Skin Manifestations of Athletes Competing

Transcription

Sports Med 2012; 42 (5): 399-413
0112-1642/12/0005-0399/$49.95/0
REVIEW ARTICLE
Adis ª 2012 Springer International Publishing AG. All rights reserved.
Skin Manifestations of Athletes
Competing in the Summer Olympics
What a Sports Medicine Physician Should Know
Jacqueline F. De Luca,1 Brian B. Adams2,3 and Gil Yosipovitch4
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4
University of Hawaii Transitional Residency Program, Honolulu, HI, USA
Department of Dermatology, University of Cincinnati, Cincinnati, OH, USA
Section of Dermatology, Veterans Affairs Medical Center, Cincinnati, OH, USA
Department of Dermatology, Wake Forest University School of Medicine, Winston-Salem, NC, USA
Contents
Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1. Endurance. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.1 Friction Bullae . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.2 Jogger’s Nipples . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.3 Athlete’s Nodules . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.4 Urticaria. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.5 Tinea Pedis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1.6 Skin Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2. Resistance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.1 Auricular Haematoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.2 Calluses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.3 Tinea Corporis Gladiatorum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2.4 Herpes Gladiatorum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3. Team Sport . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.1 Talon Noir . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.2 Piezogenic Pedal Papules . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.3 Pitted Keratolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3.4 Cutaneous Larva Migrans . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4. Performing Arts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
4.1 Green Hair . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Abstract
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Olympic athletes are vulnerable to traumatic, environmental and infectious
skin manifestations. Although dermatological complaints are frequent among
Olympians, there is a scarcity of literature that reviews sports-related dermatoses
among Olympic athletes. A comprehensive review of PREMEDLINE and
MEDLINE searches of all available literature through to January 2011 was
conducted, focusing on sports-related dermatological presentations as well as
the key words ‘Olympic athletes’ and ‘skin diseases’. Common skin conditions can be harmful and even prohibitive for competition.
Common aetiologies of dermatological conditions related to sports include:
skin infections with dermatophytes such as tinea pedis and tinea corporis,
De Luca et al.
400
bacteria such as pitted keratolysis, and folliculitis and viruses such as herpes
gladiatorum. Frictional dermatoses occur commonly and include athlete’s
nodules, jogger’s itch, frictional blisters, callosities and talon noir. Trauma
can cause haematomas such as auricular haematomas. Due to long training
hours in the sun, many endurance athletes experience high levels of UV radiation and a higher risk for both melanoma and non-melanoma skin cancer.
Pre-existing dermatoses can also be aggravated with practice and competition; in particular, atopic eczema and physical urticarias.
Infrequent dermatoses are susceptible to misdiagnosis, delay in treatment
and needless biopsies. This review highlights the diagnosis and management
of sports-related dermatoses by the following general categories of Olympic
sport: endurance, resistance, team sport, and performing arts.
‘Faster, higher, stronger’ – the most talented
and conditioned athletes worldwide live by this
creed in order to strive for the opportunity to
compete in the Olympic Games. Although these
athletes intrinsically represent health and well-being,
the extensive training and environmental conditions
can result in significant morbidity. Dermatological
conditions, in particular, are an increasing cause
of medical problems for Olympic athletes. Concordantly, the International Olympic Committee
(IOC) Medical Commission specifically surveys
dermatological problems in the Periodic Health
Assessment of elite athletes; the importance of
surveying dermatological problems, according to
the IOC Medical Commission, is because these
conditions are common, can be transmissible and
may prevent clearance to compete.[1]
Although most athletes present with many common easily identifiable dermatoses, rarer sportsrelated conditions also exist, this may confound
some physicians and create potential for misdiagnosis and unnecessary procedures. Moreover, early correct diagnosis is imperative for the
athletes to both participate and compete to their
full potential.
Common aetiologies of dermatological conditions related to sports include infections, neoplasms,
inflammatory conditions, trauma and environmental factors. Pre-existing dermatoses can also
be aggravated with practice and competition.
This is especially problematic given the fact that
prevalence of eczema and atopy are higher in the
elite athlete population.[2]
A study of Olympians from South Africa reported the use of medical services at the Olympics
and demonstrated that dermatological conditions
are increasing in their athletes. More importantly,
dermatological conditions were the most prevalent
amongst the medical (non-injury) complaints comprising 16% of the total consultations in 2004, the
last Olympics analysed.[3]
We will provide a comprehensive review, using
PREMEDLINE and MEDLINE literature through
to January 2011, focusing on sports-related dermatological presentations, and also searching
under the key words ‘Olympic athletes’ and ‘skin
diseases’. The paper will be structured to provide
sports-related dermatoses by the general categories of Olympic sport: endurance, resistance,
team sport, and performing arts (table I).
1. Endurance
Marathon runners, triathletes, long-distance
swimmers and open-water marathon swimmers
(10 K) in the Olympics serve as a paradigm for
endurance sports. The nature of these sports necessitates constant frictional and traumatic forces
to numerous areas of the body. Infectious diseases may also be more problematic for endurance
athletes, as the constant wet environment in
runners and swimmers and resultant maceration
also serve as an ideal environment for fungal
growth. Moreover, numerous hours of UV exposure in all of these sports presents a risk for the
development of skin cancer (tables II and III)
Sports Med 2012; 42 (5)
Skin Manifestations of Athletes Competing in the Summer Olympics
401
Table I. Potential traumatic, environmental, and infectious aetiologies to dermatological problems in athletes, divided by sport
Sport
Traumatic
Environmental
Cycling
Frictional alopecia
Friction bullae
Occlusive acne
UVR
Marathon running
Friction bullae[4]
Athlete’s nodules[5]
Calluses
Jogger’s nipples[6]
Piezogenic pedal papules[7]
Subungual haematoma
Talon noir[8]
Physical urticaria[8]
UVR
Rowing
Calluses
Friction bullae
Rowers rump[11]
UVR
Infectious
Endurance
Pitted keratolysis[9]
Tinea pedis[10]
Aquagenic acne[12]
Contact dermatitis[12]
Green hair[12]
Seabather’s eruption
UVR
Xerosis
Occlusive folliculitis
Tinea pedis[13]
Verruca vulgaris (warts)
Friction bullae
Athlete’s nodules
Calluses
Piezogenic pedal papules
Jelly fish stings
Seabather’s eruption
(in ocean water)
Swimmer’s itch
(in fresh water)
UVR
Tinea pedis
Boxing
Auricular haematoma and
cauliflower ear
Calluses
Knuckle pad
Contact dermatitis
Judo
cauliflower ear
Calluses
Contact dermatitis
Tinea pedis
Weightlifting
Calluses
Friction bullae
Tache noir
Contact dermatitis
MRSA[15]
Wrestling
cauliflower ear[14]
Calluses
Contact dermatitis
Folliculitis, furuncles, carbuncles
Herpes gladiatorum
Impetigo
MRSA[15]
Tinea capitis
Tinea corporis gladiatorum
Verruca vulgaris
Calluses
Fiction bullae
Talon noir[17]
Contact dermatitis
MRSA[15]
Tinea pedis
UVR
Cutaneous larva migrans
Friction bullae
Calluses[17]
Tache noir
Talon noir[17]
UVR
Contact dermatitis
Swimming
Triathlon
Resistance
Team Support
Basketball
Beach volleyball
Tennis
Continued next page
Sports Med 2012; 42 (5)
De Luca et al.
