(Trichinella spp.)





Trichinosis is a food-borne parasitic disease caused by the consumption of raw or undercooked meat, especially pork, or wild game infected with the tissue nematode Trichinella larvae. Infection is commonly seen in animals with cannibalistic and scavenging behavior [1]. While there are eight species in the genus Trichinella, the species most important and pathogenic towards humans is T. spiralis. Trichinosis infection was previously common worldwide, but its prevalence has decreased due to the establishment of new legislation regarding food preparation [2]. Today, trichinosis is mostly found in Europe and North America [2].




Trichinellosis, Trichina



Agent and taxonomy



Kingdom: Animalia
Genus: Trichinella


Figure 1. Trichinella spiralis larvae freed from cyst. (CDC) [2]




The disease-causing agent includes the eight species of Trichinella, but T. spiralis is the most important to humans due to its worldwide distribution and high pathogenicity. The other seven (T. nativa, T. nelsoni, T. britovi, T. pseudospiralis, T. murrelli, T. zimbabwensis, and T. papuae) have different ranges in host and geographic distribution [3]. Five species are encapsulated, meaning they encyst in muscle tissue, while three are nonencapsulated (T. pseudospiralis, T. zimbabwensis, T. papuae) [4].


T. spiralis - most adapted to swine and pathogenic to humans; distributed worldwide and is also present in wild game and horse meat

T. britovi – second most common species to infect humans as it can also affect domestic pig populations; distributed throughout Europe, Asia, and Northern and Western Africa.

T. nativa – distributed in Arctic and subarctic regions with the polar bear as an important reservoir; hosts include the arctic fox, walrus, and other wild game, and it has a high resistance to freezing.

T. pseudospiralis – infects both mammals, including humans, and birds; nonencapsulated, doesn’t coil; found worldwide

T. papuae – infects both mammals and reptiles, including crocodiles, pigs, and humans; found in Papua New Guinea and Thailand; nonencapsulated

T. nelsoni – found in Eastern Africa; intermediate in pathogenicity; few human cases have been documented

T. murrelli – spread among wild carnivores in North America; does not develop in swine; infects humans, especially from black bear meat

T. zimbabwensis – detected in reptiles of Africa; can infect mammals and possibly humans [5]; nonencapsulated.



History of discovery


Discovery of the parasite

Due to the lack of medical records, the circumstances surrounding the first observation and identification of Trichinella spiralis are controversial. In 1835, James Paget, a first-year medical student, first observed the larval form of Trichinella spiralis during an autopsy at St. Bartholomew’s Hospital in London. Paget took special interest in the presentation of muscle with white flecks, described as a “sandy diaphragm.” He later remarked ‘All the men in the dissecting rooms, teachers included, ‘‘saw’’ the little white specks in the muscles: but I believe that I alone ‘‘looked at’’ them and ‘‘observed’’ them.’ [6].


While Paget is most likely the first person to have noticed and recorded these findings, the parasite was named and published in a report by his professor, Richard Owen, who is now credited for the discovery of the Trichinella spiralis larval form [10].


Life cycle discovery

From 1850 to 1870, a series of experiments conducted by the German researchers Rudolph Virchow, Rudolph Leukart, and Friedrich Zenker, discovered the life cycle of Trichinella by feeding infected meat to a dog and performing the subsequent autopsy. Through these experiments, Virchow was able to describe the development and infectivity of T. spiralis [7].


Species discovery

The invention of new biotechnologies in the 1900s and experimental studies lead to the finding of seven more species in addition to Trichinella spiralis [8].






Microscopy shows that infective larvae curl up as they encyst in striated muscle tissue, newborn larvae measuring 0.08 mm long by 7µm in diameter. Free T. spiralis larvae move in a coiling and uncoiling manner [9].


Adult worms

The adult male nematodes have claspers at their posterior end and measure 1.4mm to 1.6 mm long while adult females are twice as long, with the uterus at the posterior end and hatching eggs at the anterior end. Both worms are more slender at the anterior than posterior end [9].  




