eMedicine Specialties > Pediatrics: General Medicine > Parasitology
Gnathostomiasis
Updated: Jan 22, 2009
Introduction
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
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.
Frequency
United States
Human cases of gnathostomiasis acquired in the United States have not been reported 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, Laos, 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.
Clinical
History
In patients with gnathostomiasis, mild malaise, fever, urticaria, anorexia, nausea, vomiting, diarrhea, and epigastric pain may occur as the larvae migrate through the gastric and/or intestinal wall. Right upper quadrant pain may accompany the liver-migration phase of the illness. Further symptoms depend on the subsequent migration of the larvae.
- Skin and soft tissue - One or more areas involved with tenderness or swelling; creeping eruptions; pain, pruritus, and erythema; nodules or boils
- Pulmonary - Cough, chest pain, dyspnea, and/or hemoptysis; coughing up of worm
- GI - May mimic appendicitis, cholecystitis, or an intestinal mass lesion
- Genitourinary - Hematuria
- Ophthalmologic - Decreased visual acuity, blindness, pain, and/or photophobia
- Otologic - Decreased hearing and/or tinnitus
- CNS
- Radiculomyelitis (most common), radiculomyeloencephalitis, encephalitis, and/or meningitis may result. Condition may mimic or cause subarachnoid hemorrhage.
- Agonizing neuritic pain followed by paralysis or decreased sensorium over a few days is typical.
- Migration of focal neurologic symptoms and signs (eg, cranial nerve palsies, paralysis of an extremity, urinary retention) is typical. With eosinophilic meningitis caused by A cantonensis, CNS depression, low-grade fevers, headache, and nonfocal neurologic symptoms and signs (except for occasional cranial nerve VII or VIII involvement) are more typical.
Physical
Physical examination findings depend on the area of the body into which the larvae migrate. Single or multiple regions may be involved.
- Skin and soft tissue
- Panniculitis
- Intense, nonpitting edema
- Creeping eruptions
- Subcutaneous nodules or abscesses
- Pulmonary
- Lobar consolidation or collapse
- Pleural effusions
- Pneumothorax
- Hydropneumothorax
- GI
- Tender right upper quadrant, mid epigastrium, and/or right lower quadrant
- Right lower quadrant mass
- Ophthalmologic
- Uveitis
- Iritis
- Intraocular hemorrhage
- Increased intraocular pressure
- Retinal scarring/detachment
- CNS
- Fever, stiff neck, and/or photophobia
- Evidence of increased intracranial pressure
- Migratory focal neurologic findings
- Paralysis, cranial nerve involvement, and/or urinary retention
Causes
- Travel to or from an endemic area
- Southeast Asia, especially Thailand and Japan
- Latin America, especially Mexico and Ecuador
- Australia
- Asia and the Middle East
- Dietary/occupational exposure or ingestion
- Raw or undercooked freshwater fish (ceviche in Mexico and South America, sashimi in Japan, sum-fak in Thailand)
- Other raw or undercooked flesh
- Contaminated water
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| Treatment & Medication: Gnathostomiasis |
| Follow-up: Gnathostomiasis |
| References |
| Further Reading |
| Next Page » |
References
Fuller AJ, Munckhof W, Kiers L, et al. Eosinophilic meningitis due to Angiostrongylus cantonensis. West J Med. Jul 1993;159(1):78-80. [Medline].
Rusnak JM, Lucey DR. Clinical gnathostomiasis: case report and review of the English- language literature. Clin Infect Dis. Jan 1993;16(1):33-50. [Medline].
Kraivichian P, Kulkumthorn M, Yingyourd P, et al. Albendazole for the treatment of human gnathostomiasis. Trans R Soc Trop Med Hyg. Jul-Aug 1992;86(4):418-21. [Medline].
Bussaratid V, Desakorn V, Krudsood S, et al. Efficacy of ivermectin treatment of cutaneous gnathostomiasis evaluated by placebo-controlled trial. Southeast Asian J Trop Med Public Health. May 2006;37(3):433-40. [Medline].
Bhattacharjee H, Das D, Medhi J. Intravitreal gnathostomiasis and review of literature. Retina. Jan 2007;27(1):67-73. [Medline].
Bunnag T. Gnathostomiasis. In: Strickland GT, ed. Hunter's Tropical Medicine. 1991:764-7.
Bunyaratavej K, Pongpunlert W, Jongwutiwes S, Likitnukul S. Spinal gnathostomiasis resembling an intrinsic cord tumor/myelitis in a 4-year-old boy. Southeast Asian J Trop Med Public Health. Sep 2008;39(5):800-3. [Medline].
Cameron ML, Durack DT. Helminthic infections. In: Scheld WM, Whitley RJ, Durack DT, eds. Infections of the Central Nervous System. Lippincott Williams & Wilkins; 1997:845-78.
Chai JY, Han ET, Shin EH, et al. An outbreak of gnathostomiasis among Korean emigrants in Myanmar. Am J Trop Med Hyg. Jul 2003;69(1):67-73. [Medline]. [Full Text].
Chandenier J, Husson J, Canaple S, et al. Medullary gnathostomiasis in a white patient: use of immunodiagnosis and magnetic resonance imaging. Clin Infect Dis. Jun 1 2001;32(11):E154-7. [Medline].
Despommier DD. Tissue nematodes. In: Long SS, Pickering LK, Prober CG, eds. Principles and Practice of Pediatric Infectious Diseases. Churchill Livingstone; 2003:1340-7.
Elzi L, Decker M, Battegay M, et al. Chest pain after travel to the tropics. Lancet. Apr 10 2004;363(9416):1198. [Medline].
Fox LM. Ivermectin: uses and impact 20 years on. Curr Opin Infect Dis. Dec 2006;19(6):588-93. [Medline].
