Aquatic Sports Dermatoses: Clinical Presentation and Treatment Guidelines

Aquatic sport dermatoses include a variety of skin conditions that occur in athletes who participate in sporting activities in or on the water. Chemicals and microbes inhabiting the aquatic environment are often responsible for the development of these cutaneous conditions. We review common water sports dermatoses and divide them based on activities that occur in saltwater, freshwater and activities outside the water. Some of the water sports represented in the review include swimming, diving, scuba diving, snorkeling and water polo which are mainly based in the water, as well as sailing, rowing, fishing, surfing, whitewater rafting and water-skiing which are based on the water and outside the water. Aquatic sports dermatoses are presented according to their etiology including infectious and organism-related, contact dermatitis and miscellaneous causes. We also describe conditions specifically associated with water sports including sailing, rowing, fishing and surfing. This comprehensive review focuses on the key recognizable clinical features and principles of management of aquatic sports dermatoses. Our aim is to help sports medicine physicians, dermatologists and other health care providers recognize and treat water sport dermatoses in athletes.

. Pitted keratolysis. Multiple shallow punched-out pits on anterior sole of foot (Tlougan et al., 2010a). Reproduced with permission from International Journal of Dermatology.

Bikini bottom
Bikini bottom is a deep bacterial folliculitis typically caused by Streptococcus or Staphylococcus aureus. It usually occurs in swimmers who wear tight-fitted wet swimwear for prolonged periods of time (Saltzer et al., 1997). Clinical presentation. Individuals present with firm nodules that manifest along the inferior gluteal crease (Basler et al., 1998). Management. First-line treatment includes a course of oral antibiotics for 10 days, such as Cephalexin (Basler et al., 1998). Prevention of this condition includes prompt removal of wet swimwear.

Swimmer's Itch
Swimmer's itch, also known as Schistosome dermatitis, clam-digger's itch or cercarial dermatitis, is caused by infection with larvae from the fluke family Schistosomatidae. The condition typically occurs in swimmers exposed to freshwater, but may also occur in saltwater (Mulvihill & Burnett 1990). Rodents and birds are the primary hosts that release ova containing the immature larvae which mature in snails (Wolf et al., 1995). The larvae infect humans through penetration of the skin and eventually die causing an immunologic reaction and sensitization two weeks after initial contact. Further exposures result in lesions within hours (Wolf et al., 1995). Clinical presentation. Individuals present with multiple erythematous pruritic papules (3-5 mm) with occasional urticarial plaques (Adams, 2006;Hicks, 1977). Systemic symptoms occur rarely and include fever, chills and lymphadenopathy (Cort, 1950;Wall, 1976). Management. Lesions typically resolve spontaneously within 3 to 7 days, but topical corticosteroids and antihistamines may help relieve pruritus. Only severe cases require systemic corticosteroids (Adams, 2006).  (Tlougan et al., 2010a). Reproduced with permission from International Journal of Dermatology.

Molluscum contagiosum
Molluscum contagiosum, also known as "water warts" is a cutaneous viral infection caused by the poxvirus Molluscum contagiosum (Gottlieb & Myskowski, 1994). Various studies have documented an association between this infection and water exposure (Niizeki et al., 1984;Weismann et al., 1973). Clinical presentation. Individuals present with pearly-white or skin-colored papules and nodules that may demonstrate a central dimple or umbilication (Tlougan et al., 2010a).  (Tlougan et al., 2010a). Reproduced with permission from International Journal of Dermatology.
Management. Lesions usually resolve spontaneously without scarring within one year but may persist longer. Therapeutic options to facilitate the resolution of lesions include curettage, liquid nitrogen, trichloroacetic acid and cantharidin. Other off-label options include topical 5-FU or imiquimod (Tlougan et al., 2010a).