Figure 2. a) Male adult Trichinella spiralis worm with claspers on its posterior end. b) Female adult T. spiralis ( [10]






The transmission of trichinosis occurs through the ingestion of cysts in infected undercooked or raw meat or wild game. This is especially concerning to hunters of wild game and in cultures where raw meat is prepared as food. Humans cannot infect other humans or animals unless the infected muscle is ingested. In normal circumstances humans present an end to transmission [3].


There are two cycles in which transmission of trichinosis occurs: sylvatic and domestic. The sylvatic cycle includes all Trichinella species and centers around wildlife transmission through the ingestion of infected prey or carrion. The ability of Trichinella species to remain infectious even in decaying tissue promotes effective wildlife transmission through carcasses and carrion [9].


The domestic cycle involves the feeding of garbage containing raw pork scraps and carrion to swine. Rats may also become infected through contact with swine and ingestion of the same swinefeed, and therefore spread the infection to other animals [8].



Life cycle


Ingested infectious larvae break free from their cysts due to the acidity of the stomach, allowing the larvae to enter the small intestine. There they mature into adults and mate, depositing newborn larvae into the intestinal mucosa in as little as three days. The larvae then enter the lymphatic vessels and travel around the body via the bloodstream, entering various organs such as the retina, myocardium, or lymph nodes. However, only larvae that penetrate skeletal muscle cells survive and reach their full size within a month.


Encystation involves three major stages: 1. the formation of the host cell into a nurse cell, 2. encapsulation of the larvae (excluding T. pseudospiralis and T. zimbabwensis), and 3. development of a capillary network around the nurse cell. These infected cells can remain infectious for months to years, whether or not calcification occurs [3][11][12].



Figure 3. Life cycle of Trichinella spp. (CDC) [10]





The different species of Trichinella encompass a wide range of reservoirs:

            T. spiralis: mammals, domestic swine, rats, bears

            T. britovi: foxes, raccoons, dogs, cats

            T. nativa: polar bears, walruses, sled dogs

            T. pseudospiralis: bird, mammals

            T. papuae: wild and domestic pigs, reptiles

            T. nelsoni: hyenas, large cats

            T. murrelli: wild carnivore, humans

            T. zimbabwensis: crocodiles, mammals [13]




There are no known vectors for Trichinella spp. [3]



Clinical Symptoms and Pathogenesis


Incubation period

The incubation period is the time from exposure to the pathogen to the onset of symptoms. Once the ingested larvae enter the intestine, they mature into adults in 3 days. Symptoms during the intestinal stage may be minor and go undetected. However if symptoms do appear, they do so suddenly in 2-7 days and are similar to gastroenteritis (stomach flu). While the length of the incubation period depends on the amount of larvae ingested and varies by species, it has been averaged to be 10-14 days [14].


Clinical manifestations

Symptoms for a Trichinella infection range widely according to the amount and species of larvae ingested. They can be separated by the two phases of pathogenesis: the enteral phase of adult worms at the intestinal level, and the parenteral phase, or invasion of muscle by migrating larvae [8].


Enteral phase

The symptoms during this adult phase may be minor and unnoticeable, and consist of a general gastroenteritis. Diarrhea, nausea, vomiting, and abdominal pain may present with a larger worm burden, while symptoms may be unnoticeable if the number of larvae ingested is low. These nonspecific gastroenteritis symptoms may present anywhere from 2-7 days after ingestion of Trichinella larvae. Eosinophilia, an increase in white blood cells, also presents early and increases rapidly [8].


Parenteral phase

The severity of symptoms caused by the migration of larvae into muscle tissue is dependent on the number of larvae produced by the adult worms. A moderately severe infection may present with about 50-100 larvae per gram of muscle. The body’s inflammatory response is provoked by the invading larvae and edema, muscle pain and swelling, fever, and fatigue may occur. Severe muscle pain, weakness, and hardening, as well as facial edema are common. The classic sign of trichinosis is circumorbital edema, or swelling around the eyes, and may be connected to the inflammation of blood vessels that is caused by larval migration. This vasculitis also leads to the presentation of splinter hemorrhages in the nails [3].


