Trichinella spiralis

Trichinella spiralis
Scientific classification
Kingdom: Animalia
Phylum: Nematoda
Class: Adenophorea
Order: Trichocephalida
Superfamily: Trichinelloidea
Genus: Trichinella
Species: T. spiralis
Binomial name
Trichinella spiralis
(Owen, 1835)

Trichinella spiralis is a viviperous nematode parasite, occurring in rodents, pigs, horses, bears, and humans, and is responsible for the disease trichinosis. It is sometimes referred to as the "pork worm" due to it being found commonly in undercooked pork products.

Description

Trichinella species are the smallest nematode parasite of humans, have an unusual lifecycle, and are one of the most widespread and clinically important parasites in the world.[1] The small adult worms mature in the intestines of a definitive host such as a pig. Each adult female produces batches of live larvae, which bore through the intestinal wall, enter the blood (to feed on it) and lymphatic system, and are carried to striated muscle. Once in the muscle, they encyst, or become enclosed in a capsule. Humans can be infected by eating infected pork, horsemeat, or wild carnivores such as fox, cat, or bear.[1]

Morphology

Males of T. spiralis measure between 1.4 and 1.6 mm long and are more flat anteriorly than posteriorly. The anus can be found in the terminal (side) and they have a large copulatory pseudobursa on each side.[1] The females of T. spiralis are about twice the size of the males and have an anus found terminally. The vulva is located near the esophagus. The single uterus of the female is filled with developing eggs in the posterior portion, while the anterior portion contained the fully developed juveniles.[1]

Life cycle

Trichinella spiralis is a parasitic nematode which can live the majority of its adult life in the intestines of humans. To begin its life cycle "Trichinella spiralis" adults will invade the intestinal wall of pigs and produce larvae that invade the pigs muscles [14]. The larval forms are encapsulated as a small cystic structure within the infected host. Humans typically become infected when they eat improperly cooked Trichinella infected pork or other meat. When a human eats the infected meat, the larvae are released from the nurse cell (due to stomach pH) and migrate to the intestine, where they burrow into the intestinal mucosa, mature, and reproduce.[2] Juveniles within nurse cells have an anaerobic or facultative anaerobic metabolism, but when they become activated, they adopt an aerobic metabolism characteristics of the adult.[1]

Trichinella spiralis lifecycle

Female Trichinella worms live for about six weeks, and in that time can produce up to 1,500 larvae; when a spent female dies, she passes out of the host. The larvae can then gain access to the circulation and migrate around the body of the host.[2] The migration and encystment of larvae can cause fever and pain brought upon by the host inflammatory response. In some cases, migration to specific organ tissues can cause myocarditis and encephalitis that can result in death.

Animal tissue infected with the parasite that causes the disease trichinosis. Most parasites are shown in cross section but some randomly appear in long section.

Nurse cell formation

This nematode is a multicellular parasite that lives within a single muscle cell, which it modifies according to its own requirements.[3]

T. spiralis larvae within the diaphragm muscle of a pig

Nurse cell formation in skeletal muscle tissue is mediated by the hypoxic environment surrounding the new vessel formation.[4] The hypoxic environment stimulates cells in the surrounding tissue to regulate up and secrete angiogenic cytokines, such as vascular endothelial growth factor (VEGF). This allows for the newborn T. spiralis larvae to enter and form the nurse cells. VEGF expression is detected surrounding the nurse cell right after nurse cell formation, and the continued secretion of VEGF can maintain the constant state of hypoxia.[5] Previous studies have shown VEGF can stimulate proliferation of synthesis of collagen type 1 in activated myofibroblast-like cells.[6]

