Sports-related skin infections

As the world celebrates athletics during the XXth winter Olympics in Italy, interest and participation in sports expands. An often unanticipated and undesired consequence of athletic involvement includes injury. Athletes experience myriad medical issues, and skin disorders are among the most common. Of these cutaneous conditions, skin infections cause the most significant morbidity, individual disqualification and team disruption. Athletes of all abilities, from the Olympian to the neophyte, risk cutaneous infections. These infections are not unique to athletes and may occur in any individual. However, due to several unique characteristics, athletes preferentially develop skin infections.

First, athletes’ skin represents an ideal microenvironment for infecting organisms. Sweating not only provides the moist conditions ideal for microbial growth, but also macerates the epidermis and facilitates the penetration of the various micro-organisms past the cutaneous barrier of the athlete. Second, athletes often wear protective equipment or tight fitting uniforms that also provide the warm, dark and moist environment that is ideal for organisms’ growth. Third, athletes invariably experience abrasions, cuts and lacerations that allow the microbes easier access to the epidermis. Finally, many sports involve intense skin-to-skin contact among competitors. This contact successfully promotes spread of infection amongst athletes.

This editorial discusses the role of sport in the transmission of skin infections and offers practical care guidelines for these disorders for all athletes from the neophyte to the Olympian. Specifically, this editorial will review the diagnosis, treatment and prevention of bacterial, fungal, parasitic and viral infection occurring in athletes. Knowledge of the singular effect of sports on the development of cutaneous infections permits the sports clinician to expertly care for athletes’ skin.

Bacterial infections

Staphylococcus aureus and Streptococcus (including nephritogenic Streptococcus [M-type 2]) species cause impetigo, folliculitis and furunculosis. Methicillin-resistant S. aureus (MRSA) has increasingly caused these infections in athletes. These infections have occurred in epidemic proportions in fencers, weightlifters, wrestlers and American football, rugby and soccer players [1,2]. Most bacterial infections in athletes occur on exposed skin, corresponding to locations of intense skin-to-skin contact during practice and competition, although lesions may also appear beneath athletic equipment. Acquiring turf burns, shaving body hair cosmetically, wearing athletic tape and elbow pads and not showering before using communal whirlpools increase the risk of developing the disease [2].

The clinical morphology of most cutaneous disorders depends on the age of the lesion, and the variable appearance of the same disease over time can make punctual diagnosis challenging for the sports clinician. For example, very early lesions of impetigo demonstrate small red papules that can be confused with acne vulgaris, atopic dermatitis, folliculitis, herpes gladiatorum and tinea corporis gladiatorum. On the other hand, older lesions of impetigo exhibit yellow, crusted red plaques that may demonstrate obvious pustules; tense clear fluid-filled blisters may occur rarely [3].

Also caused by S. aureus and Streptococcus, folliculitis appears differently as small, follicular red papules and pustules. Furuncles are larger and, in their mature stage, are erythematous nodules that may have an overlying pustule. The differential diagnosis of S. aureus folliculitis includes pityrosporum folliculitis, eosinophilic folliculitis, acneiform folliculitis and hot tub folliculitis. The diagnosis of mature furunculosis is generally straightforward but it may be confused for a ruptured cyst.

Cultures of bacterial infection are required for indeterminate lesions and when MRSA is considered. Athletes may also asymptomatically carry S. aureus in their perianal region and nares or Streptococcus in their throat, so clinicians should culture these areas after repeated infection or during team epidemics. It is important to realize that systemic findings (lymphadenopathy, pharyngitis and post-streptococcal glomerulonephritis) may result [3].

Foremost, the clinician needs to repair the perturbed stratum corneum; therapy includes the use of warm water soaks on lesions for 5–10 min three times per day until the lesions are clear. Effective therapy includes the application of mupirocin ointment twice daily and the administration of oral dicloxacillin or cephalexin 500 mg three times per day for 10–14 days. Athletes allergic to penicillin and similar medications should use erythromycin or clindamycin. Methicillin-resistant S. aureus infections require trimethoprim/sulfamethoxazole or clindamycin for at least 14 days. Topical mupirocin is also effective as are oral tetracycline, vancomycin, linezolid or dactinomycin.

