Gnathostoma spinigerum Owen, 1836
ETYMOLOGY:Gnathos = jaw and stoma = mouth, along with spinigerum representing the rings of spines on the anterior end of the parasite.
SYNONYMS: Cheiracanthus robustus Diesing, 1838, Cheiracanthus socialis Leidy, 1859, Filaria radula Schneider, 1866, Cheiracanthussiamensis Levinson, 1889, Gnathostomaparonai Porta, 1908, Gnathostomaspinigerum Mitter, 1912.
HISTORY: This worm was described by Owen (1836) from the stomach of a tiger in the London Zoo. It was first reported as a parasite of the domestic cat by Gedoelst (1911). Chandler (1925) reported finding Gnathostomaspinigerum in 10% to 30% of cats in India. It has since been reported from cats and other felines.
GEOGRAPHIC LOCATION: This parasite has been encountered mainly in Asia, including reports from from India (Sur and Biswas, 1988), Laos (Scholtz and Ditich, 1990), Malaysia (Rohde, 1962), Japan (Miyazaki, 1960), and Thailand (Daengsvan, 1980). The parasite has been found on several occasions in cats in Australia (Barton and McEwan, 1993; Beveridge et al., 1978; Trueman and Ferris, 1977). This worm has also bee n found in the Phillippines (Refuerzo and Garcia, 1938). It has also been reported from cats in Egypt (Arafa et al., 1978). A cat experimentally infected with fish containing larvae developed a patent infection with worms that were identified as Gnathostomaspinigerum (Wenceslao-Ollague et al., 1988).
LOCATION IN HOST: The adult worms live in the stomach. The anterior end of the worm is embedded into the mucosa of the stomach and there may be a large cyst up to 2.5 c in diameter that contains worms and a canal leading to the stomach lumen.
PARASITE IDENTIFICATION: The adult worms are large, stout, and characterized by having a large inflation or head bulb on the anterior end. The head bulb and the anterior of the body are covered with spines. Adult females are 1 to 3 cm long and the adult males are about 1 to 2.5 cm long. The vulva of the female is one-third to one half of the body length from the posterior of the worm. The eggs are 60 to 70 µm long and 35 to 40 µm wide, contain a several-celled embryo or morula stage when passed in the feces, have a rather thick brownish shell that is thickened on one end by a clear inflation that resembles the plug in the egg of Trichuris spp.
LIFE CYCLE: In the life cycle of Gnathostomaspinigerum and the other species of this genus, two different intermediate hosts are required for larval development to be completed. When the eggs passed in the feces enter fresh water, they undergo development and ultimately produce a sheathed second-stage larva. At 25ºC to 31ºC, the second-stage larva will hatch spontaneously from the egg about 9 days after development has begun. The first intermediate host is a small fresh-water crustacean, a cyclopoid copepod (Prommas and Daengsvan, 1933). The genera of copepods involved include Cyclops, Eucyclops, Mesocyclops, and Thermocyclops. After the free-swimming larva is ingested by the copepod, it sheds its sheath, penetrates the intestinal wall, and enters the body cavity of the crustacean. It takes about a week at 29ºC to 31ºC for the larva to then develop to the third stage within the copepod; this third-stage larva is about one-half mm long and has a head bulb with spines similar to the head-bulb present on the adult worms. These larvae are not infective to the final host, but require passage through a second intermediate host. The larvae of Gnathostomaspinigerum then enter the fish which ingest the copepod hosts (Prommas and Daengsvang, 1936 and 1937). The larvae first undergo a migration through the liver of the fish, and after about one week, they become encapsulated within the muscles and grow to lenghts of 3 to 4 mm. A wide variety of animals other than fish, e.g., frogs, toads, snakes, chickens, rodents, and primates, can serve as the second intermediate host after ingesting an infected copepod and will have larvae present in muscles and other viscera (Daengsvang et al., 1966). Paratenic hosts are an important part of the life cycle, and it has been found that the advanced third-stage larvae from one host can be transferred by feeding to a second host (Daengsvang, 1971). Cats and dogs become infected by eating fish or paratenic hosts that contain third-stage larvae. The larvae pentrate the stomach and enter the liver. From the liver, the larvae while growing migrate about in the muscles and connective tissue before they returen to the stomach where they mature in the tumors in the stomach wall (Ueki, 1956). The prepatent period after the ingestion of the third-stage larvae is somewhere between 100 to 225 days (Prommas and Daengsvang, 1937; Miyazaki, 1960).