Warts
Verrucae or warts are caused by human papillomavirus (HPV) and are common in swimmers and individuals that use communal showers (Gentles & Evans, 1973;Johnson, 1995;Penso-Assathiany et al., 1999). Clinical presentation. Individuals present with well-defined, papillomatous or verrucous papules with a roughened surface. Plantar warts appear as endophytic papules or plaques of the soles with black specs at the center (Tlougan et al., 2010a). Management. Therapeutic options include mechanical destruction with liquid nitrogen, laser and curettage. Methods of chemical destruction include salicylic acid, cantharidin and trichloroacetic acid. Athletes may apply imiquimod, 5-FU, squaric acid (SADBE) and diphenylcyclopropenone (DPCP) for self-management of these lesions. (Tlougan et al., 2010a). Recalcitrant warts may be treated with injected Candida antigen, mumps antigen or bleomycin. (Tlougan et al., 2010a). Oral cimetidine has been shown to be effective in some studies, although its clinical utility remains debated (Orlow & Paller, 1993;Tlougan et al, 2010a). Fig. 4. Verrucae. Plantar wart with roughened surface and black specs at the center (Tlougan et al, 2010a). Reproduced with permission from International Journal of Dermatology.

Athlete's foot
Athlete's foot, also known as tinea pedis, is a common cutaneous fungal infection caused by dermatophytes. Infection may be transmitted through swimming pools, pool decks and shower floors (Bolanos, 1991;Kamihama et al., 1997). Clinical presentation. Individuals typically present with the interdigital subtype that manifests as erythema and scaling with or without pruritus. Other clinical forms include the moccasin subtype with plantar erythema, scaling and hyperkeratosis and the inflammatory subtype with painful bullae or pruritic vesicles (Tlougan et al., 2010a). Management. First-line therapy includes topical antifungal agents used twice daily to affected areas for one to several months. Systemic antifungal agents such as terbinafine 250 mg daily or itraconazole 200 mg daily for 2 weeks may be required for more extensive or refractory lesions. Infection may be prevented by wearing protective sandals in public www.intechopen.com An International Perspective on Topics in Sports Medicine and Sports Injury 228 showers or pool decks. Athletes may prophylactically apply topical antifungal agents twice weekly to prevent reinfection (Adams, 2006).  (Tlougan et al., 2010a). Reproduced with permission from International Journal of Dermatology.

Contact Dermatosis
Offending  (Azurdia & King, 1998;Cronin & Rubber, 1980;Goette, 1984;Romaguiera et al., 1988). Diving mask dermatitis, also known as scuba diver facial dermatitis, may result from exposure to isopropylparaphenylenediamine (IPPD), a rubber antioxidant in face masks (Maibach, 1975;Maibach, 1975;Tuyp, 1983). Swim fin dermatitis may also occur from contact sensitivity to IPPD, in addition to other components including dibutylthiourea and diethylthiourea (Balestrero et al., 1999;Fisher, 1999). Swim cap dermatitis may result from contact sensitivity to mercaptobenzothiazole (Cronin & Rubber, 1980). Other components of swim gear that may elicit a contact allergy include diphenylthiourea, para-tertiary-butylphenol-formaldehyde resin and ethyl butylthiourea found in swim suits, as well as Tego103G, a disinfectant of wet suits (Boehncke et al., 1997;Munro et al., 1989;Nagashima et al., 2003;Reid et al., 1993). Clinical presentation. Individuals with swim goggles dermatitis present with pruritic, periorbital erythema with vesicles, and yellow exudative lesions in severe cases (Tlougan et al., 2010a). Diving mask dermatitis presents with redness and pruritus over areas of direct contact (Fisher, 1980;Maibach, 1975;Tuyp, 1983). Individuals with contact dermatitis to swim caps, ear plugs and nose clips present with well-defined, erythematous, scaling plaques and occasionally vesicles over areas in direct contact with the offending agent. Wet suit dermatitis manifests as a pruritic, vesicular or eczematous eruption on the neck, trunk and extremities (Tlougan et al., 2010a). Management. Mainstay treatment for swim goggle dermatitis includes the use of mediumpotency topical corticosteroids, while systemic steroids may be required in severe cases. Topical immunomodulators may also be effective in mild and chronic conditions (Tlougan et al., 2010a). For contact allergies to other types of swim gear described above, avoidance of the offending allergen and use of silicone based gear is recommended (Fisher, 1980;Goette, 1984;Taylor & Rubber, 1986).

