Trichinella sp infections are caused by roundworms (nematodes) in mammals, including humans, as well as birds and some reptile species. Most mammals, including omnivores and carnivores, can be affected. In humans, these parasites cause trichinellosis, a parasitic disease of public health importance. Infections in humans result from the consumption of insufficiently cooked infected meat or meat-derived products, usually pork from domestic or wild swine, as well as bear, horse, or walrus meat. Occasionally meat or meat products from other species have been implicated.
Naturally infected animals do not show any clinical signs of disease, except in rare instances, even though they can reportedly harbor 1,000 parasite larvae per gram of muscle tissue. There is no treatment for trichinellosis in animals, and Trichinella sp infections are only detected by means of post-mortem laboratory testing of muscle tissue samples; several specific tests are available. The number of human cases has greatly declined in the past 50 years in part because of the move to modern production facilities (reduced confinement) that decreases or eliminates exposure of domestic pigs to wild rodents and other wildlife.
The genus Trichinella is currently considered a complex of nine species and four additional genotypes (T6, T8, T9, and T13) of undetermined taxonomic status. Other than the existence of two clades defined by the presence or absence of a collagen capsule (cyst) surrounding parasite larvae in infected muscles, there are no morphologic differences. Each taxon can be identified by means of PCR assay and DNA sequencing performed on larvae collected from muscles samples from infected animals or humans.
T spiralis (T1) is the most common and widely distributed of the encapsulated species affecting humans 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 (wildlife). The other cyst-forming species include:
T nativa (T2), found in arctic and subarctic carnivores, in which larvae can survive freezing for up to 5 years
T britovi (T3), found mainly in carnivores and more rarely in domestic and wild swine throughout the entire European continent, northwest Africa, and southwest Asia
T murrelli (T5), restricted to carnivores of temperate regions of North America
T nelsoni (T7), found in carnivores and less commonly in wild swine in eastern and southern Africa
T patagoniensis (T12), found in carnivores of South America
There are four other encapsulated genotypes: Trichinella T6, which is very similar to T nativa and is found in carnivores of arctic and subarctic regions of North America; T8, which shows similarities to T britovi and is present in carnivores of southern Africa; T9, which has been identified only in carnivores of Japan; and T13, which has been recently discovered in carnivores of northwestern Canada.
There are three additional species—T pseudospiralis (T4), T papuae (T10), and T zimbabwensis (T11)—which constitute the nonencapsulated clade (ie, lacking a cyst in the infected muscle). T pseudospiralis has a cosmopolitan distribution and is the only species capable of infecting both mammals and birds. T papuae circulates among mammals (eg, wild pigs) and reptiles (saltwater crocodiles and soft-shelled turtles) of Australasia and southeast Asia. T zimbabwensis infects carnivorous mammals (eg, lions, leopards, spotted hyenas), Nile crocodiles, and Nile monitor lizards in sub-Saharan Africa.
Infection occurs by means of ingestion of larvae that parasitize striated muscle cells. The cyst wall is digested in the stomach, and the free larvae penetrate 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 weeks. 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 into 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 one per cell.
In encapsulated taxa, capsule formation begins ~15 days after infection and is completed by 4–8 weeks, at which time the larvae are infective. Infected cells degenerate as the larva grows, followed by calcification which occurs at different rates in various hosts. Larvae may remain viable within 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 frequently infected in pigs.
Most Trichinella sp infections in domestic and wild animals are undiagnosed. In people, heavy infections may produce serious illness with three clinical phases (intestinal, muscle invasion, and convalescent) and occasionally death.
Microscopic examination of a muscle biopsy sample (usually from the diaphragm) may confirm but not necessarily exclude Trichinella sp infection. ELISA testing using excretory-secretory (ES) antigens is a reliable means to detect anti-Trichinella antibodies in pigs; however, this test is useful for epidemiologic surveillance only because of long detection windows and cross-reactions with other pathogens. Seroconversion may not occur for weeks after infection, although as few as 0.01 larvae per gram of tissue can be detected. In addition, anti-Trichinella antibodies may no longer be detectable even in animals that still harbor infective larvae.
The gold-standard diagnostic test to detect Trichinella infection in animals is the artificial digestion of muscle tissue samples with an HCl-pepsin solution. This test does not include any control and requires specifically trained personnel. The use of ELISA testing with using ES antigens is the most widely used diagnostic means to detect Trichinella infections in humans with seroconversion occurring 2–3 weeks after infection. However, in people infected by few larvae, seroconversion can occur after 5–6 weeks, when complete recovery has occurred. There is generally no treatment for animals. Infected people are treated with albendazole or mebendazole and corticosteroids. Because anthelmintics are poorly absorbed by the intestinal lumen, they generally do not reach the larvae encysted in muscle cells. In general, the later treatment is prescribed the higher the probability infected people will harbor viable larvae for years.
Treatment of Trichinella sp infections is generally impractical in animals. The objective is to prevent ingestion and thus infection by any animal or human of viable Trichinella larvae. In pigs, this may be accomplished with good management that includes controlling rodents, cooking garbage (fed to the pigs) for 30 minutes at 212°F (100°C), and preventing cannibalism (ie, tail biting) and access to wildlife carcasses. Trichinella sp infection has reportedly never been detected in pigs reared under controlled housing conditions.
Inspection of meat for viable trichinae at the time of slaughter (by means of digestion methods) is effective to prevent human infection in many countries. In the EU, all Trichinella-susceptible animals intended for human consumption must be tested for these parasites by artificial digestion testing unless pigs are from controlled housing conditions. In North America, the assumption is that pork may be infected; therefore, those products labeled “ready to eat” must be processed by adequate heating, freezing, or curing to kill larvae before marketing. Other pork products 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 larvae in meat other than pork. For example, T nativa larvae can survive in the frozen muscle of bears for up to 5 years.
Wild carnivorous and omnivorous mammals serve as the major reservoir hosts of Trichinella sp parasites.
High-risk farming practices include intentional feeding of food waste, which may contain pork scraps, or unintentional exposure to carcasses of dead swine or infected wildlife via unsecured, free-range pasturing.
Naturally infected animals do not show any clinical signs of infection except in rare instances. There is no treatment.
Serology (ELISA) testing can be used to monitor the infection in pig herds but will not detect all infected animals.