Introduction
Background
Trichinosis is the result of infection by the nematode Trichinella spiralis. Humans are infected incidentally when they eat inadequately cooked meat that contains larvae of Trichinella species. Most infestations do not cause symptoms, although heavy exposure can cause various clinical manifestations, including diarrhea, fever, myalgias, and prostration.
Pathophysiology
Although 8 species of Trichinella currently exist and are described taxonomically based on genetic, biochemical, and biological data, an additional 4 genotypes are acknowledged in the genus, but their taxonomic level is uncertain.1 The table below describes the taxonomically described species, including distribution, major host reservoir, infectivity of humans, resistance to freezing, and pathogenicity to humans.1,2
Important Characteristics of Trichinella Species
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Table
Species | Distribution | Major Host Reservoir | Infectivity | Resistance to Freezing |
T spiralis (T1) | Cosmopolitan | Swine, wild boar, bear, horse, fox | High | None |
Trichinella nativa (T2) | Arctic | Bear, horse | High | High |
Trichinella britovi (T3) | Temperate | Wild boar, horse | Moderate | None |
Trichinella pseudospiralis (T4) | Cosmopolitan | Birds, omnivorous mammals | Moderate | None |
Trichinella murrelli (T5) | Temperate, near arctic | Bear | Low | Low |
Trichinella nelsoni (T7) | Tropical | Warthog | High | None |
Trichinella papuae (T10) | Papua New Guinea | Warthog | Moderate | None |
Trichinella zimbabwensis (T11) | Central Africa | Crocodiles | Unknown | None |
Species | Distribution | Major Host Reservoir | Infectivity | Resistance to Freezing |
T spiralis (T1) | Cosmopolitan | Swine, wild boar, bear, horse, fox | High | None |
Trichinella nativa (T2) | Arctic | Bear, horse | High | High |
Trichinella britovi (T3) | Temperate | Wild boar, horse | Moderate | None |
Trichinella pseudospiralis (T4) | Cosmopolitan | Birds, omnivorous mammals | Moderate | None |
Trichinella murrelli (T5) | Temperate, near arctic | Bear | Low | Low |
Trichinella nelsoni (T7) | Tropical | Warthog | High | None |
Trichinella papuae (T10) | Papua New Guinea | Warthog | Moderate | None |
Trichinella zimbabwensis (T11) | Central Africa | Crocodiles | Unknown | None |
Trichinella species require 2 hosts to maintain their life cycle. After development in a single host, they spread to the next through ingestion of infected flesh, as opposed to the traditional arthropod intermediate host. Trichinella species have 3 major life cycles in nature: pig-to-pig, rat-to-rat, and by carnivorous or omnivorous animals in the wild. Rats and pigs are the animals most commonly associated with trichinosis; however, depending on the region, walruses, seals, bears, polar bears, cats, raccoons, wolves, and foxes may also be infected. Life cycle of Trichinella species parasite is depicted in the image below.
The life cycle begins when raw or inadequately cooked meat is eaten that contains viable larvae housed inside a cyst wall, known as a nurse cell. The acidic environment in the host's stomach releases the larvae from the cyst wall. The free larvae migrate into the small intestine and attach to and penetrate the mucosa at the base of the villi. After 4 molts and over a period of 30-36 hours, they develop into adult worms and become obligate intracellular organisms. The adult male measures 1.5 X 0.05 mm, and the adult female measures 3.5 X 0.06 mm. Approximately 5 days after infection, the female begins shedding live newborn larvae (L1 stage). The female remains in the intestine for 4 weeks, releasing up to 1500 larvae. After an adequate inflammatory response develops in the intestine, the female is eventually expelled in the feces.
The newborn larvae enter the lymphatics and blood circulatory system and migrate to well-vascularized striated skeletal muscle. The parasite has a predilection for the most metabolically active muscle groups; therefore, the most frequently parasitized muscles include the tongue; the diaphragmatic, masseteric, intercostal, laryngeal, extraocular, nuchal, intercostal, and pectoral muscles; the deltoid; the gluteus; the biceps; and the gastrocnemius. In tissues other than skeletal muscle, such as the myocardium and brain, the parasites soon disintegrate, causing intense inflammation, and are then reabsorbed.