Pool and pool water dermatitis
Pool dermatitis is an irritant dermatitis to chemicals in swimming pools, particularly chlorine and bromine. Fig. 6. Pool dermatitis. Eczematous plaques in uncovered areas in a swimmer (Tlougan et al., 2010a). Reproduced with permission from International Journal of Dermatology.
One study found that swimmers developed more severe cutaneous eruptions after swimming in brominated pools compared to chlorinated pools (Penny, 1991). In contrast to pool dermatitis, pool water dermatitis is an allergic contact dermatitis to chlorinated or brominated compounds in the water. Potassium peroxymonosulfate (PPMS) which is another decontaminant used in pools and hot tubs may also cause pool water dermatitis (Gilligan et al., 2010). Clinical presentation. Individuals with pool dermatitis present with pruritic, urticarial or eczematous plaques in uncovered areas of skin (Penny, 1991;Rycroft & Penny, 1983). Individuals with pool water dermatitis present with pruritic, erythematous, scaling plaques in uncovered areas of the skin (Fitzgerald et al., 1995;Sasseville et al., 1999). Management. Avoidance of the offending irritant and halogenated water is recommended for sensitized athletes (Penny, 1991). Diligent use of emollients is also imperative.

Miscellaneous 2.3.1 Purpura gogglorum
Purpura gogglorum or periocular purpura induced by goggles is thought to be caused by collision forces, suction trauma or pressure of the goggles on the periocular soft tissue (Jonasson, 1997;Jowett & Jowett, 1997;Metzer & Berlob, 1992). Clinical presentation. Individuals present with purpura around the eyes. Management. These lesions usually heal spontaneously. In severe cases with vision changes and extensive swelling and facial tenderness, referral to the emergency department to evaluate for possible fracture of facial bones is warranted (Tlougan et al., 2010a).

Platform purpura
Platform purpura is a skin condition that occurs during a missed dive in which the forces upon entering the pool are transmitted to the skin of the thighs (Tlougan et al., 2010a). Clinical presentation. Individuals present with symmetrical, erythematous plaques on the thighs that may be painful (Tlougan et al., 2010a). Management. Supportive care includes nonsteroidal anti-inflammatory drugs and application of warm compresses for 5-10 minutes two or three times daily for pain relief. The lesions typically resolve within a few days (Tlougan et al., 2010a).

Aquagenic pruritus
Aquagenic pruritus occurs after brief exposure to water at any temperature and is associated with mast cell degranulation, elevated blood levels of histamine and local release of acetylcholine in the skin (Greaves, 1992). Clinical presentation. Individuals present with pruritus or a tingling, burning or stinging sensation after exposure to water without any apparent skin changes. The symptoms last between 10 minutes and a couple of hours (Steinman & Greaves, 1985). Management. Phototherapy, particularly PUVA and narrow-band UVB may help relieve pruritus, while some patients may respond to antihistamines (Greaves, 1992;Xifra et al., 2005).

Aquagenic, cold and cholinergic urticaria
Aquagenic urticaria is a rare type of physical urticaria that occurs upon contact with any form of water at any temperature (Hide et al., 2000;Shelley & Rawnsley, 1964). In contrast, cold urticaria occurs in athletes exposed to cold water and is also associated with winter sports (Sarnaik et al., 1986). While essential acquired cold urticaria is the most common type of cold urticaria, secondary causes include cryoglobulinemia and connective tissue disorders (Sarnaik et al., 1986). Familial cold autoinflammatory syndrome is another condition that manifests with cold urticaria in addition to periodic fever and joint pain (Hoffman et al., 2001). Cholinergic urticaria is the most common subtype of physical urticaria found in athletes, and is typically induced by physical exertion, exposure to heat or emotional stress (Jorizzo, 1987). Clinical presentation. Individuals with aquagenic urticaria present with urticarial wheals on any submerged skin surface shortly after contact with water. Occasionally, only a focal urticarial eruption may occur (Shelley & Rawnsley, 1964). Systemic symptoms occur rarely and include headache and respiratory distress (Baptist & Baldwin, 2005;Luong & Nguyen, 1998). Cold urticaria presents with erythematous, edematous papules along cold-exposed skin surfaces that are very pruritic. Individuals may also present with systemic symptoms including anaphylaxis and loss of consciousness which may result in drowning (Sarnaik et al., 1986).Cold urticaria may be differentiated from aquagenic urticaria by placement of an ice cube on the forearm for several minutes, with resulting development of a square urticarial plaque during rewarming of the skin (Blanco et al., 2000). Individuals with cholinergic urticaria typically present initially with itching or burning, with subsequent development of flushing and hives minutes after the onset of physical activity (Jorizzo, 1987). The diagnosis is supported by exercise testing, sauna test or hot bath challenge with a resulting urticarial eruption (Jorizzo, 1987). Management. Individuals with aquagenic urticaria may respond to antihistamines and anticholinergic agents. Other alternative treatment options include PUVA and UVB (Juhlin & Malmros-Enander, 1986;Parker et al., 1992). Individuals with cold urticaria generally respond well to antihistamines (Juhlin, 2004;Zuberbier et al., 2006). Health care providers should also consider secondary causes of cold urticaria including cryoglobulinemia and connective tissue disorders and treat the underlying conditions (Sarnaik et al., 1986). It is recommended that affected athletes wear protective clothing when exposed to cold environments. Traditional therapy for cholinergic urticaria includes antihistamines and leukotriene inhibitors (Otto & Calabria, 2009).

