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, and wild 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: Trichinella

Lifecycle
The typical lifecycle 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 eventually expels them from the small intestine.
Treatment-resistant and hospitalized patients may be treated concomitantly with an MAO-inhibitor, if they are closely monitored and if the initial dose of the MAO-Inhibitor is low.Increased drug actions:

Other antidepressants, barbiturates, narcotics, sedating antihistamines, anticonvulsive drugs, alcohol - resulting in increased central depression
Anticholinergics (antiparkinsonian agents, TCAs and TeCAs) - resulting in increased anticholinergic action (dry mouth, constipation etc.) Sympathomimetics (also those used in local anesthetics like noradrenaline) : sympathomimetic effects increased (increased blood pressure, pulse rate, paleness of skin etc.) Nitrates and antihypertensives (e.g. beta-blockers) - increased antihypertensive action with pronounced fall in blood pressureDecreased drug actions:

Guanethidine, Reserpine, Guanfacine : antihypertensive effects decreased
Clonidine : antihypertensive effects decreased and risk of (massive) rebound hypertension.Other types of interaction:

Drugs, which induce certain enzymes in the liver, e.g. barbiturates, phenytoin, carbamazepine and oral anticonceptive drugs, enhance the elimination of maprotiline and decrease its antidepressant effects. Additionally the blood-concentrations of phenytoin or carbamazepine may be increased, leading to a higher incidents of side effects. The concomitant use of maprotiline and neuroleptics can lead to increased maprotiline blood-levels and to seizures. Combining maprotiline and thioridazine could induce severe arrhythmias. Additionally, increased blood-levels of Maprotiline are possible, if certain beta-blocking agents (e.g. Propranolol) are given concomitantly. Maprotiline may amplify the actions of coumarin-type anticoagulants (e.g. warfarin, phenprocoumon). The plasma-prothrombin-activity must be assessed closely in order to avoid overt bleedings. Maprotiline can increase the actions of oral antidiabetic drugs (sulfonylureas) and Insulin. Diabetic patients should have regular assessments of their blood-glucose-levels.