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 are found in wild carnivores; trichinellosis has also been found in horses, rats, beavers, opossums, walruses, whales, and meat-eating birds. Most mammals are susceptible. The number of human cases has declined in the past 50 years due in part to the move to modern production facilities (confinement) that reduces or eliminates exposure to rodents and other wildlife.
Etiology and Epidemiology
The genus Trichinella is currently considered a complex of nine species and three additional genotypes (T6, T8, and T9) of undetermined taxonomic status. Other than for the existence of two clades defined by the presence or absence of a collagen capsule (cyst) surrounding the parasite in the muscle, there are few distinct morphologic differences. Taxon identification is based on characteristics such as reproductive isolation, infectivity to certain hosts, resistance to freezing, geographic cruising range, PCR and DNA sequencing, and isoenzyme analysis. T spiralis (T1) is the most common and widely distributed of the encapsulated species affecting people and domestic animals in temperate regions; it has high infectivity for pigs and rodents, exhibits low resistance to freezing, and is broadly infective for most sylvatic hosts. The other cyst-forming species include T nativa (T2), found in arctic carnivores; T britovi (T3), found throughout the entire European continent, northwest Africa, and southwest Asia; T murrelli (T5), restricted to North America; T nelsoni (T7), found only in eastern Africa; and the most recently named T patagoniensis (T12), found in Argentina. There are three other encapsulated genotypes: Trichinella T6, which is very similar to T nativa and is found in carnivores of North America; T8, which shows similarities to T britovi and is present in carnivores of Africa; and T9, which has been identified only in sylvatic hosts from Japan but is genetically more similar to T murrelli of the USA. There are three additional species—T pseudospiralis (T4), T papuae (T10), and T zimbabwensis (T11), which constitute the nonencapsulated clade (lack a cyst in the muscle). T pseudospiralis has a cosmopolitan distribution and is the only species capable of infecting mammals and birds. T papuae was first identified in pigs from Papua New Guinea, but its presence is suspected to extend into Australasia and southeast Asia. T zimbabwensis is present in sub-Saharan Africa. Both T papuae and T zimbabwensis are capable of infecting crocodiles.
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) throughout 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 people, heavy infections may produce serious illness with three clinical phases (intestinal, muscle invasion, and convalescent) and occasionally death.
Although antemortem diagnosis in animals other than people 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 exclude 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.
Treatment is generally impractical in animals. The objective is to prevent ingestion by any animal, including people, 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 to prevent 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 145°F (63°C) for roasts or 160°F (71°C) for ground meats. 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 September 2013 by Bert E. Stromberg, PhD