Skin Infections in Athletes

Brian B Adams


Expert Rev Dermatol. 2010;5(5):567-577. 

In This Article


The three main viral infections acquired by athletes are herpes simplex infection, verruca vulgaris and molluscum contagiosum.

Herpes Simplex virus Infection

Herpes simplex virus-1 (HSV) causes two primary manifestations in athletes as a result of their activity. Athletes may acquire HSV from other athletes, especially in sports with close skin-to-skin contact such as wrestling, judo and rugby.[1,32] Alternatively, as a result of reactivation of dormant HSV, athletes with intense exposure to ultraviolet radiation develop lesions. Skiers, for instance, frequently experience reactivation of herpes labialis.[36]

Skiers risk reactivation of HSV for a variety of reasons. First, the high elevation of the competition venue allows for more intense UV exposure. As there is less atmosphere to filter the harmful UV rays of the sun, athletes in the high altitudes of the snowy mountains experience a comparable amount of UV radiation as athletes competing at sea-level in Orlando (FL, USA).[37] Furthermore, the snow reflects nearly all of the UV radiation that hits it. As such, athletes who practice sun safety solely by creating shade cannot ensure protection because the UV radiation reflects back to their skin from the snow-covered ground surface.[1] One study documented a significant decrease in the prevalence of HSV reactivation in skiers after applying sunscreen.[38] Other investigators demonstrated that skiers who took acyclovir 400 mg twice-daily 12 h before UV exposure developed significantly fewer HSV lesions.[39]

Close skin-to-skin contact represents another common method by which athletes acquire cutaneous viral eruptions, namely herpes virus infection, verruca vulgaris and molluscum contagiosum.[1] Wrestlers frequently acquire HSV from other wrestlers; this eruption, termed herpes gladiatorum, has occurred in epidemic proportions. Rugby players also endure this eruption. Numerous studies have noted epidemics of herpes gladiatorum; the median prevalence is approximated to be 20%.[1,40–43]

Intense skin-to-skin contact represents the most important aspect that facilitates transmission, but sharing of equipment may also play a role; very little evidence exists to implicate the wrestling surface. Extensive epidemiologic research has documented the significant risk of sparring with an infected wrestler; a third of unaffected wrestlers who compete with infected partners will develop herpes gladiatorum.[44] Most infected athletes will develop lesions within 5 days.

Infected athletes will almost always note a burning, tingling or prickly sensation in the area of eventual infection. This prodrome, without skin lesions, precedes the manifestation of erythema and vesicles by several days. Initially, nonspecific erythematous macules and patches develop and later, the typical, grouped vesicles on an erythematous base occur (Figure 9). The most common sites of distribution include the head, neck and extremities.[1,44]

Figure 9.

Herpes gladiatorum.

To avoid epidemics, infected athletes need treatment as soon as possible. Valacyclovir rapidly clears the cutaneous eruption. A total of 4 g of valacyclovir administered in 1 day results in clearance of the virus within 4 days.[1] During isolated outbreaks of herpes gladiatorum, clinicians may use bandaging techniques along with oral antiviral agents for infected athletes. While infected athletes cannot compete for 4–5 days after institution of the oral antiviral agents, practice may continue if the athlete can easily cover the affected area with a bandage that cannot be dislodged.[1]

Like other sports-related skin infections, meticulous skin examinations by the athletes and medical staff, including the athletic trainers, will identify early infections in competitors and may help avoid team epidemics. To further minimize epidemics of herpes gladiatorum, athletes should use the same techniques described in the section on prevention of tinea corporis gladiatorum.

Susceptible athletes, especially those with a history of recurrent herpes infections, should take season-long prophylaxis. A randomized, placebo-controlled, study demonstrated the effectiveness of daily oral valacyclovir in the prevention of herpes gladiatorum.[45]

Verruca Vulgaris

Human papilloma virus causes verruca vulgaris (warts) and occurs in epidemic proportions in athletes, although no prevalence data exist in the literature. Overall, athletes with intense skin-to-skin contact with other athletes and athletes who share equipment or fail to wear sandals in the showers or locker room risk acquiring this virus.[1,46] While researchers have not extensively investigated various sports and the incidence of warts, several studies have documented an increased risk of disease among swimmers.[47] Rowers also seem particularly susceptible.[48]

Verruca commonly occur on the soles and hands of athletes. These infected athletes develop verrucous, thick scaling, well-defined plaques. Occasionally, clinicians can confuse verruca with calluses and corns. Clinicians should pare suspicious thick plaques on the palms and soles of athletes; verruca demonstrate black dots (pericapillary hemorrhages), while corns display a central core, and calluses do not possess any change in the fingerprint pattern.[1]

Verruca clear with destructive methods; an ideal regime for treating verruca includes soaking, paring and applying liquid nitrogen or cantharidin. Athletes may also apply salicylic acid in combination with dithranol. This regime also frequently leads to blister formation and pain. Unfortunately, the resultant discomfort may prevent athletic activity; athletes may prefer to apply over-the-counter or prescription treatment instead. While these self-applied chemical therapies may permit continued athletic activity, this approach takes longer to clear the warts.[1]

Molluscum Contagiosum

Molluscum contagiosum, caused by a pox virus, commonly infects athletes, especially those who share equipment, those who engage in athletic activity with close skin-to-skin contact, and those who partake in aquatic sports. Tight-fitting athletic clothing seems to place the athlete at increased risk to develop molluscum. An interesting report noted that 8% of 1500 cross-country runners developed molluscum contagiosum.[49] The origin of this epidemic was unclear, but is likely related to fomites.

While mature lesions of molluscum contagiosum demonstrate well-defined, white papules with a central indentation, athletes often present to the training room with disease early in the course (Figure 10). As such, the lesions tend to be small and often lack the central umbilication. Infectious and inflammatory folliculitis may mimic these early small lesions. Occasionally, medical staff misdiagnose and treat athletes for primary dermatitis when a player develops an eczematous reaction to a previously unidentified molluscum infection.[1]

Figure 10.


Sports clinicians should promptly treat athletes with destruction; these methods include liquid nitrogen and curettement. Commercially available metal-tipped curettes represent one instrument to treat the infection, but a tongue depressor, readily available in most training rooms, when broken longitudinally, also readily scoops out the infection. While these methods cure the athlete immediately, athletes can subsequently develop new lesions that may represent a newly acquired infection or simply growth of previously undetectable disease. Athletes, occasionally, develop hundreds of these lesions and may require daily topical therapy with tretinoin or imiquimoid. Athletes need to avoid sharing clothes, equipment, towels and razors that may transmit the organism. Tight-fitting bandages over the affected area prevent the spread of the poxvirus and allow participation in practice.[1] However, as soon as possible, the infected athlete should have the lesions removed to avoid any disruption in competition.


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