402
Table I. Contd
Sport
Traumatic
Environmental
Infectious
Soccer
Calluses
Friction bullae
Talon noir
Turf burn[18]
UVR
Contact dermatitis
MRSA[15]
Tinea pedis[19]
Volleyball
Calluses
Friction bullae
MRSA[15]
Water polo
Performing Arts
Diving
Aquagenic acne
Contact dermatitis
Green hair
UVR
Xerosis
Tinea pedis
Aquagenic acne
Green hair[12]
UVR
Xerosis
Tinea pedis
Verruca vulgaris
Gymnastics
Frictional alopecia[20]
Friction bullae
Calluses
Tache Noir
Talon Noir
Contact dermatitis
Rhythmic gymnastics
Calluses
Frictional alopecia[20]
Contact dermatitis
Synchronized swimming
Aquagenic acne
Green hair[12]
UVR
Xerosis
Tinea pedis
MRSA = Methicillin-resistant Staphylococcus aureus; UVR = UV radiation.
1.1 Friction Bullae
Friction bullae occur frequently in endurance
athletes. With an incidence of 0.2–39% in marathon
runners, it is their most frequent complaint.[6] Repetitive frictional forces, especially when combined
with moisture, cause separation of epidermal cells
at the level of the stratum spinosum, which may
fill with either transudate or blood.[38,39] The
likelihood of bullae development is positively
correlated with the magnitude of friction and frequency of cycles.[38] Bullae usually occur in areas
that have a thick stratum corneum, such as on the
palms of the hands and soles of the feet. The most
commonly affected sites are on the tips of the
toes, the balls of the feet and the posterior heel.
Prevention should be aimed, therefore, at both
decreasing frictional forces and preventing moisture. Tension can be reduced with proper-fitting
shoes that distribute frictional forces and wearing
socks with low friction, particularly on the side
facing the skin. Moisture reduction can be accomplished with acrylic or polyester socks that
work by wicking away sweat. Antiperspirants can
also prevent moisture development, but may
cause an irritant contact dermatitis. Treatment
involves sterile incision and drainage at the edge
of painful bullae while carefully maintaining
the blister roof. This should be performed early,
in the first 24 hours after blister development;
the blister roof acts as a dressing that provides
for quicker healing and lower infection rates.
Moleskin padding may also be used to minimize
additional trauma to the blister and to relieve
discomfort. Hydrocolloid dressings and silvadene
or antibacterial ointments may decrease discomfort, prevent secondary infection and augment
healing.
Sports Med 2012; 42 (5)
1.2 Jogger’s Nipples
Repetitive friction to the nipples can lead to
painful irritation, fissures and bleeding (figure 1).
A tight-fitting, course cotton fabric shirt is the
usual culprit. Among marathon runners, the prevalence is between 2–16.3%.[6] Jogger’s nipples
can be treated with petroleum jelly or topical
erythromycin.[8] For refractory cases, tacrolimus
0.1% has been successful.[21] Runners can prevent
‘jogger’s nipple’ by wearing clothes that reduce
irritation, such as supportive jogging bras for
women, and wearing lycra or silk shirts instead of
cotton shirts; cotton absorbs water, keeping the
area moist and creating more irritation. Also,
men always have the option of going without a
shirt, as the weather permits. Other preventative
Table II. Treatment: non-systemic therapies
Dermatological
condition
Treatment
Friction bullae
Hydrocolloid dressings
Silvadene
Antibacterial ointment
Jogger’s nipples
Petroleum jelly[8]
Topical erythromycin ointment[8]
Tacrolimus 0.1% (only for refractory cases)[21]
Tinea corporis
gladiatorum
1% terbinafine cream applied bid for
1–2 weeks[22]
Piezogenic pedal
papules
Three intralesional injections of
betamethasone and bupivacaine (in equal
parts)a [23]
Pitted keratolysis
Topical 20% aluminum chloride solution
applied bid
Botulinum toxin injections[24]
Topical clindamycin 1% (with or without 5%
benzoyl peroxide)[25]
Topical mupirocin applied bid[26]
Topical erythromycin 2% solution applied
bid[27]
Cutaneous larva
migrans
Topical 15% thiabendazole at bedtime[28]
Green hair
Penicillamine containing shampoo[29]
Hydrogen peroxide (2–3%)[12]
Chelating agents[12]
a
USADA prohibits systemic corticosteroid use such as IM
injections and oral/IV therapy, but has no restrictions on topical
or intralesional corticosteroid injections.[30]
bid = twice daily; IM = intramuscular; IV = intravenous.
403
strategies include lubrication and nipple protection: surgical tape, bandages or breast shields.[8]
1.3 Athlete’s Nodules
Athlete’s nodules (also known as collogenomas, ‘Nike nodule’ in runners, or ‘nuckle pad’ in
boxers) are cutaneous nodules that occur after
chronic trauma, either frictional or pressure.[4,5]
‘Nike nodules’ occur over the malleolus and dorsal
aspect of the foot and are soft skin-coloured nodules that are keratinized on its surface and range
in size from 0.5 cm to 4.0 cm (figure 2). A biopsy
confirms the diagnosis. Although dermatofibromas
appear similar, histologically, athlete’s nodule will
have a tumorous proliferation of fibroblasts in
the dermis and reactive hypertrophy of the epidermis.[5] Surgical excision assuages symptoms if
present.[40]
1.4 Urticaria
Athletes, in general, are particularly predisposed to physical urticarias. While physical urticarias represent only 2.4% of urticarial types in
the population at large, in athletes they comprise
15%.[41] Although multiple sports appear to hasten
physical urticarias, running is the most recognized.[8] The physical urticarias include cholinergic,
exercise-induced, cold, solar, pressure, dermatographical, vibratory and aquagenic varieties
(figure 3).[42] While all can occur in athletes, this
review focuses on cholinergic urticaria and exerciseinduced anaphylaxis; both entities present with
pruritus and wheals after initiation of exercise,
but the latter form is potentially life-threatening.
