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Trichinellosis is a parasitic disease of public health importance caused by the nematode Trichinella spiralis. Human infections are established by consumption of insufficiently cooked infected meat, usually pork or bear, although other species have been implicated. Natural infections occur in wild carnivores; trichinellosis has also been found in horses, rats, beavers, opossums, walruses, whales, and meat-eating birds. Most mammals are susceptible.
Etiology and Epidemiology
Trichinella spp are considered to be a complex of 8 species, with 11 genotypes (T1 to T11) that have been identified by DNA analysis. There are few distinct morphologic differences, and species identification is based on characteristics such as reproductive isolation, infectivity to certain hosts, and resistance to freezing. T spiralis (T1) is the most common species affecting humans and domestic animals in most temperate regions; it has high infectivity for pigs and rodents, low resistance to freezing, and forms muscle cysts. The other cyst-forming species include T nativa (T2), found in arctic carnivores; T britova (T3), found primarily in southern Europe; T murrelli (T5), restricted to North America; T nelsoni (T7), restricted to eastern Africa; and 3 other T nelsoni genotypes: T6 (carnivores of North America), T8 (carnivores of Africa), and T9 (Japanese wildlife). There are 3 additional species—T pseudospiralis (T4), T papuae (T10), and T zimbabwensis (T11)—all of which lack the cyst in muscle.
Infection generally occurs by ingestion of larvae encysted in muscle. The cyst wall is digested in the stomach, and the liberated larvae penetrate into the duodenal and jejunal mucosa. Within ~4 days, the larvae develop into sexually mature adults. After mating, the females (3–4 mm) penetrate deeper into the mucosa and discharge living larvae (up to 1,500) over 4–16 wk. After reproduction, the adult worms die and usually are digested. The young larvae (0.1 mm) migrate into the lymphatics, are carried via the portal system to the peripheral circulation, and reach striated muscle where they penetrate individual muscle cells. They grow rapidly (to 1 mm) and begin to coil within the cell, usually 1 per cell. Capsule formation begins ~15 days after infection and is completed by 4–8 wk, at which time the larvae are infective. The cell degenerates as the larva grows, and then calcification occurs (at different rates in various hosts). Larvae may remain viable in the cysts for years, and their development continues only if ingested by another suitable host. The diaphragm, tongue, masseter, and intercostal muscles are among those most heavily involved in pigs.
If larvae pass through the intestine and are eliminated in the feces before maturation, they are infective to other animals.
Clinical Findings and Diagnosis
Most infections in domestic and wild animals go undiagnosed. In humans, heavy infections may produce serious illness with 3 clinical phases (intestinal, muscle invasion, and convalescent) and occasionally death.
Although antemortem diagnosis in animals other than humans is rare, trichinellosis may be suspected if there is a history of eating rodents, wildlife carcasses, or raw, infected meat. Microscopic examination of a muscle biopsy sample (usually tongue) may confirm but not necessarily rule out trichinellosis. ELISA is a reliable test to detect anti-Trichinella antibodies. Seroconversion may not occur for weeks after infection, although as little as 0.01 larvae per gram of meat can be detected.
Control
Treatment is generally impractical in animals. The objective is to prevent ingestion by any animal, including humans, of viable Trichinella cysts in muscle (trichinae). In pigs, this may be accomplished with good management that includes controlling rodents, cooking garbage (fed to the pigs) for 30 min at 212°F (100°C), and preventing cannibalism (ie, tail biting) and access to wildlife carcasses.
Inspection of meat for viable trichinae at the time of slaughter (by trichinoscopic or digestion methods) is effective in preventing human infection in many countries. In North America, the assumption is that pork may be infected; therefore, those products that appear as “ready to eat” must be processed by adequate heating, freezing, or curing to kill trichinae before marketing. Other pork should be cooked to assure that all tissue is heated to an internal temperature of ≥137°F (58°C). Freezing pork at an appropriate temperature for an appropriate time is also effective (5°F [−15°C] for 20 days, −9.4°F [−23°C] for 10 days, or −22°F [−30°C] for 6 days). Freezing cannot be relied on to kill trichinae in meat other than pork.
Last full review/revision March 2012 by Bert E. Stromberg, PhD
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