Green hair
Green hair occurs in swimmers with blonde, gray or white hair after exposure to copper in pool water. Frequent hot air drying, brushing, sun exposure, peroxide bleaching and use of alkaline or tar shampoos increases the likelihood of developing green hair (Carson, 1977;Holmes & Goldsmith, 1974). Clinical presentation. Individuals present with green-colored hair after swimming (Goette, 1978). Management. Effective treatment options for green hair include 3-5% hydrogen peroxide and copper chelating shampoos (Adams, 2001).

Swimmer's shoulder
Swimmer's shoulder typically occurs during the crawl stroke in which the athlete's chin rubs against the shoulder while turning the head to breathe, with the development of irritation dermatitis (Koehn, 1991). Clinical presentation. Individuals present with erythematous and slightly roughened plaques on the anterior aspect of the shoulder after swimming (Tlougan et al., 2010a). Management. Lesions typically heal without treatment, while application of petroleum jelly or polysporin ointment may provide additional relief (Tlougan et al., 2010a).

Pool palms
Pool palms describe a type of frictional dermatitis resulting from repetitive rubbing of the skin surfaces against rough surfaces in the pool (Blauvelt et al., 1992;Wong & Rogers, 2007). Clinical presentation. Individuals present with symmetric erythematous plaques on the convexities of the palmar hands and fingers (Lacour, 1995). Management. This condition usually resolves spontaneously after cessation of the irritating activity (Tlougan et al., 2010a).

Infectious and organism-related 3.1.1 Cnidarial dermatoses
Cnidarial dermatoses result from contact with marine invertebrates of the phylum Cnidaria. These organisms contain nematocysts on their tentacles which may pierce the skin and release toxins that may result in cutaneous as well as systemic reactions. Several organisms known to affect water athletes and swimmers include Portuguese man-of-war, jelly fish, sea anemones, fire corals and red sea corals. Clinical presentation. Individuals stung by Portuguese man-of-war present with pain after the initial sting, followed by development of a pruritic, erythematous, urticarial eruption that subsides after a few days. Violaceous lesions and vesicles occasionally occur, while systemic symptoms including anaphylaxis are rare (Adams, 2006). Similarly, jellyfish stings present with initial stinging sensation followed by urticarial or papulovesicular lesions in a linear distribution (Burnett, 1992;Currie & Jacups, 2005).Delayed reactions including hyperpigmentation, lipodystrophy, keloid-like scars and erythema nodosum may result, while severe reactions including respiratory distress and cardiac arrest rarely occur (Burnett et al., 1986;Manowitz & Rosenthal, 1979;Tamanaha & Izumi, 1996;Veraldi & Carrera, 2000). Individuals stung by sea anemones present with an initial stinging or burning sensation with erythema, edema, petechial hemorrhages and ecchymoses. Eventually, an erythematous, papulovesicular eruption develops and local necrosis, ulceration and desquamation may occur (Halstead, 1988). Bathing or showering exacerbates the stinging or burning sensation. Severe side effects include acute renal failure and fulminant hepatic failure (Garcia et al., 1994;Mizuno et al., 2000). Seabather's eruption results from contact with larvae of the adult sea anemone and the thimble jellyfish and presents similarly with systemic symptoms occurring in up to 10% of cases. (Freudenthal & Joseph, 1993;MacSween & Williams, 1996;Sams, 1949;Tomchik et al., 1993). Fig. 8. Jellyfish sting. Linear erythematous plaques, which may be vesicular or urticarial (Tlougan et al., 2010b). Reproduced with permission from International Journal of Dermatology.
Individuals stung by the fire coral present with erythematous, burning lesions caused by formic acid on the coral's outer shell. Individuals stung by the red soft coral present with urticarial eruption of the hands and arms with vesicular-bullous lesions, in addition to conjunctivitis, rhinitis and asthma from release of a toxin (Addy, 1991;Canarasa et al., 1993;Fisher, 1999;Miracco et al., 2001;Onizuka et al., 2001). Management. Supportive care for Cnidarial dermatoses includes application of warm compresses, topical corticosteroids and antihistamines for symptomatic relief. Some authors recommend applying sand to the affected areas to facilitate removal of the nematocysts. Severe anaphylactic reactions require epinephrine. Clinicians should consider pain management and tetanus prophylaxis as well (Tlougan et al., 2010b).
For jellyfish stings, application of vinegar may provide relief. Some authors recommend prompt placement of meat tenderizer to help inactive toxins (Freiman et al., 2004). It is important to note that swimmers should not immerse themselves in freshwater after being stung by saltwater Cnidaria because this may activate nematocysts (Tlougan et al., 2010b). Treatment of fire coral dermatitis includes application of ammonium to neutralize formic acid (Tlougan et al., 2010b).