Cholinergic urticaria is related to the elevation
of core body temperature, as occurs during exercise, passive warming and emotional stress. It
presents with numerous punctate wheals (2–5 mm)
surrounded by erythematous large flares that may
coalesce. They usually appear on the trunk and neck
and spread distally.[43] Although brochospasm
can occur with cholinergic urticaria, only rare cases
will progress to anaphylaxis.[44] Initial treatment
for athletes should consist of antihistamines.[45]
Other treatments consist of avoiding exercise and
other triggers and taking b-blockers and Danazol,
all of which would be unappealing to the Olympic
Sports Med 2012; 42 (5)
De Luca et al.
404
Table III. Treatment: systemic therapies
Dermatological
condition
Treatment
Dosing
USADA regulations
Cholinergic urticaria
Non-sedating anti-histamines
2nd generation: (1) cetirizine
3rd generation: (2) xyzal
(1) 20 mg daily[31]
(2) 10 mg daily
No restrictions[32]
Danazol (17a-ethynyl-17bhydroxyandrost-4-eno[2,3-d] isoxazole)
Is an anabolic androgenic steroid;
prohibited in all sports, both in and
out of competition[32]
Propranolol
20 mg bid[33]
Prohibited in particular sports while
in competition
Prohibited while in and out of
competition in archery and shooting[32]
Exercise-induced
anaphylaxis
Epinephrine
0.3 mg IM PRN anaphylaxis
Prohibited while in competition
Not prohibited while out of
competition[32]
Tinea corporis
gladiatorum
Terbinafine
Treatment: 250 mg daily for
2–4 weeks[22]
No restrictions[32]
Itraconazole
Treatment: 100 mg daily for
15 days[22]
Prophylaxis: 200 mg bid, 1 day
every other week[34]
No restrictions[32]
Fluconazole
Treatment: 150 mg weekly for
3–4 weeks[22]
Prophylaxis: 100 mg weekly[35]
No restrictions[32]
Herpes gladiatorum
Valacyclovir
Other alternatives: acyclovir or
famciclovir
Primary HG: 1 g bid for
10–14 days[36]
Recurrent HG: 500 mg bid for
7 days[36]
Prophylaxis: 500–1000 mg daily
during season[36]
No restrictions[32]
Cutaneous larva
migrans
Ivermectin
200 mg/kg, single dose[37]
No restrictions[32]
Albendazole
400 mg daily for 3 days[37]
No restrictions[32]
bid = twice daily; IM = intramuscular; PRN = when necessary; USADA = National Anti-Doping Organization of the United States.
athlete.[46] The World Anti-Doping Agency classifies Danazol as a prohibited substance in all
sports, and b-blockers as prohibited during competition for many Olympic sports.[30]
Exercise-induced anaphylaxis relates to food
ingestion in some cases. In this food-dependent
exercise-induced anaphylaxis, exercise must occur
within 4 hours after ingestion of a food for a
response to occur.[47] Personal history of atopy,
aspirin or NSAID use, exposure to high pollen
levels, insect stings, extremes of weather, humidity and menses may also contribute to exerciseinduced anaphylaxis.[48-51]
On examination, the wheals are typically larger in
size than those of cholinergic urticaria (10–15 mm)
and individuals can develop angioedema, laryngeal
oedema, bronchospasm, gastrointestinal symptoms,
syncope, and/or hypotension.[43,52] Athletes that
show a relation with food should be evaluated
with prick tests and radioallergosorbent blood
tests (RAST).[53] Acute treatment should consist
of airway and cardiovascular support, and administration of epinephrine if necessary. Athletes
should prevent recurrences by identifying and
avoiding any provoking foods and medications.
They may even need to wait 6 hours after any food
ingestion to exercise. Prophylactic pharmacotherapy is not particularly effective, as antihistamines
usually prevent urticaria but not anaphylaxis. Above
all else, monitoring is crucial and should consist
of either exercising with a medically-trained companion or wearing a medical alert device.[45]
Sports Med 2012; 42 (5)
405
freshwater risk developing swimmer’s itch, which
most commonly occurs in non-covered portions
of the body. Last, jellyfish stings can cause severe
urticarial reactions and even mortality, as has
been reported with the Irukandji syndrome.[57]
Some Olympic athletes in Sydney, NSW, Australia,
experienced jellyfish stings. Detailed analysis of
this eruption is beyond the scope of this review.
1.6 Skin Cancer
Fig. 1. Painful fissures in a male runner with ‘jogger’s nipple’.
1.5 Tinea Pedis
Almost all athletes are at risk for tinea pedis,
but a higher prevalence has been specifically exposed in running, swimming, soccer, water polo
and basketball.[13] Occlusive footwear is a major
culprit as dermatophytes thrive with sweating and
maceration. Trichophyton rubrum and Trichophyton
mentagrophytes are the species most commonly
involved and are relatively equivalent in prevalence
amongst runners, 43.8% and 44.9%, respectively.
Runners are also likely under diagnosed, since
occult athlete’s foot disease has been found in up
to 48% of cases.[10] In swimmers, T. mentagrophytes
was the more common culprit of occult infection,
occurring between 70% and 85%.[13,54] It is also
speculated that the floor of swimming pool decks
and locker rooms may be a source of these occult
infections since T. mentagrophytes has been isolated
from these areas.[13,54,55]
Prevention of tinea pedis infection in athletes
should include wearing moisture-wicking synthetic
socks and changing them regularly, keeping the
feet dry, wearing well ventilated shoes, using antifungal powder, and always using sandals in the
locker room and on the pool deck.[56]
Sea water creatures can also affect Olympic
athletes, such as triathletes. Sea bather’s eruption,
caused by the larval-stage thimble jellyfish, occurs in
seawater swims and presents as erythematous
papules most commonly beneath the swimsuit.
Conversely, triathletes training or competing in
Due to long training hours in the sun many
endurance athletes experience high levels of UV
radiation (UVR), which is thought to be the most
important environmental risk factor for both melanoma and nonmelanoma skin cancer development.[58] Extremely high levels of UVR exposure
have been documented in tennis players, sailors,
cyclists and triathletes. For example, three triathletes were measured during the Ironman competition in Hawaii and were found to have a mean
personal UV of 8.3 minimal erythemal dose (MED),
exceeding international exposure limits for personal
exposure by more than 30-fold.[59] Six professional
cyclists during the Tour de Suisse race, received a
mean daily personal exposure of 8.1 MED.[60]
In addition to the total time athletes are exposed to the sun, sweating and sea or pool water
may also contribute to UVR-related skin damage. Skin hydration, in general, increases the photosensitivity of the skin, significantly decreasing the
MED to UVB.[61] It is thought that this effect is
Fig. 2. Athlete’s nodule over medial foot.
