In this issue of the journal, Taniguchi and colleagues from Mie University in Japan present a report of two patients with a form of cutaneous larva migrans (creeping eruption) which they attribute to gnathostomiasis, the larvae o^ Gnatliostoma nipponicum migrating through the skin of the patients following the ingestion of raw fish (1). The authors pursued the etiology of the skin eruption with unusual tenacity: extracting a portion of the worm from the paraffm block of the skin biopsy for scanning microscopic examination, and even engaging in "shoe leather epidemiology" to return to the rice field where the implicated fish had been caught, obtain additional fish (3,098 of them!), and document the presence of Gnathosloma larvae in some of the fish. The exquisite scanning electron micrographs illustrated as Fig 5 to their paper are of a larva found in one of the captured fish and allowed definitive morphologic speciation of the parasite as Gnathostoma nipponicum by their helminthologist colleague (1). Nematodes of the genus Gnathostoma (usually Gnathostoma spinigerum) are natural parasites of domestic cats and dogs, as well as such wild felines as leopards and tigers. They are endemic to Southeast Asia with major foci in Thailand and Japan, but are also endemic to parts of South America. The adult worms, rust colored and up to 5 cm. in length, occupy the gastric wall where they incite an inflammatory mass of hyperplastic gastric mucosa and inflammatory cells, especially eosinophils. They produce eggs which pass in the feces, hatch in water, and develop into free-swimming, first-stage larvae which are ingested by the copepod Cyclops and develop into second stage larvae. The Cyclops are in turn ingested by such aquatic creatures as eels, frogs, snakes, or, most important for human disease, a variety of fresh water fish in which third stage larvae become encysted in skeletal muscle. Numerous wild and domesticated birds and mammals, including man, may become infected from eating such infected flesh, but progression to adult organisms occurs only in the definitive hosts (cats, dogs, etc.). Man is one of the dead end hosts in whom larvae can persist but not develop further. Following ingestion of raw infected flesh, the human host may, within 24-48 h, develop acute abdominal pain as the larva penetrates the stomach wall into the peritoneal cavity. There may be abdominal symptoms such as nausea, vomiting, flushing, pruritis, and urticaria with associated abdominal tenderness, leukocytosis, and eosinophilia. An abdominal emergency, sometimes necessitating surgery, may be simulated. Within three to four weeks, the larva or larvae migrate to the subcutaneous tissues, where they tend to stay. At this point, systemic symptoms wane, blood eosinophilia decreases, and the chronic cutaneous phase begins (2, 3). In cutaneous gnathostomiasis, the larva or larvae slowly migrate through the subcutaneous fat and dermis. The clinical lesion is a palm-sized, warm, painless, pruritic swelling ("Yangtze edema") which slowly migrates and may display a more discrete, elevated, erythematous tract in its center. Episodes of more acute swelling, apparently corresponding to increased migratory activity of the larva, occur every two to six weeks and last for up to 10 days. A single larva may live in human skin for up to 10 or 12 years, causing repeated symptomatic episodes. The skin of the trunk and abdomen is usually involved, while migration to facial skin may be complicated by ocular involvement, and extension to the wrist may lead to pressure phenomena such as carpal tunnel syndrome (2). No completely effective helminthicide is available for man, and surgical removal appears to be the treatment of choice. The dermatopathoiogy of gnathostomiasis is often disappointing in that the actual larva may not be encountered in the tissue biopsy. The most intense inflammation, clinically and pathologically, is in the tissues through which the larva has already passed. For instance, in the report by Feinstein and Rodriguez-Valdes in which a 7x4 cm. incisional biopsy was performed, only a portion of the parasite was discovered in the subcutaneous fat at one edge of the specimen (4). Similarly, two biopsies in Taniguchi's Case 2 failed to eliminate the worm and the patient was treated with a helminthicide (1). On occasion, as with Taniguchi's Case 1, the biopsy will reveal the worm residing in a tract in the dermis or subcutaneous tissue (3). There are typically scattered polymorphonuclear leukocytes and eosinophils in the immediately adjacent soft tissue, with more intense representation of these cells in the vicinity of the nearby vasculature from which they are being
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