Symptoms

The first symptoms may appear between 12 hours and two days after ingestion of infected meat. The migration of worms in the intestinal epithelium can cause traumatic damage to the host tissue, and the waste products they excrete can provoke an immunological reaction.[1] The resulting inflammation can cause symptoms such as nausea, vomiting, sweating, and diarrhea. Five to seven days after the appearance of symptoms, facial edema and fever may occur. After 10 days, intense muscular pain, difficulty breathing, weakening of pulse and blood pressure, heart damage, and various nervous disorders may occur, eventually leading to death due to heart failure, respiratory complications, or kidney malfunction.[1]

In pigs, infection is usually subclinical, but large numbers of worms can be fatal in some cases.[7]

Diagnosis and treatment

Muscle biopsy is used for trichinosis detection. Several immunodiagnostic tests are also available. Typically, patients are treated with either mebendazole or albendazole, but efficacy of such products are uncertain. Symptoms can be relieved by use of analgesics and corticosteroids.[1]

In pigs, ELISA testing is possible as a method of diagnosis. Anthelmintics can treat and prevent Trichinella infections.[7]

Prevention and control

Trichinosis (also trichinellosis) is a disease caused by tissue-dwelling roundworms of the species Trichinella spiralis. In the United States, the national trichinellosis surveillance system has documented a steady decline in the reported incidence of this disease. During 1947 to 1951, a median of 393 cases was reported annually, including 57 trichinellosis-related deaths. During 1997-2001, the incidence decreased to a median of 12 cases annually, with no reported deaths. The decline of infection was largely associated with changes implemented by the U.S. pork industry that have resulted in reduced prevalence of Trichinella among domestic swine.[8] In the United States, Congress passed the Federal Swine Health Protection Act restricting the use of uncooked garbage as feed stock for pigs and creating a voluntary Trichinae Herd Certification Program.[8] The Trichinae Herd Certification Program is a voluntary preharvest pork safety program that provides documentation of swine management practices to minimize Trichinella exposure. The goal of the program is to establish a system under which pork production facilities that follow good production practices might be certified as Trichinella-safe.[9] In addition to the reduction in Trichinella prevalence in commercial pork, processing methods also have contributed to the dramatic decline in human trichinellosis associated with pork products. Through the U.S. Code of Federal Regulations, the USDA has created guidelines for specific cooking temperatures and times, freezing temperatures and times, and curing methods for processed pork products to control postharvest human exposure to Trichinella.[8] Pork products meeting these guidelines are designated certified pork.

The chances of becoming infected with Trichinella spiralis are relatively low in the United States, due to such rigorous control measures, while there are higher prevalence rates in regions such as Europe and Asia.[10] This parasite is considered to be endemic in Japan and China, while Korea just reported its first case of the parasite disease.[10]

In most abattoirs, the diaphragm of pigs is routinely sampled to detect Trichinella infections.[7]

Postharvest human exposure is also preventable by educating consumers of simple steps that can be taken to kill any larvae that can potential be in meat bought at the local supermarket. Freezing meat in an average household freezer for 20 days before consumption will kill some species of Trichinella. Cooking pork products to a minimum internal temperature of 160°F will kill most species and is the best way to ensure the meat is safe to eat.[11]

Economic Impact

Political and economic changes have caused an increase in the prevalence and incidence rates of this parasite in many European countries.[12] This complicates the meat trade industry within European countries and makes it difficult for exportation of pork outside of these countries.[12] The European Commission proposed a new regulation to implement specific rules for food safety.[12]

Illegal importation from places with low safety quality standards allows for the spread of the parasite from endemic to non-endemic countries. [12]Illegal importation and new food practices have resulted in outbreaks in many countries including: Denmark, Germany, Italy, Spain, and the United Kingdom.[12]

The economic cost for detecting trichinosis can be another cost burden. In 1998, it was estimated to cost $3.00 per pig in order to detect the parasite.[12] In order to control Trichinella infection, the European Union condemned 190 million pigs leading to a substantial economic impact of about $570 million per year.[12]

Genome

The Trichinella spiralis draft genome became available in March 2011.[13] The genome size was 58.55 Mbp with an estimated 16,549 genes.[14] The T. spiralis genome is the only known nematode genome to be subject to DNA methylation,[15] an epigenetic mechanism that was not previously thought to exist in nematodes.