Although it may not be important in the regular biology of this parasite, Daengsvang et al. (1970) also showed that the advanced third-stage larvae recovered from the snake-headed fish, Ophiocephalusstriatus, are capable of infecting cats by skin penetration if the free-larvae are placed on the skin. The penetration of the skin takes about 5 minutes to over an hour. Once the larvae have penetrated the skin, they move into the nearby muscle tissue and were later found in the liver, diaphragm, abdominal tissues,and chest wall. Ultimately, eggs were found in the feces of cats infected by the percutaneous application of these larvae 2 to 7½ months later.
CLINICAL PRESENTATION AND PATHOGENESIS: Trueman et al. (1977) describe clinical signs in three cats that were found to have gnathostomiasis. One cat died after an illness of three weeks, one stray cat was emaciated, and another stray cat was apparently normal. All three cats were necropsied, and it was found that the cat that died had died from a perforated stomach wall. The emaciated cat had a small serosal perforation on a gastric lesion, and the cat that appeared normal had a well-developed gastric lesion but no perforation of the wall. Histological examination of the lesions revealed a marked proliferation of fibrous tissues, foci of inflammatory cells, necrotic tracts, and a submucosal cavity in which the adult worms were found.
TREATMENT: Daengsvang et al. (1971) found that disophenol [2,6-diiodo-4-nitrophenol], “Ancylol” or “DNP,” was effective in removing adult Gnathostomaspinigerum from the stomachs of infected cats. All adult worms in the gastric tumors were killed by around three days after the subcutaneous administration of the drug. These authors found that larvae present in the liver, diaphragm, and skeletal muscle were not killed at the dosage level tested. To examine the potential for eliminating the larval stages, Daengsvang (1980) infected 10 cats with 50 to 99 third-stage larvae that were recovered from mice. Eight of the cats were then treated, and two cats served as untreated controls. Each cat received 12 doses of the compound at ten-day intervals. Two cats received 0.05 ml per pound, two cats received 0.04 ml per pound, two cats received 0.03 ml per pound, and two cats received 0.02 ml per pound. Necropsies were performed 19 to 24 days after the last dose. There were no worms found in the cats receiving the highest dose, one cat given 0.04 ml per pound had two larvae, and one cat given 0.03 ml per pound had one larvae. Both cats treated with 0.02 ml per pound had worms, one had an immature adult and nine larvae, the other cat had six larvae. The two control cats were necropsied 180 days after infection and had 8 immature adults and 8 larvae.
EPIZOOTIOLOGY: Cats acquire their infections with Gnathostomaspinigerum by the ingestion of infected prey. The initial larval stage requires development in fresh-water copepods, thus, the parasite is present around fresh water. In these situations it will be very difficult to prevent cats from hunting for prey that might be infected due to the wide rage of hosts that are potentially infected.
HAZARDS TO OTHER ANIMALS: The eggs passed in the feces of cats are not infectious unless first ingested by copepods. Thus, with proper disposal of feces, this parasite should not pose a threat to other animals. However, an infected cat on the premises where a pond is present may produce water that tcontains infected copepods capable of infecting other animals.
HAZARD TO HUMANS: There have been a number of human cases of gnathostomiasis. The occur from the ingestion of raw or undercooked fish or other animals containing the larval stages. On occasion, infections have proven fatal (Chitanondh and Rosen, 1967). In humans, the larvae migrate through the stomach wall and this is followed with epigastric pain and possibly peritonitis. Ther larvae migrate through the liver and peritoneum. Very typically in humans there is a cutneous involvement where the larvae migrate about under the skin. On occasion the larvae also may enter the nervous system causing life-threatening illness.
