Gnathostomiasis Acquired by British Tourists in Botswana

Joanna S. Herman; Emma C. Wall; Christoffer van Tulleken; Peter Godfrey-Faussett; Robin L. Bailey; Peter L. Chiodini

Disclosures

Emerging Infectious Diseases. 2009;15(4):594-597. 

In This Article

Conclusions

Our patients received a diagnosis of typical cutaneous gnathostomiasis, but their lack of travel to a region in which the disease was known to be endemic was perplexing. The only previous reports of this infection from Africa were in 3 persons who ate raw catfish from the Rufiji River in Tanzania (1994) and in 2 travelers who ate raw bream from the Zambezi River in Zambia (1998).[1] Before these reports, all reported cases of gnathostomiasis had been acquired in Southeast Asia and Central and South America.

Gnathostomiasis is a nematode infection caused by the late third-stage larva (L3) of the helminth Gnathostoma spp. A foodborne zoonosis, it is endemic where people eat raw or undercooked fish that harbor the infectious L3. At least 4 species are known to cause human disease, the most common being G. spinigerum. Adult nematodes live in the stomach of definitive fish-eating hosts (commonly cats and dogs).When feces containing eggs are deposited in water, free-swimming first- and then second-stage larvae develop.[2,8] Ingested by the first intermediate host (a copepod), they develop into early L3 forms. Second intermediate hosts (freshwater fish such as bream, catfish, snake-headed fish, sleeper perch, Nile tilapia, butterfish, or eel; frogs; snakes; chickens; snails; or pigs) ingest the copepods, liberating the larvae, which encyst in muscle and mature into L3 forms. When infected fish are eaten by a definitive host, the larvae mature into adults in ~6 months (see life cycle of G. spinigerum, adapted from an illustration by Sylvia Paz Diaz Camacho, available from www.dpd.cdc.gov/dpdx/HTML/gnathostomiasis.htm). Humans are accidental hosts in which the parasite fails to reach sexual maturity.

Two alternative routes of human infection have been suggested: ingestion of water that contains infected copepods or direct skin penetration of food handlers through L3-infected meat.[2,8] Symptoms in humans occur as the larva migrates through tissues, causing cutaneous and/or visceral larva migrans, which may begin within 24-48 hours after ingestion of infected meat. Initial nonspecific symptoms include fever, malaise, nausea, vomiting, diarrhea, and epigastric pain lasting 2-3 weeks and usually accompanied by a marked eosinophilia. Within 1 month, the cutaneous form may develop, with characteristic nonpitting edematous migratory swellings that may be painful, pruritic, or erythematous and may last 1-2 weeks. The swellings are typically due to 1 larva, occasionally due to 2 or more.[8] Spontaneous larval extrusion, such as occurred in 1 of our patients, has been recorded.

Visceral gnathostomiasis occurs when the larvae migrate through the internal organs such as the lungs, gut, genitourinary tract, eye, ear, and central nervous system. This form causes more illness and deaths, with mortality rates reported at 8%-25%, than the cutaneous form.[9,10] Pathogenicity is thought to result from direct mechanical injury by the larvae and by their release of secretions and excretions, which contain various compounds that cause tissue damage.[9] The result is characteristic hemorrhagic tracts that may be seen at autopsy. Untreated, infected persons may have intermittent symptoms until the larvae die, after ~12 years.

Diagnosis is suggested by eosinophilia, migratory lesions, and a history of geographic and food exposure. An immunoblot detecting 24-kDa-L3-specific antigen is considered diagnostic of Gnathostoma sp. and is the most widely used serologic test because of its high sensitivity and specificity.[11;P. Dekumyoy,pers. comm] Some laboratories use an ELISA for immunoglobulin G subclasses as a screening test.[12] In our first patient, the larva was identified based on its morphologic features, including the number and size of cephalic hooks and the character and extent of spines on its body (Figure 2).[2,13]

Figure 2.

Third-stage larva of Gnathostoma spinigerum, which was expressed from the face of a male British tourist who had visited Botswana. Photograph shows entire larva (A) and larva head with hooks (B).

For many years, treatment with various drugs was unsuccessful, and surgical excision of the larvae was the only effective management. Studies in the 1990s confirmed the efficacy of a 21-day course of albendazole, 400 mg 2x/d,[14,15] and ivermectin, 0.2 mg/kg immediately or for 2 consecutive days.[15]

The area for risk of acquiring gnathostomiasis is expanding, and travelers and physicians need to be aware of this risk. Eradication of the organism is unlikely given its complicated life cycle, but local campaigns and appropriate pretravel advice can raise awareness and change people's eating habits. Travelers must realize that culinary adventures on exotic holidays can result in acquiring unwanted parasites that may have devastating consequences.

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