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Trichinella spiralis
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Definition: Trichinella spiralis is a nematode parasite that is acquired by ingestion of larvae in undercooked meat from pigs that have themselves been infected by eating T. spiralis-infected rats or pork.
In the United States, the number of T. spiralis-infected pigs has been greatly reduced by laws requiring cooking of hog food, and this has reduced the number of reported human infections in the United States to about 100 each year. Still, trichinosis is widespread where undercooked pork is eaten.
In the human gut, T. spiralis larvae develop into adults that mate and release new larvae, which penetrate into the tissues. Larvae disseminate hematogenously and penetrate muscle cells, causing fever, myalgias, marked eosinophilia, and periorbital edema. Much less commonly, patients develop dyspnea (because of invasion of the diaphragm), encephalitis, and cardiac failure.
In striated skeletal muscle, T. spiralis larvae become intracellular parasites, increase dramatically in size, and modify the host muscle cell (referred to as the nurse cell) so that it loses its striations, gains a collagenous capsule, and develops a plexus of new blood vessels around itself.
The nurse cell-parasite complex is largely asymptomatic, and the worm may persist for years before it dies and calcifies. Antibodies to larval antigens, which include an immunodominant carbohydrate epitope called tyvelose, may reduce reinfection and are useful for serodiagnosis of the disease.
T. spiralis and other invasive nematodes stimulate a TH2 response, with production of IL-4, IL-5, IL-10, and IL-13. The cytokines produced by TH2 cells activate eosinophils and mast cells, both of which are associated with the inflammatory response to these parasites.
In animal models of T. spiralis infection, the TH2 response is associated with increased contractility of the intestine, which expels adult worms from the gut and subsequently reduces the number of larvae in the muscles.
The mechanism by which the TH2 response increases intestinal motility is unclear, although IL-4, IL-13, and mast cell degranulation have each been implicated.
While the TH2 response indirectly reduces the number of larvae in muscle by eliminating adults from the intestine, it is not clear whether the intramuscular inflammatory response, which is composed of mononuclear cells and eosinophils, is effective against the
During the invasive phase of trichinosis, cell destruction can be widespread but is rarely lethal. In the heart, there is a patchy interstitial myocarditis characterized by many eosinophils and scattered giant cells. The myocarditis can lead to scarring.
Larvae in the heart do not encyst and are difficult to identify, because they die and disappear. In the lungs, trapped larvae cause focal edema and hemorrhages, sometimes with an allergic eosinophilic infiltrate. In the CNS, larvae cause a diffuse lymphocytic and eosinophilic infiltrate, with focal gliosis in and about small capillaries of the brain.
T. spiralis preferentially encysts in striated skeletal muscles with the richest blood supply, including the diaphragm; the extraocular; and the laryngeal, deltoid, gastrocnemius, and intercostal muscles.
Coiled larvae are approximately 1 mm long and are surrounded by membrane-bound vacuoles within nurse cells, which in turn are surrounded by new blood vessels and an eosinophil-rich mononuclear cell infiltrate. This infiltrate is greatest around dying parasites, which eventually calcify and leave behind characteristic scars, which are useful for retrospective diagnosis of trichinosis.
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