The classical agent is T. Spiralis (found worldwide in many carnivorous and omnivorous animals, both domestic and sylvatic), but there are also seven primarily sylvatic species of Trichinella now recognized:
- T. Spiralis is most adapted to swine, most pathogenic in humans and is cosmopolitan in distribution.
- T. Britovi is the second most common species to infect humans; it is distributed throughout Europe, Asia, and northern and western Africa, usually in wild carnivores, wild boar and domesticated pigs.
- T. Murrelli also infects humans, especially from black bear meat; it is distributed among wild carnivores in North America.
- T. Nativa, which has a high resistance to freezing, is found in the Arctic and subarctic regions; reservoir hosts include polar bears, Arctic foxes, walruses and other wild game.
- T. Nelsoni, found in east African predators and scavengers, has been documented to cause a few human cases.
- T. Papuae infects both mammals and reptiles, including crocodiles, humans, wild pigs and domestic pigs; this species, found in Papua New Guinea and Thailand, is also nonencapsulated.
- T. Pseudospiralis infects birds and mammals, and has demonstrated infection in humans; it is a nonencapsulated species.
- T. Zimbabwensis can infect mammals, and possibly humans; this nonencapsulated species was detected in crocodiles in Africa.
- Taxonomy => Kingdom: Animalia
- Phylum: Nematoda
- Class: Adenophorea
- Order: Trichurida
- Family: Trichinellidae
- Genus: Trichinell.
The typical life cycle for T. Spiralis involves humans, pigs, and rodents. A pig becomes infected when it eats infectious cysts in raw meat, often porcine carrion or a rat (sylvatic cycle). A human becomes infected by consuming raw or undercooked infected pork (domestic cycle). In the stomach, the cysts from infected undercooked meat are acted on by pepsin and hydrochloric acid, which help release the larvae from the cysts into the stomach. The larvae then migrate to the small intestine, and burrow into the intestinal mucosa, where they molt four times before becoming adults.
Thirty to 34 hours after the cysts were originally ingested, the adults mate, and within five days produce larvae. Adult worms can only reproduce for a limited time, because the immune system will eventually expel them from the small intestine. The larvae then use their piercing mouthpart, called the "stylet", to pass through the intestinal mucosa and enter the lymphatic vessels, and then enter the bloodstream.
The larvae travel by capillaries to various organs, such as the retina, myocardium, or lymph nodes; however, only larvae that migrate to skeletal muscle cells survive and encyst. The larval host cell becomes a nurse cell, in which the larva will be encapsulated, potentially for the life of the host. The development of a capillary network around the nurse cell completes encystation of the larva. Trichinosis is not soil-transmitted, as the parasite does not lay eggs, nor can it survive long outside a host.
Diagnosis of trichinosis is confirmed by a combination of exposure history, clinical diagnosis, and laboratory testing.
Exposure history => An epidemiological investigation can be done to determine a patient's exposure to raw infected meat. Often, an infection arises from home-preparation of contaminated meat, in which case microscopy of the meat may be used to determine the infection. Exposure determination does not have to be directly from a laboratory-confirmed infected animal. Indirect exposure criteria include the consumption of products from a laboratory-confirmed infected animal, or sharing of a common exposure with a laboratory-confirmed infected human.
Clinical diagnosis => Clinical presentation of the common trichinosis symptoms may also suggest infection. These symptoms include eye puffiness, splinter hemorrhage, nonspecific gastroenteritis, and muscle pain. The case definition for trichinosis at the European Center for Disease Control states "at least three of the following six: fever, muscle soreness and pain, gastrointestinal symptoms, facial edema, eosinophilia, and subconjuctival, subungual, and retinal hemorrhages. ".
Laboratory testing => Blood tests and microscopy can be used to aid in the diagnosis of trichinosis. Blood tests include a complete blood count for eosinophilia, creatine phosphokinase activity, and various immunoassays such as ELISA for larval antigens.
The great majority of trichinosis infections have either minor or no symptoms and no complications. There are two main phases for the infection: enteral (affecting the intestines) and parenteral (outside the intestines). The symptoms vary depending on the phase, species of Trichinella, quantity of encysted larvae ingested, age, sex, and host immunity.
Enteral phase => A large burden of adult worms in the intestines promotes symptoms such as nausea, heartburn, dyspepsia, and diarrhea from two to seven days after infection, while small worm burdens generally are asymptomatic. Eosinophilia presents early and increases rapidly.
Parenteral phase => The severity of symptoms caused by larval migration from the intestines depends on the number of larvae produced. As the larvae migrate through tissue and vessels, the body's inflammatory response results in edema, muscle pain, fever, and weakness. A classic sign of trichinosis is periorbital edema, swelling around the eyes, which may be caused by vasculitis. Splinter hemorrhage in the nails is also a common symptom.
They may very rarely cause enough damage to produce serious neurological deficits (such as ataxia or respiratory paralysis) from worms entering the central nervous system. The CNS is compromised by trichinosis in 10–24% of reported cases of cerebral venous sinus thrombosis, a very rare form of stroke (3 – 4 cases per million annual incidence in adults). Trichinosis can be fatal depending on the severity of the infection; death can occur 4–6 weeks after the infection, and is usually caused by myocarditis, encephalitis, or pneumonia.