Sports Med 2012; 42 (5)
De Luca et al.
406
Fig. 3. Dermatographical ‘Olympic’ response in a runner, as evidenced by Olympic rings.
the result of stratum corneum hydration, which
shifts the absorption spectrum to shorter wavelengths and also decreases reflection and dispersion.[62] Water and sweat can wash away sunscreen
and increase the risk for UVR in this way as well.
All athletes in outdoor sports should be wearing water-resistant sunscreens and sun-protective
clothing. They should also attempt to train during times of the day with low sun exposure and
should regularly see a dermatologist.
2. Resistance
The resistance sports include weightlifting and
contact sports, such as freestyle and GrecoRoman wrestling, boxing, judo and taekwondo.
Wrestling and judo are unique amongst the contact sports in the amount of time they spend in
direct skin-to-skin contact with other athletes,
making them particularly prone to the transmission of viral, fungal and bacterial infections.
result in necrosis of the cartilage or may stimulate
formation of fibroneocartilage resulting in the
appearance of ‘cauliflower ear’.[63,64] ‘Cauliflower
ears’ date back to ancient Greek Olympians and
many coaches and athletes alike still regard this as a
sign of hard work and as a ‘badge of courage’.[65,66]
Numerous treatments exist to relieve the haematoma, but there is no consensus on which method
produces the best cosmesis due to poor study
designs. A recent Cochrane systematic review, however, suggests that treatment is superior to no
treatment.[67] In most early cases, treatment should
involve needle aspiration or possibly incision and
drainage followed by one of the various modalities to prevent re-accumulation of blood.[67,68]
If untreated, and ‘cauliflower ear’ has formed,
then reconstructive plastic surgery can help restore the pinna to its natural shape.[69] Although
head gear prevents auricular haematomas, it is
not required for Olympic or international competition. Further, if headgear is used, it must be
approved by the governing body for wrestling,
the Fédération Internationale des Luttes Associées
(FILA), prior to competition.[70] Overall, Olympic
athletes in competition seldom use headgear.
2.2 Calluses
Calluses occur among nearly all athletes, but
are most notorious in Olympic weightlifters. The
localized thickening of skin, from hyperproliferation and incomplete differentiation of epidermal
2.1 Auricular Haematoma
Olympic contact sports, such as wrestling, boxing and judo are prone to development of auricular haematomas, which may later progress to
‘cauliflower ear’ if untreated.[14] Trauma to the
athlete’s ears cause shearing forces, which can
separate the perichondrium and cartilage leading
to blood and serum accumulation, usually in the
pinna (figure 4).[63] Over time, this trauma may
Fig. 4. Acute auricular haematoma in a wrestler.
Sports Med 2012; 42 (5)
keratinocytes, serves as a protective mechanism
from repetitive friction or pressure.[71] Calluses
occur on the hands and feet and may prevent
athletes from developing painful blisters, even
giving a competitive advantage.[72]
Weightlifters typically have callosities over the
palmar metacarpophalangeal joints from gasping
the bar. The bar also causes trauma to other body
parts, such as during the ‘clean and jerk’, where
the bar rests on the clavicular region, causing lichenified plaques.[73] Other sports that may develop calluses include gymnastics, tennis, rowing
and running. Many other athletes also utilize weight
lifting for strength training and can also develop
calluses similar to Olympic weightlifters.
In most cases the callus will be asymptomatic,
but when they are painful they can be treated with
topical keratolytics, gently pared down with a blade
or debrided with a pumice stone after soaking in
warm water. In addition, preventative management can include weight-lifting gloves and modification of footwear so that friction is minimized
(extra room in the toe box, synthetic socks, shoe
inserts and placement of padding to distribute
weight more evenly).
2.3 Tinea Corporis Gladiatorum
Skin infections can be epidemic among wrestlers.
Although most infections are relatively benign,
they can exclude wrestlers from practice and
competition and can be destructive to the individual athlete and team. The wrestling environment is ideal for the transmission and survival of
bacteria, fungi and viruses through direct skin-toskin contact, warmth, moisture and traumatized
skin. Fungi cause frequent outbreaks of tinea
capitis gladiatorum and tinea corporis gladiatorum in wrestlers. The reported prevalence rates
of tinea corporis gladiatorum range from 20% to
77%.[74] Most reported cases of tinea corporis
gladiatorum have been caused by Trichophyton
tonsurans, which has recently been isolated in
>90% of cases during a 2-year analysis in Iran.[75]
This differs from the standard variety of isolates obtained from the groin and body, where
T. rubrum accounts for 32–60%, and T. tonsurans
17.7–34.3%.[76]
407
Fig. 5. Tinea corporis gladiatorum in a collegiate wrestler.
Clinically, tinea corporis gladiatorum presents
as well defined, erythematous, scaling papules and
plaques located on the head, neck and upper extremities; areas that have direct skin-to-skin contact during wrestling (figure 5). The classic features
of standard tinea corporis (annular shape, raised
leading edge and central clearing) may not be
present.[22] Treatment may consist of topical medication and/or oral treatment depending on disease severity. Many infected individuals may also
remain contagious for weeks, and may need to
keep lesions covered with bandages when practicing.[22] Preventative measures include showering,
washing uniforms and disinfecting mats daily.
Teams should also have strict surveillance by
athletic trainers who should promptly refer affected athletes to physicians.[77] Oral prophylactic
treatment with itraconazole and fluconazole significantly decreases the incidence of infection, but
may not be clinically applicable due to the high
cost and potential for adverse side effects.[35,78]
2.4 Herpes Gladiatorum
Herpes gladiatorum (HG) can be devastating
for wrestlers; not only do active lesions result in
exclusion from competition, but primary infection in the eye can result in recurrent herpes keratitis and, rarely, blindness.[79,80] Many wrestlers
are either infected or at risk for developing HG.
The prevalence of HG in wrestlers ranges between
2.6% and 40.5%, and is transmitted via skin-to-skin
Sports Med 2012; 42 (5)
De Luca et al.
408
contact or autoinoculation with herpes simplex
virus (HSV)-1.[81,82] Although clinically similar to
orolabial herpes with grouped vesicles on an erythematous base, HG occurs on different locations on the face and also affects the head, neck,
extremities and trunk (figure 6).