Fatal infections of trichinosis often involve effects on the heart, lungs, and central nervous system, giving rise to serious complications including myocarditis, pneumonia, and encephalopathy, respectively [15].




Figure 4. Classic signs of trichinosis. a) Splinter hemorrhages, b) circumorbital edema [25].



Trichinella’s pathogenic effects arise mostly from the destruction of muscle tissue during larval migration. These effects are characterized by eosinophilia, elevated creatine phosphokinase (CPK), and parasite-specific IgG. Pathogenesis varies by species, although the differences have not been thoroughly researched. A report comparing two Italian outbreaks of T. spiralis and T. britovi describe a few differences in pathogenesis: T. spiralis presents with more severe enteral phase symptoms, and a longer duration of CPK and IgG elevation [16].





History of exposure

The determination of trichinosis infection depends heavily on a history of exposure to, most commonly, raw or undercooked pork or bear meat. Often, the meat in question is home-prepared and thus provides a good source for microscopy. Besides direct consumption of confirmed infected meat, other exposure includes consumption of products from a confirmed infected animal, or sharing exposure to a common source as a confirmed infected human [12].


Clinical diagnosis

The typical clinical symptoms of circumorbital edema, splinter hemorrhages, muscle pain, and gastroenteritis may also suggest trichinosis infection. The European Center for Disease Control states as its case definition for trichinosis “At least three of the following six: fever, muscle soreness and pain, gastrointestinal symptoms, facial edema, eosinophilia, and subconjunctival, subungual, and retinal hemorrhages.” [12].


Laboratory testing


Useful laboratory indicators of infection are eosinophilia, increased levels of creatine phosphokinase (CPK), parasite-specific immunoglobulin G, and antibodies against newborn larvae [16]. Serum tests can detect eosinophilia or the presence of muscle enzymes such as CPK. Immunoassays such as ELISA, indirect immunofluorescence, or Western blot can be performed for anti-Trichinella antibodies [12].



The finding of Trichinella larvae in a muscle biopsy confirms a trichinosis infection. After the first week of infection, tissue biopsies of skeletal muscle, most commonly of calf muscle, or aspirate samples of cysts will show encysted larvae [12].




Figure 5. a) Encysted Trichinella larvae  b) Encysted Trichinella larvae in striated muscle tissue.  (CDC) [2]





Early treatment is desirable as the later an infection progresses without treatment, the greater the chance of larval encystations in the patient’s muscle. These cysts may then remain infectious for years, despite treatment [12].


Primary treatment

Anthelmintics such as albendazole and mebendazole can be prescribed to prevent newborn larvae from growing. If this treatment is given in the early stages of infection, especially in the first three days, larvae may be prevented from encysting, therefore preventing disease and pain. It is important to note that anthelmintics may be useless against long-term infections as larvae have already encysted -- therefore, treatment should be given as early as possible. Unfortunately, most cases of trichinosis are diagnosed too late and larvae have already been established [3][12].


Mebendazole is the preferred treatment, with a dosage of 200 to 400 mg three times daily for three days, followed by 400 to 500 mg three times daily for 10 days.

Alternatively, the dosage for the albendazole is 400 mg twice a day for 8 to 14 days.

These drugs should not be taken by pregnant women and are not recommended for children under two years of age [12].


New research

Extension of the effectiveness of anthelmintics to allow for later treatment of helminthic infections has been demonstrated in a mouse model by using 2-hydroxypropyl-β-cyclodextrin. Similar results were obtained using cymetidine for human cystic echinococcosis (hydatid disease), but studies in human trichinosis have not been conducted [17].


Secondary treatment

Steroids such as prednisone may be used as secondary treatment after infection to relieve muscle pain due to larval migration. Pyrantel is safe for pregnant women and children, but only effects adult worms in the intestines [12].