CONTROL/PREVENTION: Control is preventing cats from hunting in areas where the parasite is found. The wide range of intermediate and paratenic hosts make it more difficult to prevent infection in cats.
Arafa MS, Nasr NT, Khalifa R, Mahdi AH, Mahmoud WS, Khalil MS. 1978. Cats as reservoir hosts of Toxocara and other parasites potentially transmissible to man in Egypt. Acta Parasitol Polonica 25:383-392.
Barton MA, McEwan DR. 1993. Spirurid nematodes in dogs and cats from central Australia. Aust Vet J 70: 270.
Beveridge I, President PJA, Arundel JH. 1978. Gnathostomaspinigerum infection in a feral cat from New Sourth Wales. Aust Vet J 54:46.
Chitanondh H, Rosen L. Fatal eosinophilic encephalomyelitis caused by the nematode Gnathostoma spinigerum. Am J Trop Med Hyg 16:638-645.
Daengsvang S. 1971. Infectivity of Gnathostomaspinigerum larvae in primates. J Parasitol 57:476-478.
Daengsvang S. 1980a. A monograph on the genus Gnathostoma and gnathostomiasis in Thailand. 87 pages.
Daengsvang S. 1980b. Chemotherapy of feline Gnathostomaspinigerum migrating stage with multiple subcutaneous doses of Ancylol. SE Asian J Trop Med Pub Hlth 11:359-362.
Daengsvang S, Sermwatsri B, Youngyi P, Guname D. 1971. A preliminary study of chemotherapy of Gnathostomaspinigerum infections in cats with Ancylol, disophenol (2,6-diido-4-nitrophenol). SE Asian J Trop Med Pub Hlth 2:359-361.
Daegsvang S, Thienprasitthi P, Chomcherngpat P. 1966. Further investigations on natural and experimental hosts of larvae of Gnathostomaspinigerum in Thailand. Am J Trop Med Hyg 15:727-729.
Heydon GM. 1929. Creeping eruption or larva migrans in North Queensland and a note on the worm Gnathostomaspinigerum (Owen). Med J Austral 1:583-591.
Miyazaki I. 1960. On the genus Gnathostoma and human gnathostomiasis, with special reference to Japan. Exp Parasitol 9:338-370.
Prommas C, Daengsvang S. 1933. Preliminary report of a study on the life cycle of Gnathostomaspinigerum. J Parasitol 19:287-292.
Prommas C, Daengsvang S. 1936. Further report of a study on the life cycle of Gnathostomaspinigerum. J Parasitol 22:180-186.
Prommas C, Daengsvang S. 1937. Feeding experiments on cats with Gnathostomaspinigerum larvae obtained from the second intermediate host. J Parasitol 23:115-116.
Refuerzo PG, Garcia EY. 1938. The crustacean intermediate hosts of Gnathostomaspinigerum in the Philippines and its pre- and intrcrustacian development. Phil J Anim Indust 5:351-362.
Rohde K. 1962. Helminthen aus Katzen un Hunden in Malaya; Bemerkungen zu ihrer epideiologischen Bedeutung für den Menschen. Ztsch Parasitenk 22:237-244.
Scholtz T, Ditrich O. 1990. Scanning electron microscopy of the cuticular armature of the nematode Gnathostomaspinigerum Owen, 1836 from cats in Laos. J Helminthol 64:255-262.
Sur SK, Biswas G. 1988. Cat - a source of human parasitic infection. Ind J Publ Hlth 32:211.
Trueman KF, Ferris PBC. 1977. Gnathostomiasis in three cats. Austral Vet J 53:498-499.
Ueki T. 1957. Experimental studies on the third-sttage larva of Gnathostomaspinigerum. Egaku Kenkyu Fukuoka 27:1162-1196.
Wenceslao-Ollague L., Eduardo-Gomez L, Manuel Briones I. 1988. Infeccion experimental de un gato domestico adulto con el tercer estado larvaio de Gnathostomaspinigerum procedente de un pez de agua dulce. Medicina Cutanea Ibero-Latino-Americana 16:295-297.