Germann R, Schachtele M, Nessler G, et al. Cerebral gnathostomiasis as a cause of an extended intracranial bleeding. Klin Padiatr. Jul-Aug 2003;215(4):223-5. [Medline].
Gillespie SH. Cutaneous Larva Migrans. Curr Infect Dis Rep. Feb 2004;6(1):50-53. [Medline].
Gutierrez Y. Other tissue nematode infections. In: Guerrant RL, Walker DH, Weller PF, eds. Tropical Infectious Diseases: Principles, Pathogens, & Practice. Churchill Livingstone; 1999:933-48.
High WA, Bravo FG. Emerging diseases in tropical dermatology. Adv Dermatol. 2007;23:335-50. [Medline].
Intapan PM, Morakote N, Chansung K, Maleewong W. Hypereosinophilia and abdominopulmonary gnathostomiasis. Southeast Asian J Trop Med Public Health. Sep 2008;39(5):804-7. [Medline].
Kraivichian K, Nuchprayoon S, Sitichalernchai P, et al. Treatment of cutaneous gnathostomiasis with ivermectin. Am J Trop Med Hyg. Nov 2004;71(5):623-8. [Medline]. [Full Text].
Laummaunwai P, Sawanyawisuth K, Intapan PM, Chotmongkol V, Wongkham C, Maleewong W. Evaluation of human IgG class and subclass antibodies to a 24 kDa antigenic component of Gnathostoma spinigerum for the serodiagnosis of gnathostomiasis. Parasitol Res. Aug 2007;101(3):703-8. [Medline].
Ligon BL. Gnathostomiasis: A review of a previously localized zoonosis now crossing numerous geographical boundaries. Semin Pediatr Infect Dis. Apr 2005;16(2):137-43. [Medline].
Magana M, Messina M, Bustamante F, Cazarin J. Gnathostomiasis: clinicopathologic study. Am J Dermatopathol. Apr 2004;26(2):91-5. [Medline].
Michaels MG. Eosinophilic meningitis. In: Long SS, Pickering LK, Prober CG, eds. Principles and Practice of Pediatric Infectious Diseases. Churchill Livingstone; 2003:312-5.
Moore DA, McCroddan J, Dekumyoy P, Chiodini PL. Gnathostomiasis: an emerging imported disease. Emerg Infect Dis. Jun 2003;9(6):647-50. [Medline].
Nawa Y, Hatz C, Blum J. Sushi delights and parasites: the risk of fishborne and foodborne parasitic zoonoses in Asia. Clin Infect Dis. Nov 1 2005;41(9):1297-303. [Medline].
Parola P, Bordmann G, Brouqui P, Delmont J. Eosinophilic pleural effusion in gnathostomiasis. Emerg Infect Dis. Sep 2004;10(9):1690-91. [Medline].
Pearson RD, Weller PF, Guerrant RL. Chemotherapy of parasitic diseases. In: Guerrant RL, Walker DH, Weller PF, eds. Tropical Infectious Diseases: Principles, Pathogens, & Practice. Churchill Livingstone; 1999:215-37.
Preechawat P, Wongwatthana P, Poonyathalang A, Chusattayanond A. Orbital apex syndrome from gnathostomiasis. J Neuroophthalmol. Sep 2006;26(3):184-6. [Medline].
Robertson J, Shilkofski N. Drug doses. In: The Harriet Lane Handbook: A Manual for Pediatric House Officers. Philadelphia, PA: Mosby; 2005:679-1009.
Rojas-Molina N, Pedraza-Sanchez S, Torres-Bibiano B, et al. Gnathostomosis, an emerging foodborne zoonotic disease in Acapulco, Mexico. Emerg Infect Dis. Mar-Apr 1999;5(2):264-6. [Medline].
Sawanyawisuth K, Chlebicki MP, Pratt E, Kanpittaya J, Intapan PM. Sequential imaging studies of cerebral gnathostomiasis with subdural hemorrhage as its complication. Trans R Soc Trop Med Hyg. Jan 2009;103(1):102-4. [Medline].
Sithinamsuwan P, Chairangsaris P. Images in clinical medicine. Gnathostomiasis - neuroimaging of larval migration. N Engl J Med. Jul 14 2005;353(2):188. [Medline].
Stechenberg BW. Eosinophilic meningitis. In: Feigin RD, Cherry JD, Fletcher J, eds. Textbook of Pediatric Infectious Diseases. WB Saunders; 2004:494-6.
Weller PF. Eosinophilic meningitis. Am J Med. Sep 1993;95(3):250-3. [Medline].
Wilson CM, Freedman DO. Antiparasitic agents. In: Long SS, Pickering LK, Prober CG, eds. Principles and Practice of Pediatric Infectious Diseases. Churchill Livingstone; 2003:1547-58.
Wilson ME, Chen LH. Dermatologic Infectious Diseases in International Travelers. Curr Infect Dis Rep. Feb 2004;6(1):54-62. [Medline].
Keywords
gnathostomiasis, CNS infection, chokofishi, consular disease, encephalitis, eosinophilia, eosinophilic meningitis, eosinophilic myeloencephalitis, Gnathostoma binucleatum, G binucleatum, G doloresi, G hispidum, G nipponicum, G procyonis, G spinigerum, hematuria, hydropneumothorax, intraocular hemorrhage, iritis, meningitis, nodular (migratory) eosinophilic panniculitis, panniculitis, parasitic infection, photophobia, pleural effusions, pneumothorax, radiculomyelitis, radiculomyeloencephalitis, Shanghai rheumatism, Tau-cheed, tinnitus, urticaria, uveitis, Woodbury bug, Yangtze River edema
