Introduction The genus Trichinella has undergone revision, due to the advent of reliable DNA probes that can be used to distinguish the various species that have been recently described.1, 2 There are 8 recognized genotypes (two are provisional).3 Members of the genus Trichinella are able to infect a broad spectrum of mammalian hosts, making them one of the world’s most widely-distributed group of nematode infections. Trichinella spp. are genetically related to Trichuris trichiura and Capillaria spp; all belong to the family Trichurata. These roundworms constitute an unusual group of organisms in the phylum Nematoda, in that they all live a part of their lives as intracellular parasites. |
The diseases that Trichinella spp. cause are collectively referred to as trichinellosis. Currently, prevalence of trichinellosis is low within the United States, occurring mostly as scattered outbreaks,4 and the majority of human cases are due to Trichinella spiralis and T. murrelli. The domestic pig is the main reservoir host for T. spiralis. This species is significantly higher in prevalence in people living in certain parts of Europe, Asia, and Southeast Asia than in the United States. It is now considered endemic in Japan and China. A large outbreak of trichinellosis occurred in Lebanon in 1997, infecting over 200 people.5 Trichinella spiralis infection in humans has been reported from Korea for the first time.6 In contrast, trichinella infections in wildlife within the United States are now thought to be largely due to the T5 strain, tentatively designated T. murrelli.7
Life Cycle
Infection is initiated by ingesting raw or undercooked meats harboring the Nurse cell-larva complex (Fig. 21.1). Larvae are released from muscle tissue by digestive enzymes in the stomach, and then locate to the upper two-thirds of the small intestine. The outermost cuticular layer (epicuticle) becomes partially digested.17,18 This enables the parasite to receive environmental cues19 and to then select an infection site within the small intestine. The immature parasites penetrate the columnar epithelium at the base of the villus. They live within a row of these cells, and are considered intra-multi-cellular organisms (Figs. 21.2, 21.7).20 | | |

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Larvae molt four times in rapid succession over a 30-hour period, developing into adults. The female measures 3 mm in length by 36 µm in diameter (Fig. 21.3), while the male measures 1.5 mm in length by 36 µm in diameter (Fig. 21.4).
Patency occurs within five days after mating. Adult females produce live offspring — newborn larvae (Fig. 21.5) — which measure 0.08 mm long by 7 µm in diameter. The female produces offspring as long as host immunity does not develop. Eventually, acquired, protective responses interfere with the overall process of embryogenesis and creates physiological conditions in the local area of infection which forces the adult parasites to egress and relocate further down the intestinal tract. Expulsion of worms from the host is the final expression of immunity, and may take several weeks.

The newborn larva is the only stage of the parasite that possesses a sword-like stylet, located in its oral cavity. It uses it to create an entry hole in potential host cells. Larvae enter the lamina propria in this fashion, and penetrate into either the mesenteric lymphatics or into the bloodstream. Most newborn larvae enter the general circulation, and become distributed throughout the body.
Migrating newborns leave capillaries and enter cells (Fig. 21.6). There appears to be no tropism for any particular cell type. Once inside, they can either remain or leave, depending upon environmental cues (yet to be determined) received by the parasite. Most cell types die as the result of invasion. Skeletal muscle cells are the only exception. Not only do the parasites remain inside them after invasion, they induce a remarkable series of changes, causing the fully differentiated muscle cell to transform into one that supports the growth and development of the larva (Figs 21.8, 21.9). This process is termed Nurse cell formation.21 Parasite and host cell develop in a coordinated fashion. T. spiralis is infective by the 14th day of infection, but the worm continues to grow in size through day 20.22 The significance of this precocious behavior has yet to be appreciated.
Parasites inside cells other than striated muscle cells fail to induce Nurse cells, and either reenter the general circulation or die. Nurse cell formation results in an intimate and permanent association between the worm and its intracellular niche. At the cellular level, myofilaments and other related muscle cell components become replaced over a 14-16 day period by whorls of smooth membranes and clusters of dysfunctional mitochondria. The net result is that the host cell switches from an aerobic to an anaerobic metabolism.23 Host cell nuclei enlarge and divide,24 amplifying the host’s genome within the Nurse cell cytoplasm.25 The Nurse cell-parasite complex can live for as long as the host remains alive. Most do not, and are calcified within several months after forming. In order for the life cycle to continue, an infected host must die and be eaten by another mammal. Scavenging is a common behavior among most wild mammals, and this helps to ensure the maintenance of T. spiralis and its relatives in their respective host species.

What are the symptoms of a trichinellosis infection?
Nausea, diarrhea, vomiting, fatigue, fever, and abdominal discomfort are the first symptoms of trichinellosis. Headaches, fevers, chills, cough, eye swelling, aching joints and muscle pains, itchy skin, diarrhea, or constipation follow the first symptoms. If the infection is heavy, patients may experience difficulty coordinating movements, and have heart and breathing problems. In severe cases, death can occur.
For mild to moderate infections, most symptoms subside within a few months. Fatigue, weakness, and diarrhea may last for months.

How soon after infection will symptoms appear?
Abdominal symptoms can occur 1-2 days after infection. Further symptoms usually start 2-8 weeks after eating contaminated meat. Symptoms may range from very mild to severe and relate to the number of infectious worms consumed in meat. Often, mild cases of trichinellosis are never specifically diagnosed and are assumed to be the flu or other common illnesses.

Trichinosis usually isn't serious and often gets better on its own, usually within a few months. However, fatigue, mild pain, weakness and diarrhea may linger for months or even years. Symptomatic infections may respond to treatment with medication. * Anti-parasite medication. Anti-parasite (anti-helminthic) medication is the first line of treatment against trichinosis. If the trichinella parasite is discovered early, in the intestinal phase, albendazole (Albenza) or mebendazole can be effective in eliminating the intestinal worms and larvae. You may have mild gastrointestinal side effects during the course of treatment. If the disease is discovered after the larvae bury themselves in tissues, the benefit of anti-parasite medications is less certain, but your doctor may prescribe anti-parasitic medication if you have central nervous system, cardiac or respiratory problems as a result of the invasion. * Pain relievers. After muscle invasion, pain relievers may be given for muscle aches. Eventually, the larvae cysts in your muscles tend to calcify, resulting in destruction of the larvae and the end of muscle aches and fatigue. * Corticosteroids. Some cases of trichinosis cause allergic reactions when the parasite enters muscle tissue or when dead or dying larvae release chemicals in your muscle tissue. Your doctor may prescribe a corticosteroid to control inflammation during larval migration.

Kingdom: Animalia
Phylum: Nematoda
Class: Adenophorea
Order: Trichurida
Family: Trichinellidae
Genus: Trichinella
Species: T. spiralis

http://www.trichinella.org/index_synopsis.htm http://www.cdc.gov/ncidod/dpd/parasites/trichinosis/factsht_trichinosis.htm http://www.mayoclinic.com/health/trichinosis/DS00689/DSECTION=treatments-and-drugs