The location affected corresponds with skinto-skin contact and often reflects the handedness
of the wrestler. In one study, 86% of the wrestlers
were right-handed and 74% had the herpetic lesion on the right side, since opponents typically
lock-up with their dominant side.[83] When the
lesions don’t display vesicles, as they do early and
late in the course of an outbreak, the differential
diagnosis includes tinea corporis gladiatorum,
impetigo, acne and atopic dermatitis. Also, some
wrestlers complicate accurate diagnosis when they
attempt to conceal the infection, using sandpaper
or bleach to alter the rash.[84] Diagnosis can be
made with Tzanck smear, which is quick but less
sensitive, or with more reliable tests such as viral
culture, polymerase chain reaction (PCR) or direct
fluorescent antibody testing. Treatment for active
infections can be accomplished with oral antiviral
agents: acyclovir, valacyclovir or famciclovir.
Prevention is complicated by the fact that viral
shedding occurs before the appearance of the skin
lesions.[85,86] Valacyclovir may be given prophylactically during the wrestling season to both wrestlers with recurrent herpes gladiatorum and in
HSV-1 naı̈ve athletes. Valacyclovir reduced outbreaks to 21% of those receiving valacyclovir 500 mg
daily and 8% of those receiving valacyclovir 1000 mg
daily. In wrestlers whose primary outbreak was
more than 2 years prior taking valacyclovir 500 mg
daily was 100% effective.[87] The potential for drug
resistance is concerning, but at this time is not problematic; the reported acyclovir resistance in immunocompetent individuals is only 0.3%.[88] Again,
as in tinea gladiatorum, prevention should also
be directed at good hygienic practices.
3. Team Sport
Teams currently competing in the summer
Olympics include basketball, baseball, field hockey,
handball, rowing, sailing, soccer, tennis, volleyball
and water polo. Although many of the dermatological problems faced by these athletes have considerable overlap with endurance athletes, as
mentioned in section 1, they are also at risk for
some unique traumatic and infectious entities.
3.1 Talon Noir
Basketball, soccer, tennis, gymnastics and running, all of which require frequent starts and stops,
can lead to talon noir. Also known as black heel or
calcaneal petechiae, repeated lateral shearing forces
creating intraepidermal haemorrhages cause these
lesions. Although completely benign, they can often
clinically resemble verruca with thrombosis or acral
melanomas, as they appear as blue-to-black linear,
circular or oval shaped macules on the posterior or
posterolateral aspect of the heel (figure 7).[8,89]
Tennis players, gymnasts and weightlifters can also
have similar lesions on the thenar eminence called
tache noir, palmar petechiae or black palm.
Dermatoscopic examination may help rule out
melanoma.[90,91] If the diagnosis remains unclear,
biopsy will reveal the diagnosis.
3.2 Piezogenic Pedal Papules
Fig. 6. Herpes gladiatorum.
Piezogenic pedal papules, which result from
the herniation of subcutaneous fat through the
dermis, may occur more frequently in athletes,
usually among long-distance runners, triathletes,
volleyball players and basketball players.[7,16]
One review of the literature suggests that athletes
have a higher prevalence of the painful variety of
Sports Med 2012; 42 (5)
409
injections of botulinum toxin, reduces hyperhydrosis
and make the sole a less hospitable environment for
the microorganism.[24] Topical treatment includes
clindamycin (with or without 5% benzoyl peroxide),
mupirocin or erythromycin.[25-27,100]
Another common bacterial skin manifestation
in athletes who profusely sweat is occlusive folliculitus with Staphylococcus (see table I).
3.4 Cutaneous Larva Migrans
Fig. 7. Talon noir in a professional tennis player.
papules; however, no study has compared the
prevalence of piezogenic papules or the associated pain in athletes versus non-athletes.[7]
Piezogenic pedal papules appear as yellow or
skin-coloured nodules, usually occurring bilaterally on the medial, posterior and lateral aspects
of the heels (figure 8). Placing one’s weight on the
affected foot would accentuate the lesions. Athletes with painful lesions may benefit from foot
pads or heel cups, compression stockings, electroacupuncture, injections of betamethasone and
bupivacaine (in equal parts), or surgery (deep
punch biopsy or small excision).[23,92-94]
3.3 Pitted Keratolysis
Pitted keratolysis, a gram-positive bacterial infection of the plantar surface of the feet, reportedly
occurs in runners, and in tennis and basketball
players.[9] A hyperhydrotic, occluded, and macerated foot hosts Corynebacterium, Micrococcus
sedentarius (now renamed as Kytococcus sedentarius), and Dermatophilus congolensis, which
produce proteinases that degrade the stratum
corneum.[95-99] Athletes will have multifocal, discrete erosions ranging from 0.5 mm to 7.0 mm in
diameter and from 1 mm to 2 mm in depth, and a
foul odour (purportedly due to the production of
sulphur-compound by-products).[96,97]
Preventative measures include the use of synthetic
socks and avoidance of prolonged use of occlusive
shoes. Topical 20% aluminum chloride solution or
Beach volleyball players risk developing a chronic
parasitic infection, cutaneous larva migrans, via
animal hookworm larva, most commonly Ancylostoma braziliense.[101] The larvae of A. braziliense
emerge from dog or cat faeces in the sand and can
penetrate the skin of the player’s lower extremities.[101,102] The larvae then migrate within the
skin and thereby produce erythematous, serpiginous, elevated tunnels, which gradually advance
with time. The intensity of the pruritus with these
lesions may disturb sleep.[103] Players will most likely
develop cutaneous larva migrans from practice or
competitions in subtropical or tropical endemic
areas.[104] First-line treatments include ivermectin, albendazole or topical thiabendazole.[105,106]
4. Performing Arts
Diving, synchronized swimming and rhythmic
gymnastics are sports that are included in this
category. Overall, they acquire many of the same
Fig. 8. Piezogenic pedal papules in a runner.
Sports Med 2012; 42 (5)
De Luca et al.
410
dermatological problems as other sports, such as
those exposed to trauma or sharing equipment.
Divers and synchronized swimmers, like other
aquatic athletes, can develop contact dermatitis:
irritant from the chemicals (chlorine and bromine)
in the pool, or allergic from the nose clips, ear plugs,
swimming caps, fins, goggles or pool water.[107]
They are also prone to swimmer’s xerosis; pools
both dilute the skin’s sebum and draw water from
the skin (via osmosis). This xerosis may paradoxically result in aquagenic acne, which is primarily thought to be a result of rebound hyperactivity of
the sebaceous glands. Another contributing factor
is pilosebaceous obstruction, which may be caused
by overhydration of the stratum corneum or by
chlorine irritating the follicular orifice.[12]
4.1 Green Hair
Green hair occurs in water sport athletes: divers, synchronized swimmers, water polo players
and swimmers. Athletes with blonde, grey or white
hair are prone to pigmentation by copper ions in
pools, which originate from the water’s source, the
pipes or the algicides.[12,108] Physical and chemical
damage to the hair, including sunlight and chlorinated water, also contributes to the development
of green hair.[109] Green hair can be prevented
by wearing a cap and using a chelating shampoo.
