Sea Bather's Eruption

 

SE, also known as marine dermatitis and often misnamed sea lice infestation, is an acute dermatitis that begins shortly after bathing in seawater. SE is often confused with swimmer's itch (cercarial dermatitis, see previous section), not only because they both occur after exposure to water but also because the common names of these two conditions are easily confused. For many years, the cause of SE remained a mystery, but it is now known that the responsible agents in at least two types of SE are the larval forms of marine coelenterates. In waters off the coast of Florida and in the Caribbean, the tiny larvae of the thimble jellyfish, Linuche unguiculata, are to blame. Off the coast of Long Island, New York, researchers found that the larval forms of the sea anemone Edwardsiella lineata were responsible for the eruption.

In addition to having a different etiology, SE can be distinguished from cercarial dermatitis by several other characteristics: SE primarily involves areas of the body covered by bathing suits from which water evaporates slowly, as opposed to uncovered areas as is typical of swimmer's itch. Most symptoms are not noted until the bather has left the water (although some of those affected have complained of a prickling sensation while still in the water).

The eruption is caused by minute stings from the nematocysts of the coelenterate larvae, which become trapped underneath swimwear or may adhere to hairy areas of the body. In addition to SE after contact with the larvae, which are most abundant in May and June, swimmers and bathers may also develop SE after contact with the other two free-swimming stages of L. unguiculata, the ephyrae and medusae stages.

The lesions begin within 4 to 24 hours after exposure as erythematous macules, papules, or wheals that may itch or burn  These lesions may progress to vesiculopapules, which crust over and heal in 7 to 10 days. Associated systemic symptoms may include chills and a low-grade fever as well as nausea, vomiting, diarrhea, headache, weakness, muscle spasms, and malaise. Febrile and systemic symptoms are more common in children and adolescents. In the presence of such constitutional symptoms, caregivers who fail to recognize the pattern of the eruption or who fail to take a history of exposure to saltwater may mistakenly make the diagnosis of a viral syndrome.

In waters along the coast of south Florida, the season for SE is between March and August with a peak in May. The incidence among bathers during May and June 1993 in Palm Beach County was reported to be 16 percent. The strongest risk factor for developing SE is a previous history of the condition, which is consistent with the theory that SE represents a hypersensitivity response to the nematocyst stings. Other risk factors include age younger than 16 years and surfing. Showering with swimwear removed was found to be a protective measure.

 

 

Prevention of SE includes the measures listed in Table 209-5. Treatment of SE is symptomatic and includes the use of antipruritic lotions, colloidal baths with starch or oatmeal, antihistamines, and topical glucocorticoids. Severe unremitting cases may warrant systemic glucocorticoid therapy. Secondary bacterial infections may complicate the condition and should be diagnosed and treated appropriately.

Injuries Caused by Mollusks

 

CONE SHELL ENVENOMATIONS

Cone shells are univalvular gastropods whose ornate cone-shaped shells are highly prized by shell collectors and divers. A number of species have a highly developed venom apparatus that can inflict a lethal sting. Most of the dangerous cone shell species are found in the shallow waters of the Indo-Pacific. Cone shells are carnivorous. They live on the ocean bottom and, depending on the species, may hunt worms, other mollusks, or fish. Cone shells kill their prey by means of a spear-like venomous radular tooth that is thrust out from the animal's proboscis. Cone shell venom contains several different kinds of neurotoxins, and death may result from respiratory paralysis. There is so far no antivenin for cone shell toxin, and mortality rates after envenomations from the more dangerous species (Conus geographicus and C. magus) may be as high as 15 percent to 20 percent.

Injuries from cone shells are of the puncture wound variety. The degree of pain is variable, ranging from a mild stinging sensation, similar to that of an insect bite, to excruciating pain. Early symptoms may include edema, ischemia, numbness, and paresthesias of the wound site. Paresthesias may become widespread, with the lips and mouth commonly affected. Localized muscular paralysis may progress to generalized weakness or paralysis with eventual respiratory distress and cardiopulmonary failure. Neurotoxic symptoms that indicate severe envenomation include diplopia, blurred vision, aphonia, dysphagia, and coma. Rare cases of disseminated intravascular coagulation have been reported after cone shell envenomation.

Great care must be exercised in handling live cone shells. Thick protective gloves should be worn, and the soft under portion of the animal should be avoided. Cone shells should never be placed in pockets of clothing or swimwear, because they have been known to sting through clothing.

Treatment of cone shell envenomations is supportive. The victim should be kept at rest and the sting area kept dependent and immobilized. A compression dressing should be applied to occlude lymphatic-venous, but not arterial, flow. Local suction may be helpful if it can be applied immediately to the wound site with a plunger device, such as the Extractor Vacuum Pump (Sawyer Products, Safety Harbor, Florida).