Duration of disqualification from close contact with other competitors is controversial but 3 days after starting therapy seems to be a reasonable time period. Continued practice is allowed if the lesions can be adequately and securely covered. Athletes should launder equipment in very hot water and whirlpools need to be regularly drained and cleaned. All athletes must avoid body shaving and sharing equipment, towels, ointments and tape, although no evidence-based medicine supports this tactic. Decreasing the exposed skin area by wearing loose-fitting, moisture wicking and synthetic clothing, athletes can inhibit the spread of infection. All trainers and other sports clinicians must carefully sanitize their hands between seeing athletes.

Athletes with positive methicillin-sensitive or -resistant S. aureus nasal or crural cultures must apply topical mupirocin to each nares or the perianal area twice daily for 1 week; this application must be repeated every 6 months [3].

Fungal infections

Tinea pedis

Swimmers, runners, and soccer, water polo and basketball players experience tinea pedis 2–4 times more commonly than non athletes [4,5]. Trichophyton, Epidermophyton and Microsporum cause almost all types of tinea pedis, although Candida can also cause disease. The three clinical types of tinea pedis include moccasin, vesicular and interdigital. The moccasin type demonstrates ill-defined scaling plaques on the lateral aspects of the soles. Athletes may mistake this type for simple dry skin. The interdigital variety demonstrates macerated, scaling plaques in the web spaces, and the vesicular variety exhibits moderately pruritic, well defined, moderately red, scaling papules, plaques and vesicles on the sole’s instep. Most often, tinea pedis is asymptomatic [6].

The differential diagnosis includes xerosis (dry skin), eczema, psoriasis and pitted keratolysis. Potassium hydroxide examination confirms the diagnosis and cultures designate species identification.

Topical therapy twice daily for several weeks clears the eruption. The fungicidal (allylamines) creams are optimal, as they possess fungicidal and antibacterial properties [7]. Oral anti fungal therapy will clear resistant disease. Topical aluminum chloride 30% may prevent tinea pedis [8]. Very thick skin requires topical urea preparations in varying concentrations. Domeboro soaks or a vinegar/water mix twice daily dries wet areas and moderate potency topical corticosteroids, such as triamcinolone 0.1% ointment, improve pruritus. Wearing synthetic socks wicks moisture from the foot and prevents hyperhydration of the foot.

Tinea corporis gladiatorum

Epidemics of tinea corporis have affected up to 75% of a wrestling team. However, any athlete with intense skin-to-skin contact may develop ringworm. Trichophyton tonsurans has caused more than 100 reported cases of tinea corporis gladiatorum; this dermatophyte resides asymptomatically in some athletes’ scalps [9]. Athletes develop nonannular, red, round, scaling papules and plaques on the head, neck and arms (which correlate to the skin-to-skin contact areas). Very early lesions may be confused for acne, eczema, early herpes gladiatorum and early impetigo. Potassium hydroxide examination confirms the diagnosis and cultures designate species identification. Evidence-based medicine recommends once-weekly oral fluconazole (200 mg) for 3 weeks [10]. Other oral therapies, without evidence-based support, include ketoconazole 200 mg daily for 2–4 weeks and itraconazole 200 mg daily for 1–2 weeks. The duration of disqualification is controversial but infected athletes should not compete or practice for 3 days after beginning therapy. Athletes may cover affected areas during practice but will not be eligible to compete without proper therapy. While no study has confirmed transmission of the dermatophyte via equipment and mats, athletes should avoid sharing equipment [3].

Prevention of epidemics includes a multistaged approach. Trainers and athletes themselves should carefully examine the athletes’ skin to discover lesions at the earliest possible point. Prompt therapy and isolation will inhibit spread among the team or competitors. Oral prophylaxis with every-other-week itraconazole (400 mg) [11] or once weekly fluconazole (100 mg) [12] decreases the incidence of tinea corporis gladiatorum.

Parasitic infestations

Scabies

All athletes with close skin-to-skin contact (such as judo and wrestling) risk contracting scabies from other infected athletes. The mite Sarcoptes scabiei causes scabies, which is a significantly pruritic eruption, whose lesions predominately occur on the trunk, extremities and groin. While the organism’s burrows occur on the wrist and elbows, distant skin demonstrates eczematous reaction, which represents a sensitization to the mite and its feces. It is critical to note that athletes develop pruritus, not limited to the direct area of scabies infestation.