Treatment with a penicillamine containing shampoo, hydrogen peroxide (2–3%) or chelating agents,
also clears green hair.[12,29,109]
5. Conclusion
There are numerous dermatological conditions that may occur in Olympic athletes due to
the extreme nature of their training, and their
constant environmental exposures to heat, sweat,
trauma, sun and various other exogenous factors.
Sports medicine physicians, as well as dermatologists, should be aware of these findings for
prompt and appropriate management.
Acknowledgements
No funding was received to assist in the preparation of this
review. The authors have no conflicts of interest that are directly relevant to the content of this review.
References
1. Ljungqvist A, Jenoure PJ, Engebretsen L, et al. The International Olympic Committee (IOC) consensus statement
on periodic health evaluation of elite athletes. Clin J Sport
Med 2009; 19: 347-65
2. Carlsen KH, Kowalski ML. Asthma, allergy, the athlete
and the Olympics. Allergy 2008; 63: 383-6
3. Derman WE. Profile of medical and injury consultations
of Team South Africa during the XXVIIIth Olympiad, Athens 2004. South African J Sports Med 2008; 20:
72-6
4. Dickens R, Adams BB, Mutasim DF. Sports-related pads.
Int J Dermatol 2002; 4: 291-3
5. Uchiyama M, Tsuboi R, Mitsuhashi Y. Athlete’s nodule.
J Dermatol 2009; 36: 608-11
6. Mailler EA, Adams BB. The wear and tear of 26.2: dermatological injuries reported on marathon day. Br J
Sports Med 2004; 38: 498-501
7. Redbord KP, Adams BB. Piezogenic pedal papules in a
marathon runner. Clin J Sport Med 2006; 16: 81-3
8. Adams BB. Dermatologic disorders of the athlete. Sports
Med 2002; 32: 309-21
9. Kantor GR, Bergfeld WF. Common and uncommon dermatologic diseases related to sports activities. Exerc Sport
Sci Rev 1988; 16: 215-53
10. Auger P, Marquis G, Joly J, et al. Epidemiology of tinea
pedis in marathon runners: prevalence of occult athlete’s
foot. Mycoses 1993; 36: 35-41
11. Tomecki KJ, Mikesell JF. Rower’s rump. J Am Acad
Dermatol 1987; 16: 890-1
12. Basler RS, Basler GC, Palmer AH, et al. Special skin
symptoms seen in swimmers. J Am Acad Dermatol 2000;
43: 299-305
13. Kamihama T, Kimura T, Hosokawa JI, et al. Tinea pedis
outbreak in swimming pools in Japan. Public Health
1997; 111: 249-53
14. Giffin CS. Wrestler’s ear: pathophysiology and treatment.
Ann Plast Surg 1992; 28: 131-9
15. Kirkland EB, Adams BB. Methicillin-resistant Staphylococcus aureus and athletes. J Am Acad Dermatol 2008
Sep; 59 (3): 494-502
16. Brzeziński P. Piezogenic pedal papules: a chronic disease of
athletes. Polish J Sports Med 2009; 25: 183-8
17. Basler RS, Garcia MA. Acing common skin problems in
tennis players. Phys Sportsmed 1998; 26: 37-44
18. Wright JM, Webner D. Playing field issues in sports medicine. Curr Sports Med Rep 2010; 9 (3): 129-33
19. Pickup TL, Adams BB. Prevalence of tinea pedis in professional and college soccer players versus non-athletes.
Clin J Sport Med 2007; 17: 52-4
20. Biolcati G, Berlutti G, Bagarone A, et al. Dermatological
marks in athletes of artistic and rhythmicgymnastics. Int
J Sports Med 2004; 25: 638-40
21. Tomi NS, Altmeyer P, Kreuter A. Tacrolimus ointment for
‘jogger’s nipples’. Clin Exp Dermatol 2007; 32: 106-7
22. Kohl TD, Lisney M. Tinea gladiatorum: wrestling’s emerging foe. Sports Med 2000; 29: 439-47
Sports Med 2012; 42 (5)
23. Doukas DJ, Holmes J, Leonard JA. A nonsurgical approach to painful piezogenic pedal papules. Cutis 2004;
73: 339-40, 346
24. Tamura BM, Cucé LC, Souza RL, et al. Plantar hyperhidrosis and pitted keratolysis treated with botulinum
toxin injection. Dermatol Surg 2004; 30: 1510-4
25. Vlahovic TC, Dunn SP, Kemp K. The use of a clindamycin
1%-benzoyl peroxide 5% topical gel in the treatment of
pitted keratolysis: a novel therapy. Adv Skin Wound Care
2009; 22: 564-6
26. Vazquez-Lopez F, Perez-Oliva N. Mupirocine ointment for
symptomatic pitted keratolysis. Infection 1996; 24: 55
27. Ramsey ML. Pitted keratolysis: a common infection of
active feet. Phys Sportsmed 1996; 24: 51-6
28. Whiting D. The successful treatment of creeping eruption with topical thiabendazole. S Afr Med J 1976; 50:
253-4
29. Person JR. Green hair: treatment with a penicillamine
shampoo. Arch Dermatol 1985; 121: 717-8
30. World Anti-Doping Agency. The World Anti-Doping
Code. The 2010 Prohibited List International Standard
[online]. Available from URL: http://www.wada-ama.org/
rtecontent/document/2010_Prohibited_List_FINAL_EN_
Web.pdf [Accessed 2010 Nov 22]
31. Zuberbier T, Münzberger C, Haustein U, et al. Doubleblind crossover study of high-dose cetirizine in cholinergic
urticaria. Dermatology 1996; 193: 324-7
32. Global DRO United States [online]. Available from URL:
http://www.globaldro.com/us-en/default.aspx [Accessed
2011 Nov 14]
33. Feinberg JH, Toner CB. Successful treatment of disabling
cholinergic urticaria. Mil Med 2008 Feb; 173: 217-20
34. Hazen PG, Weil ML. Itraconazole in the prevention
and management of dermatophytosis in competitive
wrestlers. J Am Acad Dermatol 1997 Mar; 36 (3 Pt 1):
481-2
35. Kohl TD, Martin DC, Nemeth R, et al. Fluconazole for the
prevention and treatment of tinea gladiatorum. Pediatr
Infect Dis J 2000; 19: 717-22
36. Anderson BJ. Managing herpes gladiatorum outbreaks in
competitive wrestling: the 2007 Minnesota experience.
