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20. Encounters with Animals 20. Encounters with Animals This is the last chapter in the section on sports-related conditions induced by the environment and the last chapter of this book. This chapter discusses the myriad skin reactions to members of the animal kingdom encountered in the athlete’s venue. The type of skin eruption is largely related to the specific organ- ism involved. Athletes whose competition take them to the outdoor turf or surf risk involvement. Although the overall incidence of skin reactions likely is greater in the grounded athlete, the variety of skin conditions experienced by the aquatic athlete is vast. Seabather’s Eruption Epidemiology Many epidemics of seabather’s eruption, also termed sea lice, have occurred. In 1980 on the south shore of Long Island, several thousand swimmers developed the condition. In 1992 along the coast of South Florida, at least 10,000 swimmers were affected. Seabather’s eruption typically creates havoc in the ocean along the Atlantic coast, Bermuda, Bahamas, and other Caribbean islands. Outbreaks occur between March and August but peak in May. Snorkelers and swimmers, but not deep-sea divers, develop the condition. The organisms causing seabather’s eruption do not live at deep-sea depths. It is widely believed that Cnidaria larvae cause seabather’s eruption. Cnidaria is a phylum consisting of jellyfish, corals, sea anemones, and hydroids. Investi- gators have identified the larvae (planula) of Linuche unguiculata as the cause of epidemics in Florida and the Caribbean (Tomchik et al., 1993). However, the larvae of Edwardsiella lineata cause seabather’s eruption on the coast of New York. Observations suggest that in addition to the larval forms of Cnidaria, adult medusa and immature medusa (ephyra) can cause seabather’s eruption (Segura- Puertas et al., 2001). The ephyra range in size from 0.5 to 6mm and prevail during January and March. Adult medusas are small jellyfish and grow to 2.5cm; they predominate from March to May. The planula predominate from May to June. These organisms are 0.5mm in size and are barely visible with the naked eye. The finding that all forms of L. unguiculata can cause seabather’s eruption explains how a swimmer can develop seabather’s eruption in the early spring when mature medusas exist. It is thought that the small-sized organisms flow through bathing suits, become trapped, and discharge their nematocysts onto the swimmer’s skin. Several factors impact the probability of disease. First, host factors are nec- essary, as not all exposed swimmers develop seabather’s eruption. A swimmer’s 312 Sports Dermatology skin not only responds to the toxic effect of the nematocysts but also may develop an immunologic response to the antigen. The cell-mediated immunity is critical. The organisms are not distributed evenly in the water and can appear as cloudy areas. Finally, longer water exposure and swimsuits that cover greater areas of the body increase the likelihood of disease. Clinical Presentation Swimmers may experience a prickling sensation while they are still in the water. The skin lesions typically develop 4 to 24 hours after exposure, but may take up to four days to appear. One study showed that swimmers who had seabather’s eruption in the past were statistically more likely to experience the prickling sensation while they were in the water (Tomchik et al., 1993). The distribution of seabather’s eruption is distinctive. Swimmers develop lesions concentrated beneath the swimming suit or on uncovered areas of the body that experience a great deal of friction (e.g., axillae and thighs). Lesions also occur under bathing caps and swimming fins. Surfers develop lesions on their chest and abdomen that result from trapping the stinging organisms as the surfers lie on the board heading out to catch a wave. Morphologically, the lesions of seabather’s eruption appear as well-defined, discrete macules and papules; vesicles may be seen (Figure 20-1). The lesions can be painful or pruritic. In general the eruption clears within 1 to 2 weeks; most clear in 1 week. Figure 20-1. In seabather’s eruption, athletes develop erythematous papules and vesicles beneath swim wear. 20. Encounters with Animals 313 Investigators have documented persistent vesicular eruptions even 1 year after initial exposure. It is important to note that although the larva die in the bathing suit, the nematocysts persist and can continue to discharge their toxin. Associated systemic findings include fever, chills, headache, malaise, arthralgia, myalgias, and diarrhea. Complications include conjunctivitis, hyperpigmenta- tion, keloidal formation, and atrophy. Diagnosis The distinctive distribution of seabather’s eruption should alert the clinician. If the swimmer has been stung by the adult medusa, bell-shaped erythema may be noticed. The differential diagnosis is vast and includes swimmer’s itch, insect bite reaction, urticaria (unrelated to sea creatures), sponge-diver’s disease (ghost anemone), and viral or drug eruptions. Biopsy reveals a hypersensitivity reac- tion and is not particularly helpful in delineating the