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In 1909 Dr. Robert Leiper, helminthologist to the London School of Tropical Medicine, wrote: "The natives of Siam are occasionally affected by subcutaneous tumors that have been found to be due to the presence of a small nematode worm, named by Levinsen (1889) Cheiracanthus siamensis" and he went on to give a detailed description of the worm, reclassifying it as Gnathostoma siamense. The first human case had been described by Levinsen in 1889, but in 1836 Richard Owen had discovered and described Gnathostoma spinigerum in the stomach of a young tiger that had died after rupture of its aorta in the London zoo. It was not until 1934 that the next series of human cases was reported and since then the literature has grown and so have the number of freshwater animals known to be naturally infected. Perhaps the most intriguing aspect of this introductory story is the question of how a young tiger in the zoo in London could become infected with a worm normally found in fish, cats, and dogs in Southeast Asia. Unfortunately, we may never be able to solve that problem.


Gnathostomiasis. Creeping eruption. Larva migrans. Yangtze edema. Choko-Fuschu Tua chid. Wandering swelling. Visceral larva migrans results when there is migration of nematode larvae through visceral tissues.


Gnathostomiasis is infection by the nematode Gnathostoma spinigerum, and rarely by G. hispidum. Larva migrans can be from Toxocara canis or cati, Ascaris lumbricoides, or other nematodes (WHO).

Geographic Distribution

Human gnathostomiasis is endemic in Southeast Asia (Thailand, Malaysia, Vietnam) and Japan and China. It has been reported from India, the Philippines, and Israel. There are many different species of the genus Gnathostoma found in animals in North and South America, Africa, and Arabia, but so far no human infection has been reported from them.

Epidemiology and Life Cycle

The life cycle of G. spinigerum includes two freshwater hosts: Cyclops and the freshwater fishes which normally feed on these infected crustacea. Man becomes infected by eating raw, poorly cooked, or marinated fish and meat. Because man is not part of the normal life cycle, the parasite fails to mature and migrates through the tissues for as long as 12 years. The common animal hosts are the dog and cat, and the worms have also been recovered from domestic pigs, chickens, fish-eating birds, snakes, frogs, eels, and, as was originally described, tigers and leopards.

Ingestion by a dog or cat of infected fish or meat results in the liberation of the parasite in the stomach; from there it migrates through the wall into the peritoneal cavity, and then through the liver into the skeletal muscle and connective tissues. The cycle is completed when, about 3 months later, the parasite reenters the stomach and buries itself in the gastric mucosa. After another 6 months it reaches maturity and is 2 to 3-cm in length. Histologically in man, while the larva are moving, the tissue damage appears to be mainly mechanical. There are edema, small hemorrhages, and a moderate cellular reaction. However, once the parasite is stationary, there is an intense inflammatory response, with many eosinophils. The periphery is walled off by granulomatous and fibrous tissue. Because this reaction may occur anywhere in the body the clinical results may be variable. If the reaction occurs within the central nervous system, for example, the resulting symptomatology can be bizarre. Within the stomach the gastric mucosa is heaped up around the worm and results in a firm mucosal swelling.

Laboratory Diagnosis

Cross-reactions with other nematodes make serological diagnosis unreliable: recovery of the worm (there is usually and fortunately only one worm per human patient) is the accurate way to make the diagnosis. Other causes of cutaneous larva migrans have to be differentiated, e.g., paragonimiasis, sparganosis, toxocariasis, and the swelling caused by maggots (the tumbu fly) or the sand flea (jiggers: Tunga penetrans). None of the above are as mobile and active as Gnathostoma.

Clinical Characteristics

Symptoms develop within 24 to 48 hours after eating infected fish or meat (and poorly cooked chicken must be remembered as a significant source of infection). There will be nausea, salivation, vomiting, flushing, pruritus, urticaria, and upper abdominal pain. At this stage there is a marked eosinophilia, which may reach 90%. As the larvae escape from the stomach, their movement within the abdomen or chest, or later in the muscles, may cause brief but sharp pain. Symptoms have suggested cholecystitis, appendicitis, cystitis, and salpingitis. When the worm is in the lung there may be blood-streaked sputum or a pneumothorax. Three or four weeks after ingestion the worm is in the subcutaneous tissues and its migration can be observed. It moves at the rate of 1-cm per hour or even more rapidly when subcutaneous. For example, movement from one arm across the chest and down the other arm has been recorded overnight. Attempts to remove the worm surgically are often unsuccessful because of the rate at which it can move. Progress can be prevented in certain anatomical sites, such as the wrists, by the use of tourniquets. The worm seldom migrates deeply once it has reached the subcutaneous tissue. At this stage the systemic symptoms decrease, the eosinophilia is less marked, and the illness becomes chronic. Intermittent subcutaneous swellings appear, single or multiple, depending on the number of larvae migrating. They may last as long as 10 days and recur every 2 to 6 weeks, but gradually the episodes subside and the intervals are increased.

When the larva enters specific organs, the clinical symptoms depend entirely on the situation. For example, it may penetrate the eye, and damage to every part of the orbit and its contents has been described. It rarely enters the central nervous system but when it does it may cause meningitis, encephalitis, or, in the peripheral nerve, neuritis. In the lungs, there are focal necrosis and acute inflammation resulting in localized consolidation, hemorrhage, and often atelectasis resembling infarction. There may be a pleural effusion or pneumothorax if the worm penetrates the pleura. The symptomatology can arise from any organ or system. Toothache, uterine bleeding, hematuria, excess salivation, drowsiness, facial paralysis, severe nerve root pain, transverse myelitis (the CSF will be bloody or xanthochromic, with increased pressure), and abdominal masses have all been reported. Appendicitis, cystitis, peptic ulcer, and cholecystitis have all been mistakenly suspected.

Imaging Diagnosis

The radiological findings are as nonspecific as the clinical symptoms. The mucosal mass within the gastric wall resembles a neoplasm or edematous ulcer of the stomach. The bowel is not usually involved, but intra-abdominal masses may form and be indistinguishable from ovarian cysts or any other intra-abdominal tumor.

The radiological changes in the chest have been described as resembling tuberculosis (particularly when there has been hemoptysis). Localized but changeable pulmonary consolidation has also been recorded, with areas of segmental atelectasis. A pneumothorax seldom occurs without evidence of lung edema, but otherwise there are no distinguishing characteristics. The finding of numerous eosinophils in the sputum (as well as in the blood) may be a better indication of the etiology than the chest radiograph!

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Copyright: Palmer and Reeder