Anisakiasis is caused by several related larval nematodes, especially
those of the genera Anisakis, Phoconema, and Contracaecum, that
are ingested when eating raw or insufficiently cooked marine fish,
as in sushi or sashimi.1 Adult nematodes are found
mainly in the gastrointestinal tract of cetaceans (dolphins, porpoises, and
whales), and nematode eggs shed in the feces of these definitive hosts
are ingested by small crustaceans, where they develop into third-stage
larvae.2 Fish and cephalopod mollusks become infected
by eating crustaceans infected by larval forms, which invade the
tissues of the fish. Definitive hosts and humans usually become
infected by eating fish containing these larval stages. Most cases
are associated with mackerel, but other fish, such as cod, whiting,
haddock, herring, and salmon, may be infected.
There has been a dramatic increase in the incidence of anisakiasis
since 1980, probably due to a (1) improvement in endoscopic procedures needed
to make the definitive diagnosis; (2) increasing global demand for
seafood and a growing preference for raw or lightly cooked food, especially
in Western countries; and (3) the impact of regulatory controls
on harvesting of marine mammals, leading to increased populations of
potential definitive hosts. Human infection is most common in Japan,
where consumption of raw fish is common and approximately 2000 anisakiasis
cases are reported annually (accounting for 90% of all
reported cases worldwide). However, incidence is also increasing
in the United States (with about 50 annual cases) and in Europe
(with about 500 annual cases).
Clinical Manifestations, Diagnosis,
Several clinical manifestations are seen depending on whether
the worm localizes in the stomach or small intestine.3 In
the former, acute gastritis with severe epigastric pain, nausea,
and vomiting may occur, often within the first 12 hours of ingestion. More
severe symptoms with fever, chills, and urticaria may develop with
repeated exposure because of Arthus-type allergic reactions. The relationship
between anisakiasis and strong allergic reactions, ranging from
isolated swellings to urticaria and life-threatening anaphylaxis,
has become clearer in recent years. Most cases of allergic manifestations
have been reported from Spain, where cases reported have demonstrated
elevated IgE responses against A simplex. There
is also speculation that initial sensitization may occur from exposure
to dead parasites, as well as after exposure to live parasitic larvae.
Intestinal anisakiasis may not become symptomatic until up to
a week after initial infection. Usually, the worms are regurgitated
or expelled by coughing or defecating, which terminates the episode.
Invasion of the gastric or intestinal wall may be associated with
a severe eosinophilic granulomatous reaction that may become chronic,
causing gastric or right lower quadrant pain, eosinophilia, and
fecal occult blood. Occasionally, the stomach or intestine may be
perforated by the invading worm, causing an acute surgical abdomen.
Gastric anisakiasis is often misdiagnosed as peptic ulcer, and intestinal
infection may mimic appendicitis or peritonitis.
Diagnosis can be difficult. Serodiagnosis generally is not available, ...