Infectious diseases Internal Medicine

Anisakiasis (Herring Worm Disease)

Anisakiasis
Anisakiasis - Parasitic Worm

Introduction – Anisakiasis

Anisakiasis is a nematode infectious disease that can be caused by, among other species, Anisakis simplex (herring worm) and Pseudoterranova decipiens (cod worm). These species are roundworms in the order Ascaridida, and in the Anisakidae family.

Species belonging to the Anisakidae family are found all over the world. Most descriptions come from cultures where it is common to eat raw fish dishes, such as in some parts of Asia and South America. Anisakiasis is also uncommon in these regions. In the United States, fewer than 10 cases are diagnosed per year. The Netherlands and Spain have had some cases in the past, which have, however, decreased in number in recent years in parallel with the tightening of fish handling recommendations in these countries.

Cod worm infection, human pseudoterranovosis, has been described in Chile, Japan and Korea, but is very rare. It is not required to report Anisakiasis cases under the Infection Protection Act.

The life cycle of the worms

The worm has a complex life cycle. The adult worm lives in marine mammals, in water seals, whose feces contain eggs. In the eggs, larvae are found that mature to the next stage, L2. The eggs hatch and L2 larvae swim freely. They are eaten by crustaceans in which they develop into L3 larvae. The crustaceans are eaten by fish (many different species) which in turn are eaten by marine mammals where the L3 larvae develop into adult worms that lay eggs in the mammal’s intestine. This completes the life cycle of the worm.

Sometimes humans can enter the place of the mammal; L3 larvae can then develop into a fourth stage, L4, but thereafter the larvae cannot develop into adult worms. Therefore, in those cases, the infected human being becomes the final station in the worm’s life cycle.

In adult mammals, the adult worm looks like a flush worm. The size of the larvae varies depending on the host, but the L3 larvae are usually about 3 cm long. A. simplex is about 0.5 mm thick, P. decipiens about 1 mm thick.


Symptoms and Clinical Findings

Most of the Anisakidae infections probably go unnoticed, or, if symptoms persist, remain undiagnosed and self-resolve.

If the worm (A. simplex or P. decipiens) is consumed alive in larval stage L3, severe abdominal pain in the epigastric region, as well as nausea and vomiting may debut a few hours after ingestion. Ingestion of one or two worms is sufficient for symptoms to develop. The larvae, which hook into the lining of the stomach, can at this stage be seen by gastroscopy.

Sometimes the larvae can be regurgitated and crawl over from the esophagus to the trachea, causing coughing or giving rise to a crawling/tickling sensation in the rear pharynx as they move there.

A. simplex is the more pathogenic of the two species. It can pass further down the gut and after one to two weeks cause eosinophilic granulomatous disease similar to Crohn’s disease. Acute abdomen, small bowel obstruction, and perforation have been described due to the infection. A. simplex can also leave the gut and cause abscesses in the abdominal cavity and its parenchymatous organs.

Acute allergic manifestations, such as urticaria and anaphylaxis, have been described in A. simplex infection – even in the absence of abdominal symptoms. Chronic events also occur. Dead larvae can also cause acute hypersensitivity reactions with fever and eosinophilia as a result. Worm allergic reactions with respiratory symptoms and dermatitis in fish cleaners have been reported.

Infection with P. decipiens (cod worm infection, human pseudoterranovosis) can give rise to the same clinical picture as described above for A. simplex . There are two cases of invasive pseudoterranovosis described in the United States. One was a 44-year-old man with ALS. The larva penetrated the esophagus and emerged from an ulceration in the throat. The second case was involved the finding of a larva in an iliac aneurysm in a 76-year-old man.

In a case from Japan, it was found that what was believed to be a liver tumor turned out to be granuloma caused by P. decipiens.


Diagnostics – Anisakiasis

Diagnosis is usually made by coughing or spitting out the worm. Sometimes, the infection is detected by gastroscopy. Suspicion of anisakiasis has at some times been raised after pathological CT angiogram findings. Serological methods are available. Feces microscopy has no place in diagnostics.


Treatment – Anisakiasis

Man is the end station for Anisakidae; The larvae cannot survive in a human host. Symptomatic treatment, including removal by gastroscopy, is sufficient in most cases.

Surgery may be necessary in bowel obstruction due to A. simplex infection. Treatment with albendazole PO 400 mg x 2 in the wide range of 3 to 21 days (!) has been recommended – may be an option.


Prophylaxis

Fish that have been adequately cooked are risk-free with respect to living larvae. The larvae die when heated to 70 degrees or frozen for two days. When salting herring, the worm dies after one month at 22-24% salinity. The worm dies in hot-smoked fish, but not in cold smoked. All sushi fish must have been frozen before eating it.


Further Reading