See also

References

  1. 1 2 3 4 5 6 7 8 Roberts, Larry S., John Janovay (2005). Foundations of Parasitology (7th ed.). New York: McGraw-Hill. pp. 405–407.
  2. 1 2 Crowley, Leonard (2009). An Introduction to Human Disease: Pathology and Pathophysiology Correlations (8th ed.). Jones and Bartlett.
  3. ↑ Combes, Claude (2005). The art of Being a Parasite (English translation ed.). The University of Chicago Press.
  4. ↑ Fong GH (2008). "Mechanism of adaptative angiogenesis to tissue hypoxia". Angiogenesis 11: 121–140. doi:10.1007/s10456-008-9107-3.
  5. ↑ Capo VA, Despommier DD, Polvere RI (1998). "Trichinella spiralis: vascular endothelial growth factor is up-regulated within the nurse cell during the early phase of its formation". J. Parasitol. 84: 209–214. doi:10.2307/3284472.
  6. ↑ Novo E, Cannito S, Zamara E, Valfre di Bonzo L, Caligiuri A, Cravanzola C, et al. (2007). "Proangiogenic cytokines as hypoxia-dependent factors stimulating migration of human hepatic stellate cells". Am. J. Pathol. 170: 1942–1953. doi:10.2353/ajpath.2007.060887.
  7. 1 2 3 "Trichinella". WikiVet. Retrieved 12 October 2011.
  8. 1 2 3 Roy, Sharon L., Adriana S. Lopez, and Peter M. Schantz. "Trichinellosis Surveillance --- United States, 1997--2001." Center for Disease Control
  9. ↑ National Pork Board. Trichinae Herd Certification. Des Moines, Iowa: National Pork Producers Council, 2000. Available at http://www.aphis.usda.gov/vs/trichinella/.
  10. 1 2 "Epidemiology of Trichinella". www.trichinella.org. Retrieved 2016-05-05.
  11. ↑ Morbidity and Mortality Weekly Report: Surveillance Summaries (2003): 1-8. JSTOR. Centers for Disease Control & Prevention (CDC). Web. 1 Dec. 2014.
  12. 1 2 3 4 5 6 7 Gottstein, Bruno; Pozio, Edoardo; Nöckler, Karsten (2009-01-01). "Epidemiology, Diagnosis, Treatment, and Control of Trichinellosis". Clinical Microbiology Reviews 22 (1): 127–145. doi:10.1128/CMR.00026-08. ISSN 0893-8512. PMC 2620635. PMID 19136437.
  13. ↑ "Trichinella spiralis". Genome. NCBI. Retrieved 2012-04-19.
  14. ↑ Mitreva M, Jasmer DP, Zarlenga DS, Wang Z, Abubucker S, Martin J, Taylor CM, Yin Y, Fulton L, Minx P, Yang SP, Warren WC, Fulton RS, Bhonagiri V, Zhang X, Hallsworth-Pepin K, Clifton SW, McCarter JP, Appleton J, Mardis ER, Wilson RK (March 2011). "The draft genome of the parasitic nematode Trichinella spiralis". Nat. Genet. 43 (3): 228–235. doi:10.1038/ng.769. PMC 3057868. PMID 21336279.
  15. ↑ Gao F, Liu X, Wu XP, Wang XL, Gong D, Lu H, Xia Y, Song Y, Wang J, Du J, Liu S, Han X, Tang Y, Yang H, Jin Q, Zhang X, Liu M (October 2012). "Differential DNA methylation in discrete developmental stages of the parasitic nematode Trichinella spiralis". Genome Biol. 13 (10): R100. doi:10.1186/gb-2012-13-10-r100. PMID 23075480.

14 "Microbiology: An Introduction 9/e" (2006)

Bibliography

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