Gnathostomiasis in Mexico
SPECIAL COVERAGE
Source: Ogata K, et al. Short report: Gnathostomiasis in Mexico. Am J Trop Med Hyg 1998;58:316-318.
Ogata and colleagues examined the recent epidemiology of human gnathostomiasis in Mexico. In excess of 1000 cases were diagnosed based on clinical findings in the six endemic sites of Culican, Sinaloa, Culiacan (Sinaloa State), Tepic (Nayarit), Acapulco (Guerrera), Temascal and Tuxtepec (Oaxaca), Tierra Blanca (Veracruz), and Tampico (Tamaulipas).
The first four areas are on the Pacific Coast and include sites frequented by tourists (See Figure 1). The sites in Oaxaca and Veracruz are near a large inland dam. Most patients reported having eaten cebiche, a dish of raw freshwater fish, especially tilapia.
The most common finding was migrating areas of erythema with associated local edema which usually involved the extremities or the head. Lesions characteristic of creeping eruption were noted in one-third of the cases. Ocular migration of the parasite was noted in only one subject. Relapses occurred over several years.
Larvae obtained by excisional biopsy resembled those of Gnathostoma spinigerum when examined microscopically. Three-fourths of 60 patients in Culiacan and Temascal had antibody to Gnathostoma antigens, with those in the early stages of infection or those receiving corticosteroids together with albendazole being most likely to be seronegative.
COMMENT BY STAN DERESINSKI, MD, FACP
While gnathostomiasis is prevalent in many areas of Asia, it has also been identified in the Western Hemisphere.1 The first report of this parasitic infection in Mexico was published in 1970, six years after the introduction and cultivation of tilapia in dammed waters.
There are at least 12 species of Gnathostoma, four of which have caused human disease. Three of these, G. spinigerum, G. hispidum, and G. doloresi are widely distributed in Asia, while G. nipponicum may be limited to Japan.2 The incidence of creeping eruption due to gnathostomiasis has been increasing in Japan over the last two decades as the result of the popularity of dining on small live loaches (doju).
The most studied of the species associated with human disease is G. spinigerum, which is prevalent in Thailand and China as well as Indonesia, Japan and the Philippines, and has also been reported to be the agent of gnathostomiasis in Ecuador. The adult worm, which is rust-colored and 2-3 cm in length, lives in tumorous swellings in the intestinal wall of fish-eating mammals. Eggs produced by the adult erupt into the intestinal lumen, are passed in the feces, and, in an aquatic environment, produce motile larvae. The latter are ingested by the first intermediate host, Cyclops, a tiny crustacean, in which they molt twice to become early third-stage larvae. The larvae are in turn ingested by a second intermediate host, either a fish, reptile, or amphibian. In the host, further development to late third stage larvae takes place, making them infectious for the definitive host. Ingestion by the definitive host, which may be a cat, dog, or other mammal, restarts the cycle.
Ingestion of infected flesh, most commonly raw or inadequately cooked pork (14.9% of pigs examined in China in 1991 were infected with G. hispidum), poultry, or fish, by humans, however, leads to a dead end since the worms do not reach maturity in man.3 Penetration of the skin, prenatal transmission, and ingestion of water containing infested Cyclops are also theoretical modes of infection. The larvae, which are approximately 1 cm in length penetrate the wall of the stomach and then migrate to other tissues. The motility of the third stage larvae is achieved by contractile movements of its cephalic bulb.
Figure 1
Areas endemic for gnathostomiasis in Mexico
Reprinted with permission from Ogata K, et al. Short report: Gnathostomiasis in Mexico. Am J Trop Med Hyg 1998;58:316-318.
Nausea, vomiting, and diarrhea may develop within 24-48 hours of ingestion of a larvae.4 However, the presence of Gnathostoma infestation is most commonly recognized as a result of the migration of the nematode through the dermis, where it usually produces either transitory erythematous edematous swellings or typical larva migrans (creeping eruption). It is a potential cause of eosinophilic panniculitis.5 Cutaneous lesions may first develop weeks to years after ingestion and persist for one to two weeks; they may recur at irregular intervals for decades. The larva may instead migrate to more critical areas such as the eye, the lung, the genitourinary tract, and the central nervous system.6,7,8 In Thailand, the major causes of eosinophilic meningitis are infestation due to Angiostrongylus cantonensis, cystercosis, and gnathostomiasis. The gastrointestinal tract may also be a target of the migrating larvae; G. doloresi, mimicking intestinal anisakiasis, has caused an obstructing colonic mass requiring resection in a man who ate raw snake meat in Japan.9
Once the parasite begins its migration, eosinophilia is the rule. The value of serological studies is uncertain. The definitive diagnosis depends upon epidemiological history and clinical suspicion and can only be unequivocally made by demonstration of the parasite in tissue. In patients with typical migratory swelling, however, this is often not possible, since exploration is commonly unsuccessful, at least in part due to the fact that the approximately 1 cm long nematode larva migrates in the dermis at the rate of 1 cm/hr. The organism is more readily found, however, when the dermatological lesion is typical creeping eruption, a nodule or an abscess.
Figure 2
Life cycle of G. spinigerum
Reprinted with permission from Rusnak JM, Lucey DR. Clinical gnatho- stomiasis: Case report and review of the English language literature. Clin Infect Dis 1993;16:33-50.
The optimal therapy, if the organism can be located, is surgical excision; since humans are most often infected with only a single larva, cure may be achieved by extraction or excision. Treatment with albendazole may also have some activity.10 A recommended regimen is 400-800 mg daily for 21 days.11
References
1. Ollague W, et al. Human gnathostomiasis in Ecuador (nodular migratory eosinophilic panniculitis). First finding of the parasite in South America. Int J Dermatol 1984;23:647-561.
2. Nawa Y. Historical review and current status of gnathostomiasis in Asia. Southeast Asian J Trop Med Public Health 1991;22(Suppl):217-219.
3. Chen QQ, Lin XM. A survey of epidemiology of Gnathostoma hispidum and experimental studies of its larvae in animals. Southeast Asian J Trop Med Public Health 1991;22:611-617.
4. Rusnak JM, Lucey DR. Clinical gnathostomiasis: Case report and review of the English language literature. Clin Infect Dis 1993;16:33-50.
5. Adame J, Cohen PR. Eosinophilic panniculitis: Diagnostic considerations and evaluation. J Am Acad Dermatol 1996;34:229-234.
6. Biswas J, et al. Intraocular Gnathostoma spinigerum. Clinicopathologic study of two cases with review of literature. Retina 1994;14:384-344.
7. Charoeneratanakul S. Tropical infection and the lung. Monaldi Arch Chest Dis 1997;52:376-379.
8. Norcross WA, et al. Urinary gnathostomiasis in a Laotian refugee. J Am Fam Pract 1992;5:533-535.
9. Seguchi K, et al. A case report of colonic ileus due to eosinophilic nodular lesions caused by Gnathostoma doloresi infection. Am J Trop Med Hyg 1995;53: 263-266.
10. Kraivichian P, et al. Albendazole for the treatment of human gnathostomiasis. Trans R Soc Trop Med Hyg 1992;86:418-421.
11. Anon. Med Lett Drugs Ther 1995;37:99-107.
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