Proper diagnosis includes identifying the organism under the microscope after scraping the burrow onto a drop of mineral oil on a glass slide. Athletes with scabies should apply permethrin 5% cream to every skin surface from the neck down or take oral ivermectin at a dose of 200 µ/kg. Both treatment regimens should be repeated one week later; housemates need coexistent therapy. All clothing and equipment used 3–5 days prior to diagnosis should be carefully cleaned. Once treated, the athlete may return to practice and competition.

Viral infections

Herpes labialis

Nearly all athletes at the XXth winter Olympics risk reactivating prior herpes simplex virus (HSV) infection. These winter athletes appear particularly prone, because at high altitudes the atmosphere absorbs less ultraviolet radiation and snow powerfully reflects radiation onto the athlete. One study demonstrated that the ultraviolet radiation experienced by a winter athlete at 11,000 feet on a snow-covered mountain in Colorado, USA, is comparable to that experienced by an aquatic athlete at the beach in Orlando, Florida [13].

Herpes labialis begins first with a prodrome of tingling or burning on the lip at the site of a future red papule and ultimately a vesicle; this process takes several days. Recent studies document the effectiveness of very short-term therapy [14]. Treatment includes two 1 g tablets of valacyclovir taken in just two doses within 1 day. Competitive outdoor winter athletes with a history of oral herpes labialis should consider taking daily suppressive therapy with valacyclovir 1 g. Lip balm with sunscreen should be compulsory outdoor winter athlete equipment.

Herpes simplex in contact sports

All athletes with close skin-to-skin contact risk acquiring HSV infection on skin other than their lips. Wrestlers and rugby players most frequently develop (median prevalence 20%) this type of HSV infection termed herpes gladiatorum and rugbieorum, respectively [6]. Clinically, the athlete experiences a prodrome of stinging and burning in the area of subsequent skin lesions (often on the head and neck). Early lesions are nonspecific red papules or plaques, but progress to display grouped vesicles upon an erythematous base. Early lesions can easily be confused for acne vulgaris, atopic dermatitis, molluscum contagiosum, tinea corporis gladiatorum and impetigo. A quarter of the athletes develop fever, sore throat, malaise, myalgias, arthralgias or swollen lymph glands [6]. Culture or direct immunofluorescence confirm HSV infection. Rare complications of herpes gladiatorum or rugbieorum include herpes conjunctivitis, blepharitis and keratitis [15], monoarticular arthritis [16] and HSV-related meningitis [17].

Treatment includes two 1 g tablets of valacyclovir, taken in just two doses within 1 day. Athletes can compete and practice 96 h after starting oral therapy, assuming all lesions have crusted and the athlete has not had any new blisters for 3 days or any systemic symptoms. Prevention of epidemics is challenging, as athletes are infectious before obvious skin lesions exist and herpes gladiatorum is often initially mistaken for other banal skin disorders. An athlete competing against an infected opponent risks a 33% chance of contracting HSV [18].

Prevention of epidemics includes a multistaged approach. Trainers and athletes themselves should carefully examine the athletes’ skin to discover lesions at the earliest possible point. Prompt therapy and isolation will inhibit spread among the team or competitors. One study demonstrated that at-risk athletes could prevent infection with daily oral valacyclovir (1 g) during the season [19].

Molluscum contagiosum

Poxvirus causes molluscum contagiosum in multiple contact (rugby players and wrestlers) and noncontact sports (gymnasts, swimmers and volleyball players) [20]. Over areas of skin-to-skin contact or in equipment occluded areas, athletes develop multiple, small (occasionally pinpoint), asymptomatic, white or skin-colored papules with a central indentation. Small lesions present a diagnostic challenge; the differential diagnosis includes acne vulgaris, folliculitis and warts.

Molluscum resolve spontaneously, but currettement with a commercially available currette or the end of a tongue depressor, broken longitudinally, rapidly removes the lesions. Destruction with liquid nitrogen, trichloroacetic acid or cantharidin also cures molluscum. Athletes alternatively may apply topical imiquimod, tretinoin or tazarotene. Prevention of epidemics includes a multistaged approach. Trainers and athletes themselves should carefully examine the athletes’ skin to discover lesions at the earliest possible point. Prompt therapy and isolation will inhibit spread amongst the team or competitors.

Summary

Athletes represent a unique group of patients. The variety of skin infections experienced by athletes does not differ from nonathletes. However, a specialized approach to sports-related skin infections optimizes therapy and prevention. Skin infections not only cause significant individual morbidity, but also create significant team disruption. Future research needs to focus on prompt diagnosis and improved pharmacological prevention plans.