Curr Sports Med Rep 2008 Nov-Dec; 7 (6): 323-7
37. Ghosh SK, Bandyopadhyay D. Dermacase. Can you
identify this condition? Cutaneous larva migrans. Can
Fam Physician 2009 May; 55 (5): 489, 491
38. Knapik JJ, Reynolds KL, Duplantis KL, et al. Friction
blisters. Pathophysiology, prevention and treatment.
Sports Med 1995; 20: 136-47
39. Gerhardt LC, Strässle V, Lenz A, et al. Influence of epidermal hydration on the friction of human skin against
textiles. J R Soc Interface 2008 6; 5: 1317-28
40. Cohen PR, Eliezri YD, Silvers DN. Athlete’s nodules: treatment by surgical excision. Sports Med 1990; 10: 198-203
41. Mikhailov P, Berova N, Andreev VC. Physical urticaria
and sport. Cutis 1977; 20: 381-4, 389-90
42. Dice JP. Physical urticaria. Immunol Allergy Clin North
Am 2004; 24: 225-46, vi
43. Nichols AW. Exercise-induced anaphylaxis and urticaria.
Clin Sports Med 1992; 11: 303-12
411
44. MacKnight JM, Mistry DJ. Allergic disorders in the athlete. Clin Sports Med. 2005; 24: 507-23, vii-viii
45. Schwartz LB, Delgado L, Craig T, et al. Exercise-induced
hypersensitivity syndromes in recreational and competitive athletes: a PRACTALL consensus report (what the
general practitioner should know about sports and allergy). Allergy 2008; 63: 953-61
46. Wong E, Eftekhari N, Greaves MW, et al. Beneficial effects
of danazol on symptoms and laboratory changes in cholinergic urticaria. Br J Dermatol 1987; 116: 553-6
47. Del Giacco SR, Manconi PE, Del Giacco GS. Allergy and
sports. Allergy 2001; 56: 215-23
48. Gerth van Wijk R, Roovers MH, Dieges PH. Exercisedependent anaphylaxis. Ned Tijdschr Geneeskd 1991;
135: 2293-5
49. Shadick NA, Liang MH, Partridge AJ, et al. The natural
history of exercise-induced anaphylaxis: survey results
from a 10-year follow-up study. J Allergy Clin Immunol
1999; 104: 123-7
50. Wade JP, Liang MH, Sheffer AL. Exercise-induced anaphylaxis: epidemiologic observations. Prog Clin Biol Res
1989; 297: 175-82
51. Volcheck GW, Li JT. Exercise-induced urticaria and anaphylaxis. Mayo Clin Proc 1997; 72 (2): 140-7
52. Lee HB, Ahn IS, Choi JH, et al. A case of wheat-dependent
exercise-induced anaphylaxis. Ann Dermatol 2009; 21:
447-9
53. Romano A, Di Fonso M, Giuffreda F, et al. Diagnostic
work-up for food-dependent, exercise-induced anaphylaxis. Allergy 1995; 50: 817-24
54. Attye A, Auger P, Joly J. Incidence of occult athlete’s foot
in swimmers. Eur J Epidemiol 1990; 6: 244-7
55. Bolaños B. Dermatophyte feet infection among students
enrolled in swimming courses at a university pool. Bol
Asoc Med P R 1991; 83: 181-4
56. Field LA, Adams BB. Tinea pedis in athletes. Int J Dermatol 2008; 47: 485-92
57. Little M, Pereira P, Carrette T, et al. Jellyfish responsible
for Irukandji syndrome. QJM 2006; 99 (6): 425-7
58. Gloster Jr HM, Brodland DG. The epidemiology of skin
cancer. Dermatol Surg 1996; 22: 217-26
59. Moehrle M. Ultraviolet exposure in the Ironman triathlon.
Med Sci Sports Exerc 2001; 33: 1385-6
60. Moehrle M, Heinrich L, Schmid A, et al. Extreme UV exposure of professional cyclists. Dermatology 2000; 201:
44-5
61. Moehrle M, Koehle W, Dietz K, et al. Reduction of minimal erythema dose by sweating. Photodermatol Photoimmunol Photomed 2000; 16: 260-2
62. Blazek V, Wienert V. The influence of corneal stratum
hydratation on the chronological development of acute
ultraviolet injury (author’s transl). Strahlentherapie 1981;
157: 280-6
63. Ohlsén L, Skoog T, Sohn SA. The pathogenesis of cauliflower ear: an experimental study in rabbits. Scand J Plast
Reconstr Surg 1975; 9: 34-9
64. Lee EC, Soliman AM, Kim J. Traumatic auricular hematoma: a case report. J Craniomaxillofac Trauma 1997; 3:
32-5
Sports Med 2012; 42 (5)
412
65. Masterson DW. The ancient Greek origins of sports medicine. Br J Sports Med 1976; 10: 196-202
66. Kordi R, Mansournia A, Nourian RA, et al. Cauliflower ear
and skin infections among wrestlers in Tehran. J Sports Sci
Med 2007; 6: 39-44
67. Jones SE, Mahendran S. Interventions for acute auricular
haematoma. Cochrane Database Syst Rev 2004; (2):
CD004166
68. Ghanem T, Rasamny JK, Park SS. Rethinking auricular
trauma. Laryngoscope 2005; 115: 1251-5
69. Yotsuyanagi T, Yamashita K, Urushidate S, et al. Surgical
correction of cauliflower ear. Br J Plast Surg 2002; 55:
380-6
70. USA Wrestling. International rule book & guide to wrestling: freestyle, Greco-Roman, women’s wrestling, and
beach wrestling. 2010 ed [online]. Available from URL:
http://www.themat.com/forms/Rulebook.pdf [Accessed
2010 Oct 25]
71. Kim SH, Kim S, Choi HI, et al. Callus formation is associated with hyperproliferation and incomplete differentiation of keratinocytes, and increased expression of
adhesion molecules. Br J Dermatol 2010; 163: 495-501
72. Helm TN, Bergfeld WF. Sports dermatology. Clin Dermatol 1998; 16: 159-65
73. Scott Jr MJ, Scott NI, Scott LM. Dermatologic stigmata in
sports: weightlifting. Cutis 1992; 50: 141-5
74. Adams BB. Tinea corporis gladiatorum. J Am Acad Dermatol 2002; 47: 286-90
75. Bassiri-Jahromi S, Khaksar AA. Outbreak of tinea gladiatorum in wrestlers in Tehran (Iran). Indian J Dermatol
2008; 53: 132-6
76. Foster KW, Ghannoum MA, Elewski BE. Epidemiologic
surveillance of cutaneous fungal infection in the United
States from 1999 to 2002. J Am Acad Dermatol 2004; 50:
748-52
77. Hand JW, Wroble RR. Prevention of tinea corporis in
collegiate wrestlers. J Athl Train 1999; 34: 350-2
78. Hazen PG, Weil ML. Itraconazole in the prevention and
management of dermatophytosis in competitive wrestlers.
