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Anisakiasis is a zoonosis caused by nematodes (roundworms) belonging to the Anisakidae family. Various species of these roundworms like Anisakis simplex (herring worm), Pseudoterranova (Phocanema, Terranova) decipiens (cod or seal worm), Contracaecum spp., and Hysterothylacium (Thynnascaris) spp. have been implicated in human infections and all are acquired by eating raw or undercooked fish or squid. Adult worms live embeded in the stomach mucosa of marine mammals (whales, dolphins, porpoises, seals, sealions, walruses, etc.). Adult females produce unembrionated eggs which pass in the feces into the sea. In the water, the eggs embryonate , and larvae develop into first and second stage larvae. These hatch from the eggs and are free-swimming in the water where crustaceans (like krill) ingest them. In the tissues of crustaceans they molt to third stage larvae. When an infected crustacean is eaten by a fish or squid, they acquire the third stage larva which penetrate through the intestine to the tissues in the peritoneal cavity and then migrate to the muscle tissues. Through predation, the larvae are transferred from fish to fish. Finally, when fish or squid containing third-stage larvae are ingested by marine mammals, the larvae molt twice and develop into adult worms. The adult females produce eggs that are shed by the marine mammals and the life cycle starts again. Humans are accidental hosts that become infected by eating raw or undercooked infected marine fish or squid that contain the third stage larvae. These larvae may enter the tissue of the gastrointestinal tract and then can cause different problems associated with gastric and abdominal infections; occasionally the worm can migrate to another viscera. Symtoms can start as early as 50 minutes after ingestion when the patient complains of feeling a tingling, tickling throat and coughs up or manually extracts a nematode. Depending on what part of the gastrointestinal tract is involved, the disease can be classified as follows: LUMINAL FORM The larvae that cause luminal anisakiasis are incapable of penetrating the mucosal surface of the digestive tract, and are accompanied by a tingling, tickling throat until the patient actually coughs up or can otherwise extract a nematode. Symptoms occur 50 minutes to two weeks after consumption, and usually only one nematode is recovered. GASTRIC FORM This form is usually caused by the Anisakis species, and symptoms mimic gastritis or an ulcer, accompanied by nausea, vomiting, and abdominal pain. Symptoms first occur 12 hours after consumption of the larvae. INTESTINAL FORM is characterized by the burrowing of the larval nematodes into the wall of the intestines, possibly even burrowing through to the cavity, causing intraperitoneal anisakiasis (see below). Any portion of the intestines may be invaded, but the terminal ileum is the most common site. The larvae produce a substance that recruits eosinophils to the site, causing the formation of a granuloma around the worm in the tissue. Penetrated worms that die in the tissues are eventually removed by the host's phagocytic cells. When they do not burrow into the intestinal wall, larvae can remain in the intestinal lumen. Anisakids rarely reach full maturity in humans and usually are eliminated spontaneously from the digestive tract lumen within 3 weeks of infection. In severe cases, the larvae may completely penetrate the intestinal wall and migrate to the liver, gallbladder, lymph nodes, and mesenteries of the host. Often, symptoms mimic gastric cancer, appendicitis, pancreatic cancer, or peritonitis. The prognosis of this form of anisakiasis is the worst. Additionally , it has been observed that persons previously sensitized to anisakid larvae can develop an allergic reaction within the next 72 hours of ingesting parasitized fish. Symptoms vary and they can present wheals, urticaria, angioneurotic edema, diarrhea, vomiting or asthma reactions. Some patients can present severe allergic reactions (anaphylaxis) that can lead to death. In these cases symptoms are not caused by a migrating worm, instead it is the immune system of the allergic and sensitized patient that is hyperreactive. In cases where the patient vomits or coughs up the worm, the disease may be diagnosed by morphological examination of the nematode. Other cases may require a fiber optic device that allows the attending physician to examine the inside of the stomach and the first part of the small intestine. These devices are equipped with a mechanical forceps that can be used to remove the worm. Other cases are diagnosed upon finding a granulomatous lesion with a worm on laparotomy. A specific radioallergosorbent test has been developed for anasakiasis, but is not yet commercially marketed Treatment of gastrointestinal anisakiasis involves removal of the worm. Acute cases are extremely painful and require surgical intervention. Physical removal of the nematode(s) from the lesion is the only known method of reducing the pain and eliminating the cause (other than waiting for the worms to die). The symptoms apparently persist after the worm dies since some lesions are found upon surgical removal that contain only nematode remnants. Stenosis (a narrowing and stiffening) of the pyloric sphincter was reported in a case in which exploratory laparotomy had revealed a worm that was not removed. Recently it has been reported that administering albendazole during at least 2 weeks can eliminate anisakid larvae in patients presenting chronic symptoms. (Moore DA, Girdwood RW, Chiodini PL.Treatment of anisakiasis with albendazole. Lancet. 2002 Jul 6;360(9326):54 ) Allergic reactions are treated following standard procedures for this type of complication. Suggested reading: http://www.dpd.cdc. gov/dpdx/HTML/Anisakiasis.htm http://www.cdfound.to.it/html /ani1.htm http://europa .eu.int/comm/food/fs/sc/scv/out05_en.html http://www.conganat. org/iicongreso/comunic/052/ http://www.redalergia.com.ar/profesionales/contenidos/bibliodi/trab ajos/ani sakisguiadeact.htm http://www.hrs.sas.junta- andalucia.es/NOTICIAS/alergia_anisakis.htm
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