagiosum.

Diagnosis

An umbilicated papule with peripheral erythema is very characteristic. In cases of uncertainty, curettage with a histopathologic examination is diagnostic and curative.

Treatment

Molluscum contagiosum usually resolves spontaneously within 1 year. Curettage is more effective than topical medications. The site should be covered after tissue removal.

Return-to-Play Recommendations

Playing after curettage with the site covered is permitted. ²¹

Noninfectious Conditions

Acne Mechanica

Known as “sport-induced acne,” acne mechanica is a type of acneiform folliculitis caused by heat, pressure, occlusion, and repeated friction of hair-bearing skin.^7,8 Athletes with acne vulgaris have a predisposition for and higher likelihood of infection.

Clinical Presentation

Acne mechanica manifests as red papules, pustules, and nodules usually located in the distribution of protective equipment. Common truncal or thigh involvement results from the use of cotton undergarments. The differential diagnosis includes contact dermatitis caused by the chemicals used to clean athletic equipment and playing surfaces. Football and hockey players present with rashes under pads, helmets, or chinstraps; golfers with a rash in a golf bag strap pattern; and equestrians with rash in a chinstrap pattern.

Treatment

Benzoyl peroxide, topical and systemic antibiotics, and topical retinoids, such as tretinoin cream, are the recommended treatments. For severe and refractory acne, systemic isotretinoin can be used; however, there is a risk of myopathy and tendinitis.

Prevention

Wearing moisture-wicking clothes or clean absorbent cotton shirts under sports equipment and diligently cleansing the skin after intense physical activity are recommended.

Blisters

Moist skin increases frictional force, which in turn increases the likelihood of blisters. ²⁸ Aggravating factors include heat, ill-fitting shoes, and excessive or unusual exercises early in training. Frequent locations are the posterior heel, tips of the toes, and balls of the feet. This is the most common complaint of marathon runners. The palms and fingers of racquet sports players are also often affected. ²⁸

Treatment

Small blisters resolve spontaneously if left alone. Needle compression with a sterile blade or needle can be applied to large blisters that interfere with activity to release the fluid after the site has been cleansed with alcohol. The blister roof should be left intact to minimize the likelihood of infection and to promote healing. After the blister has been drained, petrolatum and an adhesive bandage or second skin product may be applied to minimize further friction. This process may be performed up to 3 times within 24 hours.

Prevention

The use of dry, moisture-wicking acrylic or polyester socks is recommended. Wet socks should be changed frequently. For long-distance runners, acrylic socks are more beneficial than cotton socks. Fewer and smaller blister events occur with 100% acrylic socks. If hyperhidrosis is a factor, talc powders or 10% tannic acid soaks may be beneficial. Once pain has been relieved, the athlete may return to play with monitoring for infection and continued skin abrasion.

Contact Dermatitis

Contact dermatitis is an inflammatory reaction triggered by contact with a substance. Both irritant and allergic contact dermatitis can be seen in athletes.^8,17,22 Athletes are frequently exposed to irritant factors, such as trauma, heat, and moisture, and may have contact with sport-specific allergens and chemicals. These eruptions present on a spectrum of acute to subacute to chronic dermatitis. Athletes with a history of atopic dermatitis are more prone to these eruptions.^8,17,22

Clinical Presentation

Acute dermatitis presents as erythema, crusting, and scaling, with variable vesiculation. Subacute dermatitis is characterized by pruritic, scaling, ill-defined erythematous patches and thin plaques. Chronic dermatitis results in progressive skin thickening (acanthosis) and may demonstrate lichenification, where natural skin lines appear exaggerated.

Treatment

Contact dermatitis, when allergic, improves or resolves when the contact sensitizer is identified and avoided. Topical corticosteroids to relieve skin inflammation and pruritus are first-line interventions.

Prevention

Contact with the offending agent should be avoided and the effect of low-grade irritants producing xerosis can be minimized with bland emollient moisturizers.

Conclusion

Specific dermatologic conditions show an increased prevalence in athletes. Correct diagnosis and treatment facilitate a faster return to play and prevent larger team-related adverse effects.

Clinical Recommendations

• Overlying crust removed frequently to improve antibiotic absorption for the treatment of impetigo.

• Treatment of ecthyma is the same as for impetigo, except that oral antibiotics are recommended.

• Prophylactic therapy in wrestling camps has been found to reduce recurrent outbreaks of herpes gladiatorum by 87%.

• Molluscum contagiosum usually resolves spontaneously within 1 year. Curettage is more effective than topical medications.

• Wearing moisture-wicking clothes or clean absorbent cotton shirts under sports equipment is recommended to prevent acne mechanica.

• The blister roof should be left intact to minimize the likelihood of infection and to promote healing.