Gnathostomiasis 

  • Author: Robert W Tolan Jr, MD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Jan 9, 2012
 

Background

Gnathostomiasis is a rare infection that most often results from ingestion of the third-stage larvae of the nematode Gnathostoma spinigerum, although several other species also cause human disease. The larvae may be found in raw or undercooked meat (eg, freshwater fish, chicken, snails, frogs, pigs) or in contaminated water. Rarely, larvae penetrate the skin of individuals who are exposed to contaminated meat or water.

Any organ system can be involved, but the most common manifestation of infection is localized, intermittent, migratory swelling in the skin and subcutaneous tissues. Such swelling may be painful, pruritic, and/or erythematous. Angiostrongylus cantonensis and Gnathostoma species are common causes of parasitic eosinophilic meningitis, which results from their random migration into the CNS.[1] Infection is typically associated with peripheral eosinophilia, in which the eosinophils may exceed 50% of the circulating WBCs. The classic triad of infection is intermittent migratory swelling, eosinophilia, and travel to endemic areas (mainly Southeast Asia).[2]

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Pathophysiology

Definitive hosts for Gnathostoma species include dogs, cats, tigers, leopards, lions, mink, opossums, raccoons, and otters, in which the adult worms live in a tumor in the gastric wall. Eggs leave an aperture in the tumor that opens on the stomach lumen and pass into water in the feces. After approximately one week, the eggs develop into larvae, which hatch and are then ingested by the first intermediate host, minute crustaceans of the genus Cyclops. Larvae penetrate the gastric wall of the copepods, migrate through the body cavity, and mature into second-stage and early third-stage larval forms. The copepods are ingested by the second intermediate hosts or definitive hosts (eg, fish, frogs, snakes, chicken, pigs), in which they again penetrate the gastric wall, migrate into muscles, and mature into advanced third-stage larvae before encysting.

When flesh from these hosts is eaten, the larvae excyst in the stomach, penetrate the gastric wall, migrate through the liver, and travel to the connective tissue and muscles. After 4 weeks, they return to the gastric wall to form the tumor, where they mature into adults in 6-8 months. At 8-12 months after initial ingestion, the worms mate, and eggs begin to pass into the feces of the host.

Humans become infected when they ingest third-stage larvae in raw or undercooked meat of the definitive host or when they drink, work in, or bathe in water contaminated with larvae or infested copepods. Cases of probable prenatal transmission in humans have occurred as well. In humans, the larvae do not return to the stomach wall, but rather, they migrate randomly throughout the body for as long as 10-12 years. For this reason, eggs are rarely, if ever, found in human feces.

Within 24-48 hours of ingestion, larvae invade the gastric and/or intestinal wall, resulting in eosinophilia and local symptoms. They migrate to and through the liver. Their migration through the body begins 3-4 weeks to several years after ingestion. Typically, episodes last 1-2 weeks. Over time, episodes are often less frequent, less intense, and shorter. Disease is thought to result from mechanical damage to tissues caused by gnathostome migration; gnathostome production and/or the action of toxins that resemble those of acetylcholine, hyaluronidase, protease, and hemolysin; and the host's response to the infestation.

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Epidemiology

Frequency

United States

A single, unconfirmed, human case of gnathostomiasis acquired in the United States has been reported[3] and it remains rare in individuals who are exposed abroad.

International

Gnathostomiasis is an uncommon disease, even in endemic areas of Southeast Asia (including Japan, Korea,[4] Laos,[5] Malaysia, Taiwan, and Thailand) and Latin America (mainly Mexico and Ecuador), although its incidence appears to be increasing, possibly because of changing dietary habits. It is most common in Thailand and Japan. In Thailand, it is the most common parasitic infection of the CNS. In Thailand, 6% of subarachnoid hemorrhages in adults and 18% of those in infants and children are due to gnathostomiasis.

Mortality/Morbidity

Gnathostomiasis can persist 10-12 years and may cause significant morbidity because of its propensity to involve any part of the body. Random invasion of the CNS, which is the major cause of mortality, may lead to death in 8-25% of patients or long-term sequelae in 30% of patients with CNS involvement.

Race

No predilection has been reported.

Sex

No predilection has been reported, except in cases in which occupational or dietary exposure is related to gender roles.

Age

No predilection has been reported, except in cases affected by factors related to occupational or dietary exposure.

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Proceed to Clinical Presentation
 
 
Contributor Information and Disclosures
Author

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Specialty Editor Board

Glenn Fennelly, MD, MPH  Director, Division of Infectious Diseases, Lewis M Fraad Department of Pediatrics, Jacobi Medical Center; Clinical Associate Professor of Pediatrics, Albert Einstein College of Medicine

Glenn Fennelly, MD, MPH is a member of the following medical societies: Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Martin Weisse, MD  Program Director, Associate Professor, Department of Pediatrics, West Virginia University

Martin Weisse, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Daniel Rauch, MD, FAAP  Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine

Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine

Disclosure: Baxter Honoraria Consulting

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

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