Vaccine research

While there are currently no vaccines for Trichinosis, experimental mice studies have suggested a potential vaccine may be produced. In one such study, microwaved larvae of T. spiralis were used to immunize mice and results ranged from a decreased larval count to complete protection depending on dosage. This technology may be used to create an effective barrier to human or animal transmission [18].


A candidate vaccine for use in domestic swine herds has been developed and may help in management of the disease. However, the production of the vaccine may be too costly [19].





The worldwide prevalence of trichinosis infection has declined largely due to legislation requiring proper preparation of garbage used as hog food, storage of pork products, public awareness, and possibly a decline in the consumption of pork [3]. Reported cases of trichinosis today occur mainly in developed countries, including Europe, Asia, and North America [12].


Cultural factors such as the traditional preparation of dishes based on raw or undercooked meat is often the source of occasional outbreaks. These eating habits range from raw horse meat delicacy in France [26], dog meat in China and the Slovak Republic, and the consumption of improperly cooked wild game by hunters worldwide. Interestingly, in Muslim populations where the consumption of pork is forbidden, trichinosis infection has only been found in Europeans [12].



In the 1990s, trichinosis was labeled as a “reemerging zoonosis” despite the previous veterinary efforts to control it in the past century. This may be due to the relaxation of veterinary public health systems, the changing climate, increasing sylvatic transmission, and expanding food marketing systems, among other factors [19].


It is suggested that the success of trichinosis control in the 1960s led to inspectors and food workers letting down their guard and relaxing inspection protocol. Other reasons for the reemergence of trichinosis include the mass marketing of meat products in transferring the disease to non-endemic areas as well as a shift in human behavior towards consuming more game meat [12].


Increased outbreaks in recent years by the sylvatic Trichinella species indicates an increase in transmission to the domestic cycle and therefore to humans. These outbreaks were seen with T. pseudospiralis in Thailand [20], T. nativa in indigenous Arctic populations [21], and potentially T. zimbabwensis in Taiwan [5]. This may be a result of “risky behaviour” that subjects wildlife to exposure of the parasite, such as the habit of hunters in leaving carcasses in the wild. These outbreaks not only provide more information about the different Trichinella species, but also indicate that the Trichinella epidemiology is changing [19].


Changing political arenas may also lead to the reemergence of Trichinosis, as indicated by Serbia. An outbreak in 2001 was determined to have resulted from a weak veterinary public health system and economy affected by the breakup of the former Federation of Yugoslavia [22].



Prevention and Public Health Strategies



Outbreaks can be prevented by legislation requiring standards and control for food packaging companies. To improve food safety for consumers, the European Commission established rules for the control of Trichinella in meat, including required inspections, rodent control, and hygiene standards. [12]. In the United States, the United States Department of Agriculture (USDA) guidelines for establishment responsibilities in the inspection of meat and poultry include procedures to follow in identifying cysts in pork products [23]. These rules targeting food –packaging companies may aid in the prevention of a trichinosis outbreak.


Legislation that sets standards for pig farming may also help in preventing transmission through the establishment of hygienic conditions, certified feedstuff, and veterinary control [12].


Education and training

Public and consumer education about the risks of consuming raw or undercooked meat products of both domestic animals and wild game may reduce infection rates [12]. As hunters are part of the at-risk population, some states such as New York require the completion of an education course which includes food preparation in order to apply for a hunting license [24].


Food preparation

Trichinella larvae can be inactivated by heating, freezing, and irradiation of meat.


Heating: at 71°C for at least one minute until “the meat must change the color from pink to gray, and muscle fibers are easily separated from each other” [12]

Freezing: Cuts of meat up to 15 cm thick must be frozen at a minimum of -15°C for at least 3 weeks. This only applies to T. spiralis infections, as other species, particularly the freeze-resistant T. nativa, may survive cold temperatures.

Irradiation: In countries where irradiation of food is permitted, irradiation at 0.3 kGy inactivates Trichinella and is only recommended for seals packaged food [12].