J Am Acad Dermatol 1997; 36: 481-2
79. Holland EJ, Mahanti RL, Belongia EA, et al. Ocular involvement in an outbreak of herpes gladiatorum. Am J
Ophthalmol 1992; 114: 680-4
80. Wilhelmus KR. The treatment of herpes simplex virus epithelial keratitis. Trans Am Ophthalmol Soc 2000; 98: 505-32
81. Becker TM, Kodsi R, Bailey P, et al. Grappling with herpes:
herpes gladiatorum. Am J Sports Med 1988; 16: 665-9
82. Strauss RH, Leizman DJ, Lanese RR, et al. Abrasive shirts
may contribute to herpes gladiatorum among wrestlers.
N Engl J Med 1989; 320: 598-9
83. Anderson BJ. The epidemiology and clinical analysis of
several outbreaks of herpes gladiatorum. Med Sci Sports
Exerc 2003; 35: 1809-14
84. Adams BB. New strategies for the diagnosis, treatment,
and prevention of herpes simplex in contact sports. Curr
Sports Med Rep 2004; 3: 277-83
85. Wald A, Zeh J, Selke S, et al. Virology characteristics
of subclinical and symptomatic genital herpes infections.
N Engl J Med 1995; 333: 770-5
De Luca et al.
86. Koelle DM, Wald A. Herpes simplex virus: the importance
of asymptomatic shedding. J Antimicrob Chemother
2000; 45 Suppl. T3: 1-8
87. Anderson BJ. The effectiveness of valacyclovir in preventing reactivation of herpes gladiatorum in wrestlers. Clin
J Sport Med 1999; 9: 86-90
88. Bacon TH, Levin MJ, Leary JJ, et al. Herpes simplex
virus resistance to acyclovir and penciclovir after two decades of antiviral therapy. Clin Microbiol Rev 2003; 16:
114-28
89. Urbina F, León L, Sudy E. Black heel, talon noir or calcaneal
petechiae? Australas J Dermatol 2008 Aug; 49: 148-51
90. Zalaudek I, Argenziano G, Soyer HP, et al. Dermoscopy
of subcorneal hematoma. Dermatol Surg 2004; 30:
1229-32
91. Wolf IH. Dermoscopic diagnosis of vascular lesions. Clin
Dermatol 2002; 20: 273-5
92. Böni R, Dummer R. Compression therapy in painful piezogenic pedal papules. Arch Dermatol 1996; 132: 127-8
93. Woodrow SL, Brereton-Smith G, Handfield-Jones S. Painful
piezogenic pedal papules: response to local electroacupuncture. Br J Dermatol 1997; 136: 628-30
94. Lebovits PE, Kouskoukis CE, Weidman AI. Piezogenic
pedal papules. Cutis 1982; 29: 276-7, 280
95. Takama H, Tamada Y, Yano K, et al. Pitted keratolysis:
clinical manifestations in 53 cases. Br J Dermatol 1997;
137: 282-5
96. Singh G, Naik CL. Pitted keratolysis. Indian J Dermatol
Venereol Leprol 2005; 71: 213-5
97. Nordstrom KM, McGinley KJ, Cappiello L, et al. Pitted
keratolysis: the role of Micrococcus sedentarius. Arch
Dermatol 1987; 123: 1320-5
98. Woodgyer AJ, Baxter M, Rush-Munro FM, et al. Isolation
of Dermatophilus congolensis from two New Zealand
cases of pitted keratolysis. Australas J Dermatol 1985; 26:
29-35
99. Longshaw CM, Wright JD, Farrell AM, et al. Kytococcus
sedentarius, the organism associated with pitted keratolysis, produces two keratin-degrading enzymes. J Appl
Microbiol 2002; 93: 810-6
100. Shah AS, Kamino H, Prose NS. Painful, plaque-like, pitted
keratolysis occurring in childhood. Pediatr Dermatol
1992; 9: 251-4
101. Biolcati G, Alabiso A. Creeping eruption of larva migrans:
a case report in a beach volley athlete. Int J Sports Med
1997; 18: 612-3
102. Davies HD, Sakuls P, Keystone JS. Creeping eruption:
a review of clinical presentation and management of 60
cases presenting to a tropical disease unit. Arch Dermatol
1993; 129: 588-91
103. Jackson A, Heukelbach J, Calheiros CM, et al. A study in a
community in Brazil in which cutaneous larva migrans is
endemic. Clin Infect Dis 2006; 43: e13-8
104. Edelglass JW, Douglass MC, Stiefler R, et al. Cutaneous
larva migrans in northern climates: a souvenir of your
dream vacation. J Am Acad Dermatol 1982; 7: 353-8
105. Van den Enden E, Stevens A, Van Gompel A. Treatment
of cutaneous larva migrans. N Engl J Med 1998; 339:
1246-7
Sports Med 2012; 42 (5)
106. Ang CC. Images in clinical medicine: cutaneous larva migrans. N Engl J Med 2010; 362: e10
107. Tlougan BE, Podjasek JO, Adams BB. Aquatic sports
dermatoses: part 1. In the water: freshwater dermatoses.
Int J Dermatol 2010; 49 (8): 874-85
108. Blanc D, Zultak M, Rochefort A, et al. Green hair: clinical,
chemical and epidemiologic study. Apropos of a case.
Ann Dermatol Venereol 1988; 115: 807-12
413
109. Mascaró Jr JM, Ferrando J, Fontarnau R, et al. Green
hair. Cutis 1995; 56: 37-40
Correspondence: Dr Gil Yosipovitch, Department of Dermatology, Wake Forest University School of Medicine, Medical
Center Boulevard, Winston-Salem, NC 27157-1071, USA.
E-mail: [email protected]
Sports Med 2012; 42 (5)

Skin Manifestations of Athletes Competing

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Tech Deck:

ALL KINDS OF CHILDREN`SPARTIES TO SUIT 5

FIX THAT SPORTS BRAIN