Echinodermata dermatoses
Echinodermata dermatoses result from contact with marine invertebrates from the phylum Echinodermata. Organisms which may result in injury to aquatic athletes and swimmers include sea stars, sea urchins and sea cucumbers. Clinical presentation. Individuals in contact with the spines of seastars may present with puncture wounds and a burning sensation which may persist for one month (Auerbach, 1991). Contact with sea urchin spines may result in a painful puncture wound with surrounding erythema and edema, while broken spines may remain lodged in the skin. Rarely, tenosynovitis and systemic reactions including nausea, syncope and respiratory distress may occur (Baden, 1987). Contact with sea cucumbers may present as a burning irritant dermatitis. The sea cucumber toxin holothurin, a potent cardiac glycoside, may cause a chemical conjunctivitis and even blindness, while ingestion may result in death (Tlougan et al., 2010b). Fig. 9. Sea urchin spine. Spine punctured through the skin with resulting pain, redness and swelling (Tlougan et al., 2010b). Reproduced with permission from International Journal of Dermatology.
Management. Symptomatic relief for individuals affected by seastars and sea urchins includes warm compresses, topical corticosteroids and antihistamines. Anaphylaxis should be promptly treated with epinephrine. Athletes affected by sea cucumbers should immediately irrigate the wound with warm water, soap, vinegar or isopropyl alcohol to rinse off the holothurin toxin. Healthcare providers should treat eye injury with topical anesthesia, irrigation and consultation with an ophthalmologist (Tlougan et al., 2010b).

Sponge dermatitis
Marine sponge dermatitis results from contact with marine invertebrates of the phylum Porifera. Marine sponges with sharp spicules can cause minor abrasions upon contact with swimmers. In addition, marine sponges may cause an irritant dermatitis as well as local and systemic reactions from the production of crinitoxins by some species (Brown & Shepherd, 1992;Sims & Irei, 1979). Clinical presentation. Individuals present with a stinging sensation followed by pain, pruritus, and swelling shortly after contact with the organism. Severe effects may result from the crinitoxins with cutaneous manifestations including vesiculations, bullae, desquamation, in addition to delayed allergic contact reactions, erythema multiforme and rarely anaphylaxis (Brown & Shepherd, 1992). Management. Similar to Cnidarial dermatoses, management includes symptomatic relief as described above and epinephrine for anaphylactic reactions (Tlougan et al., 2010b).