diagnosis. Some investiga- tors have suggested ELISA may be a useful serologic test to confirm the diagnosis (Burnett et al., 1995). Treatment The most important treatment is removal of the swimming suit as soon as possible after the swimmer gets out of the sea water. Swimmers should not remove the suit while taking a shower because tap water may actually cause nematocyst activation. Many agents have been used to deactivate the nemato- cysts before they fire and include vinegar, baking soda, and isopropyl alcohol. Unfortunately, these compounds occasionally can conversely cause nematocysts to activate. No studies support the use of any particular therapy. Once injected by the nematocysts, the swimmer should take antihistamines throughout the day. Topical steroids may benefit the swimmer. Some authors have used oral thiabendazole 1.5 g twice per day for 2 days (Burnett, 1992). Systemic steroids may be necessary in severe cases. The affected swimming suit should not be worn until it has been laundered (Table 20-1). Table 20-1. Treatment of Seabather’s Eruption Immediate removal of swimming suit (not in tap water) Application of vinegar or baking soda Oral antihistamines Topical steroids Oral steroids (if severe) Oral thiabendazole 314 Sports Dermatology Prevention Swimmers should avoid cloudy areas (representing groups of organisms) in the ocean and areas with high density of adult medusa. Swimmers should avoid wearing T-shirts (they should wear water-resistant sunscreen instead), and women should consider wearing a two-piece suit. Because a swimmer’s suit traps the nematocysts, decreasing the area covered by clothing is critical. Surfers and divers can wear wets suits with restrictive cuffs. A topical product that reduces the incidence of dermatitis from firing nematocysts is available and should be worn in oceans with high infestations. Finally, a sure method to prevent seabather’s eruption is to avoid swimming along the eastern seaboard during peak months. It is interesting to note that some swimmers develop antibodies that may protect certain chronically exposed individuals. Swimmer’s Itch Epidemiology Several authors have noted epidemics of swimmer’s itch, sometimes termed schistosome dermatitis, cercarial dermatitis, or clam digger’s itch (Hoeffler, 1997). Fifty-six percent of snorkelers in one series developed swimmer’s itch as did 250 swimmers in England in June and July 1970. An epidemiologic study in Quebec noted a 12% incidence of swimmer’s itch. Sixty-nine percent of all cases were related to exposure to one specific beach (Levesque et al., 2002). In contrast to seabather’s eruption, this condition occurs in fresh water. It occurs primarily in the northern United States and Canada, but it also is seen in California, Louisiana, Texas, and Washington. It has been noted on all continents except Antarctica. The peak density of schistosomes in the northern United States correlates with mid-summer. Cercarial shedding from snails increases with increasing light and warm water temperatures. Shedding still occurs, albeit at a much lower rate, during the fall and early spring. Cercariae of schistosomes cause swimmer’s itch. Ducks and rodents, not humans, are the normal hosts for these microorganisms. Cercariae typically invade the feet of the normal host and reproduce in the mesenteric veins. The schistosomes’ eggs are deposited in the host’s feces, which infect intermediately aquatic snails. Once the cercariae emerge, they attempt to complete their life cycle by penetrating the feet of ducks or rodents. The cercariae must find their next host within 12 to 24 hours or face death. The cercariae may, at this point, unintentionally invade the human skin. The penetration results in a cutaneous hypersensitivity reaction. Snails particularly like shallow water, so, not surpris- 20. Encounters with Animals 315 ingly, most swimmers develop swimmer’s itch while swimming in shallow water (Levesque et al., 2002). Clinical Presentation The swimmer develops pruritus approximately 1 hour after cercarial pene- tration. Within 24 hours, the athlete develops intensely pruritic, well-defined, erythematous, small (<0.5cm) papules, macules, and occasionally vesicles on all exposed skin. Development of lesions on the face is very unusual. Most swimmers have more than 20 lesions, 23% of swimmers have between five and 20 lesions, and less than 10% of swimmers have fewer than five lesions. The lesions resolve without therapy in 1 to 2 weeks. Lengthy exposures to infested water and lack of extensive swimming suit coverage increase the severity of disease. Systemic symptoms such as fever, chills, and lymphadenopathy are reported (Levesque et al., 2002). Postinflammatory hyperpigmentation is an occasional complication. Diagnosis The clinician should make the diagnosis of swimmer’s itch based on the find- ings of temporal association with swimming and typical distribution of lesions. The differential diagnosis includes arthropod bite reaction, seabather’s eruption, urticaria (unrelated to sea creatures), sponge-diver’s disease (ghost anemore), and viral or drug eruptions (Table 20-2).
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