Unsafe methods of preparation include cooking by microwave ovens, curing, drying, and smoking of meat, as those methods vary and are difficult to control [12].



Useful Web Links







[1] Kapel CMO. “Experimental infections with sylvatic and domestic Trichinella species in wild boars, infectivity, muscle larva distribution and antibody response”. J Parasitol 2000;93:263-278.


[2] "DPDx - Trichinellosis." Laboratory Identification of Parasites of Public Health Concern. CDC. Web.


[3] John D and William A. Petri. Markell and Voge's Medical Parasitology. 9th ed. Philadelphia: Saunders, 2006.


[4] Pozio E, et al. “Trichinella zimbabwensis n.sp. (Nematoda), a new non-encapsulated species from crocodiles (Crocodylus niloticus) in Zimbabwe also infecting mammals.” Int J Parasitol. 2002 Dec 19;32(14):1787-99. <>.


[5] Lo YC, et al. “Human Trichinosis after Consumption of Soft-Shelled Turtles, Taiwan.” Emerging Infectious Diseases 2009:15(12).


[6] Buchanan W. “Heberden Historical Series: Sir James Paget.” Rheumatology 2003;42:1107–1108 doi:10.1093.


[7] Blumer G. “Some remarks on the early history of Trichinosis (1822-1866).” Yale Journal of Biology and Medicine 1(6)581-588.


[8] Bruschi F, Murrell KD. “New aspects of human trichinellosis: the impact of new Trichinella species.” Postgrad Med J 2002;78:15-22 doi:10.1136/pmj.78.915.15 .


[9] Hartwell G, 2003. "Trichinella spiralis" (On-line), Animal Diversity Web.




[11] Fabre MV, “Immunity to Trichinella spiralis muscle infection.” Veterinary Parasitology 159 (2009) 245–248.


[12] Gottstein B, et al. “Epidemiology, Diagnosis, Treatment, and Control of Trichinellosis.” Clinical Microbiology Reviews, January 2009, p. 127-145, Vol. 22, No. 1.


[13] Despommier et al “Parasitic Diseases” Apple Trees Productions, LLC NY, 5th ed.


[14] "Trichinosis." New York State Department of Health. Web. 26 <>.


[15] A. Srikiatkhachorn. “Trichinosis – Clinical summary” Medlink 2006.


[16] Pozio E, et al. “Comparison of Human Trichinellosis Caused by Trichinella spiralis and by Trichinella britovi.” Am. J. Trop. Med. Hyg., 48(4), 1993, pp. 568-575.

[17] Luder, PJ, et al. "Treatment of hydatid disease with high oral doses of mebendazole. Long-term follow-up of plasma mebendazole levels and drug interactions." European Journal of Clinical Pharmacology 31.4 (1986): 443-48. (


[18] Ali SM, et al. “Immunization against trichinellosis using microwaved larvae of Trichinella spiralis.” J Egypt Soc Parasitol. 2007 Apr;37(1):121-33.


[19] Murrell KD, Pozio E. “Trichinellosis: the zoonosis that won’t go quietly.” International Journal for Parasitology. 30(2000)1339-1349.


[20] Jongwutiwes S et al “First outbreak of human trichinellosis caused by Trichinella pseudospiralis.” Clin Infect Dis. 1998 Jan;26(1):111-5.


[21] Hotez P. “Neglected Infections of Poverty among the Indigenous Peoples of the Arctic.” PLoS Negl Trop Dis. 2010 January; 4(1): e606.


[22] Djordjevic M et al. “Social, political, and economic factors responsible for the reemergence of Trichinellosis in Serbia: a case study.” The Journal of Parasitology, 89(2)226-231, Apr 2003.


[23] United States Department of Agriculture – Food Safety and Inspection Service. “NSS NRTE/RTE Establishment Responsibilities.” (2006).


[24] New York State Department of Environmental Conservation – Hunting Licenses


[25] Photos courtesy of


[26] MMWR Weekly. “Horsemeat-Associated Trichinosis – France.” May 09, 1986 / 35(18);291-2,297-8