Pathogenesis

T. spiralis is an obligate intracellular parasite in both its larval (striated skeletal muscle cell) and adult (cytoplasm of a row of enterocytes in the small intestine) niches. In both settings, it induces a series of changes through its secreted proteins, which alter the host, allowing the infection to proceed (Capo and Despommier, 1996). Encysted Trichinella larvae ingested in raw or inadequately cooked meat products are released after gastric digestion of the cyst wall. The larvae then invade the columnar epithelium in the mucosa of the small bowel. Within 48 hours, female worms molt four times to the adult stage and are fertilized. Larval deposition begins within 5-6 days. Each female worm is capable

Fig. 19b.2 Press preparation of striated muscle demonstrating numerous encysted larvae of Trichinella spiralis

of producing up to 1500 larvae during its lifetime. Larviposition generally continues for approximately 5 weeks before a combination of immune responses forces the expulsion of the adults from the small intestine (Despommier, 1986). Newborn larvae penetrate the mucosa to enter the capillaries and lymphatics of the small intestine, from which they are distributed systemically. Immature larvae that reach striated muscle will enter and induce the myocyte to differentiate into a 'nurse-cell' unit, which subsequently contributes to and supports the process of encystation or encapsulation (Figure 19b.2). These cystic structures may begin to calcify as early as 6 months following the initial infection. However, larvae may remain viable within cysts for several years. If infection occurs in wild game or animals destined for slaughter, the cycle may be reinitiated when a human eats the infected meat. Larvae that reach non-striated muscles or other tissues do not encyst. These larvae continue to migrate within the tissues, which results in marked inflammation and local tissue necrosis. Although this process is usually self-limited, severe multi-organ disease and chronic sequelae may develop.

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