Contact dermatitis 3.2.1 Seaweed dermatitis
Seaweed dermatitis is a type of contact dermatitis that results from irritants produced from Lyngbya majuscula, a blue-green alga that is prevalent in the Pacific, Indian, and Caribbean oceans (Chu, 1959;Osborne et al., 2001). Clinical presentation. Individuals present with blisters and desquamation with associated stinging, burning, or pruritic sensation within 24 hours after contact (Gauer & Arnold, 1961;Izumi & Moore, 1987). The lesions progress to an erythematous dermatitis that commonly surrounds the perineal and perianal areas lasting for about one week. Ingestion or inhalation of the irritants may result in burning of the upper gastrointestinal tract and respiratory irritation (Anderson et al., 1988;Marshall & Vogt, 1994). Management. Supportive therapy includes symptomatic relief with cool compresses, treatment with topical corticosteroids, antihistamines and analgesics (Izumi & Moore, 1987).

Sailing/rowing 4.1.1 Pulling boat hands
Pulling boat hands is due to a combination of mechanical injury and exposure to cold, and is usually seen in sailors, rowers and crew team members (Toback et al., 1985). There is a strong association between this condition and Raynaud's phenomenon, which causes pallor and numbness of the distal digits with resulting color changes from white to blue to red (Toback et al., 1985). Clinical presentation. Individuals present with erythematous papules, macules, nodules and blisters that may be painful and pruritic. The lesions typically manifest over the distal dorsal aspect of the hands and proximal phalanges , w i t h s p a r i n g o f t h e s k i n o v e r t h e metacarpophalangeal (MCP) joints and fingertips (Tlougan et al., 2010c). Management. The mainstay treatment includes topical corticosteroids, while supportive care includes use of moisturizers, gloves and freshwater soaks (Tlougan et al., 2010c).

Sailor's marks
Sailor's marks are associated with repetitive contact and friction between the rope and hands of sailors, with resulting thickening of the skin (Unal et al., 2005).
Clinical presentation. Individuals present with hyperkeratotic thickening of the superficial skin, with band-shaped calluses that manifest bilaterally on the dorsolateral and palmar regions of the first MCP joint and the mediopalmar site of the fifth MCP joint (Tlougan et al., 2010c). Management. Prevention of the condition includes wearing protective gloves while sailing (Tlougan et al., 2010c).

Rowing blisters
Rowing blisters result from friction between rower's hands and the oar handles (Rumball et al., 2005). Clinical presentation. Individuals present with painful blisters that typically manifest on the anterior surfaces of the fingers and palms (Tlougan et al., 2010c). Management. Treatment consists of supportive care of the blisters by draining the lesions without disruption of the roof of the blister up to three times in the first day, and application of petroleum jelly and occlusive dressing (Tlougan et al., 2010c).

Fishing 4.2.1 Fishing rod dermatitis
Fishing rod dermatitis is a contact dermatitis that results from exposure to isopropylparaphenylenediamine (IPPD) or other closely related components of carbon-fiber fishing rods (Minciullo et al., 2004). Clinical presentation. Individuals present with unilateral erythematous, scaly hand plaques (Tlougan et al., 2010c). Fig. 10. Fishing rod dermatitis. Erythematous, scaly plaques on the hand (Tlougan et al., 2010c). Reproduced with permission from International Journal of Dermatology.
Management. Treatment consists of topical corticosteroids and oral antihistamines. Preventive methods include using a protective cover and insulating tape over the fishing handles and avoidance of IPPD fishing rods (Tlougan et al., 2010c).

Live fish bait allergy
Live fish bait allergy occurs from exposure to the insects and worms used as fish bait. Contact dermatitis may result from exposure to various species of worms such as Lumbrinereis latreilli, Nereis versicolor and Chironomus thummi thummi, as well as larvae of the maggot Calliphora vomitoria De Jaegher & Goossens, 1999;Janssens et al., 1995;Usamentiaga et al., 2005;Virgili et al., 2001). Additionally, fisherman may develop allergic contact dermatitis to azo compounds used to dye maggots (Warren & Marren, 1997). Clinical presentation. Individuals typically present with bilateral pruritus and edema of the hands, and occasionally with hyperkeratotic lesions of the thumbs and index fingers (Virgili et al., 2001). Fish bait allergy may cause an urticarial eruption, respiratory reactivity or rhinoconjunctivitis (Bernstein et al., 1983;Siracusa et al., 1994). Management. Individuals gradually improve with avoidance of the offending allergens (Tlougan et al., 2010c).

