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Epidemiology and Pathology

The adult Anisakis spp. inhabits the stomachs of sea mammals, such as small whales, dolphins and seals, and passes eggs with feces into the oceans. Larvae hatch and are ingested by tiny crustaceans, which become infected and are in turn eaten by fish and squid. The larvae mature in the viscera and muscles of the fish until reaching an infective stage. The infected fish are then eaten by marine mammals to complete the life cycle. Humans are accidental hosts and larvae do not multiply or develop into adult worms in humans. The larval stage is found in a wide variety of fish, of which herring, cod and the Alaskan pollack are the most significant for human infection because they are the most frequently eaten raw. However, larvae are also found in haddock, mackerel, pike, bonita, squid, cuttlefish, Pacific red snapper and salmon. Pseudoterranova decipiens has a similar life cycle, with seals and cod being the usual hosts for this parasite, which can also infect humans.

Human infections are all due to ingestion of the larvae, which are thread-like, 1.5 to 2.5 cm long and 1 mm in diameter. Following ingestion, larvae may migrate retrograde up the esophagus where they may cause tingling in the throat, inducing coughing and expectoration. Larvae can also pass through the gastrointestinal tract and be excreted in the feces. However, in most infections the larvae will attach to the mucosa of the stomach (Fig. 11.1) or small bowel, which are the most common sites of infection, although lesions have rarely been found in the colon and rectum. Macroscopically, a larva may occasionally be recognized with its anterior end embedded in the mucosa (Fig. 11.2). If the immature worms become invasive, they may penetrate the gastric or intestinal mucosa and cause a localized intramural inflammatory mass (an eosinophilic phlegmon), or they may occasionally migrate to such sites as the omentum, mesentery, pancreas, liver and lung. Penetration of the wall of the ileum can occasionally occur, with resulting peritoneal irritation and fluid.

Fig. 11.1 Scanning electron micrograph of an Anisakis larva penetrating the gastric mucosa in vitro. (Reprinted with permission from J Parasitol 76:626, 1990 and from D.H. Connor and F.W. Chandler (eds): Pathology of Infectious Diseases, 1997).


Fig. 11.2 (A) Endoscopic view of a live Anisakis, the head of which is still attached to the gastric mucosa (arrow) of a Japanese patient. (B) The worm is being withdrawn from the stomach by forceps. (Courtesy of Dr. Yoshihiro Hiramatsu, Tokyo, Japan).

The pathogenesis of anisakiasis is governed by the immunological reaction of the host to metabolic products secreted or excreted by the worms and to larval antigens as the parasite degenerates. The infected region of gut feels edematous, and is indurated, congested and covered by a fibrinous exudate. The regional lymph nodes are enlarged and feel rubbery. The gastric mucosa is covered with small petechial hemorrhages and ulcers and is indurated where the parasite has penetrated; the folds are swollen, granular and reddened.

Histologically there is submucosal necrosis, often containing sections of the parasite, and a marked eosinophilic reaction in the tissue around the site of perforation, far more than would be expected if it were due merely to the burrowing of the parasite. This suggests that the local lesion is probably a specific reaction to the parasite occurring in a presensitized host. There is edema in the tissue surrounding the larva, especially in the submucosa, and a massive cellular reaction, particularly eosinophilic, but also containing neutrophils and lymphocytes and often acidophilic and amorphous material (Splendore-Hoeppli substance). The inflammatory and eosinophilic reaction is more marked in intestinal than in gastric anisakiasis. In the more chronic infections, the reaction becomes granulomatous with some eosinophils present.

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