Erysipeloid
Erysipeloid, also known as "fish poison", "shrimp poison", "crab poison" and "scallop poison" is a bacterial infection of traumatized skin by Erysipelothrix rhusiopathiae, mostly seen in fisherman (Burke et al., 2006;Reboli & Farrar, 1989). Infection most commonly results in localized cutaneous disease, while disseminated cutaneous disease and generalized systemic infections may occur as well (Barnett et al., 1983). Clinical presentation. Patients typically present with well-circumscribed, violaceous, edematous plaques on the fingers and hands that are painful and tender to palpation. The lesions generally display central clearing over time and vesicles may develop as well (Gorby & Peacock, 1998;Reboli & Farrar, 1989). Systemic infection may manifest with constitutional symptoms such as fever and malaise, as well as septicemia, arthritis, empyemas, endocarditis and cerebral abscesses (Gorby & Peacock, 1998;Reboli & Farrar, 1989). Management. Mainstay treatment of localized cutaneous and diffuse cutaneous forms of disease includes a one week course of penicillin (Varella & Nico, 2005). Severe systemic reations require larger doses of penicillin G (Reboli & Farrar, 1989). Erythromycin may be used in individuals with penicillin allergy.

Rubber boot dermatitis
Rubber boot dermatitis is an allergic contact dermatitis that fisherman develop after exposure to rubber fishing boots (Ross, 1969). Clinical presentation. Individuals present with a diffuse eczematous eruption throughout the leg. If the lesions progress without treatment, a pompholyx-like eruption may manifest on the palms and soles with scaling, thickening, fissures and exfoliation of the skin (Tlougan et al., 2010c). Management. Topical corticosteroids and antihistamines are the mainstay treatment. Oral steroids may be required for severe infections. Prevention includes avoidance of rubber boots in sensitized fisherman (Tlougan et al, 2010c).

Surfing 4.3.1 Surfer's nodules
Surfer's nodules are a type of athlete's nodules and occur from repetitive contact and pressure between the surfboard and surfer's bony prominences such as the knees and ankles (Basler., 1989;Erickson & Von Gemmingen, 1967). Some authors also propose that this condition may represent a foreign body reaction to sand or other foreign material (Pharis et al., 1997). Clinical presentation. Individuals usually present with nontender, fibrotic nodules on the pretibial surface of the leg or the mid-dorsum of the foot (Cohen et al., 1990).
Management. Treatment consists of topical keratolytics such as salicylic acid and lactic acid. Other therapeutic modalities include intralesional corticosteroids, topical corticosteroids and excision of the lesions (Adams et al., 2006). Prevention of this condition includes the use of protective padding on the knees and ankles (Cohen et al., 1990).

Surf rider's dermatitis
Surf rider's dermatitis is a type of irritant contact dermatitis that is generally seen in surfers and users of belly boards, boogie boards and body boards. Friction, shearing forces and pressure between the athlete's body and the surfing board contribute to the development of the eruption (Bischof, 1995). Allergic reactions to surfing board polymers and wax may also occur (Tennstedt et al., 1981). Clinical presentation. Individuals present with painful erythematous and edematous lesions on the nipples. Surfers may also present with small abrasions and fissures (Tlougan et al., 2010c). Management. The lesions resolve spontaneously without treatment. Supportive care includes analgesics for pain relief as well as protective dressings and soft clothing (Tlougan et al., 2010c).

Conclusion
Aquatic sports dermatoses consist of a variety of cutaneous conditions that occur in athletes who participate in activities on or in the water. Certain conditions are specifically associated with freshwater or saltwater, while others may occur in both settings. Furthermore, participation in particular sporting activities predisposes athletes to certain dermatoses. The approach to athletes with water-related dermatoses consists of taking an appropriate history to recognize the type of water sport, nature of the water exposure with regards to duration in or on the water, saltwater versus freshwater, and any related equipment or contact with organisms. The etiologies of water-related dermatoses are usually infectious and organismrelated or result from contact dermatitis. Our review highlights the key physical findings that are most consistent with particular aquatic sports dermatoses. We discuss first-line treatment guidelines and preventive measures that should help guide healthcare providers in the management of athletes with water-related skin conditions.