The larvae continue to grow over the next 2-3 weeks until they reach the fully developed L1 infective stage, when they increase in size up to 10-fold. The adult worms are viviparous. The larvae coil and develop a surrounding cyst wall, or nurse cell (except for T pseudospiralis, which does not encyst). The complete cycle takes 17-21 days. The larvae within the cyst wall reach an average size of 400 X 260 µm; however, lengths of 800-1000 µm have been described. The nurse cell–L1 complex may persist for 6 months to several years before calcification and death occur. The life cycle is complete when a compatible host ingests the infected muscle.
The intensity and frequency of exposure to infected meat determine the severity of the disease. The degree of infection is categorized as light (0-10 larvae ingested), moderate (50-500 larvae ingested), and severe (>1000 larvae ingested).
Frequency
United States
From 1997-2001, 72 cases of trichinosis were reported to the Centers for Disease Control and Prevention (CDC).3 Most cases were associated with eating wild game (43%), although 17% were associated with commercial pork products and another 13% from noncommercial pork products. Infections may also occur during foreign travel, especially to Mexico and Asia. The percentage of infected domestic swine in the United States is 0.001%; however, one autopsy study documented a 4% incidence of old infection. Data have also shown the presence of T murrelli in raccoons and coyotes.4
International
In Europe, where pork inspection is mandatory, most cases of trichinosis are associated with horse or wild boar meat. In Latin America and Asia, domestic pork is the chief source of infection. The rate of Trichinella infection in swine in China is as high as 20%. Studies have also reported increase rates of trichinosis in former European countries such as Romania due to political changes and regional food habits.5 In addition, the European Centre for Disease Prevention and Control and the European Safety Authority reported 779 human cases of trichinellosis in the European Union found in farm animals and wild animals, particularly in the latter.6
Mortality/Morbidity
- Although Trichinella infections are most likely underreported in the United States, fewer than 25 cases are documented per year, with a very low mortality rate.
- Patients with light infection are usually asymptomatic. Those with mild symptoms improve in 2-3 weeks. Symptoms associated with heavy infections may persist for 2-3 months.
- Factors that may affect morbidity include the quantity of larvae ingested, the species of Trichinella (most notably T spiralis), and the immune status of the host. Patients succumb to exhaustion, pneumonia, pulmonary embolism, encephalitis, or cardiac failure and/or arrhythmia. Death from trichinellosis usually occurs in 4-8 weeks but may occur as early as in 2-3 weeks.
Race
Trichinella infections are related to cultural differences in food cooking and storing methods, specifically the inadequate cooking or freezing of meat.
Sex
- No differences in the rates of trichinosis between males and females are reported.
- Pregnant patients milder trichinosis symptoms than patients who are not pregnant; however, abortions and stillbirths have been reported.
- Symptoms of trichinosis are typically worse in females who are lactating than in females who are not.
Age
Children appear to be more resistant to Trichinella infection; however, their symptoms may be more intense. Children also have fewer complications and recover more rapidly.
Clinical
History
The European Center for Disease Control has proposed definitions and algorithms for diagnosis of acute trichinellosis in humans.1 They focus on clinical, laboratory, and epidemiological criteria, along with a series of symptoms. The criteria can also be used to differentiate very unlikely, suspected, probable, highly probable, and confirmed cases (see Staging). Knowledge of the incubation period can help pinpoint the source of the infection, both in individual cases and in outbreaks.
Trichinellosis may progress from an enteric (ie, intestinal) phase to a parenteral (ie, invasive) phase to a period of convalescence.
- The intestinal phase usually causes symptoms in the first week of illness.
- Diarrhea is the most common symptom.
- Constipation, anorexia, and diffuse weakness may occur.
- Occasionally, severe enteritis due to a massive inoculum of Trichinella species occurs.
- Symptoms typically last 2-7 days but may persist for weeks.
- With certain Trichinella species and in certain population groups and geographic regions, the disease may not progress beyond the intestinal stage.
- Nausea is reported in 15% of patients, vomiting in 3%, and diarrhea in 16%.
- Dyspnea may occur with exertion.
- Abdominal discomfort and cramps may occur.
- The invasive phase corresponds to the migration of the larvae from the intestine to the circulatory system and eventually to the striated muscles. This phase is associated with a higher rate of symptoms than the intestinal stage.
- The duration varies from weeks to months.
- Severe myalgia develops in 89% of patients.
- The central nervous system (CNS) is involved in 10%-24% of patients, with a mortality rate of 50%. Approximately 52% of patients present with headaches. Other symptoms include deafness, ocular disturbances, weakness, and monoparesis.
- Cardiac system involvement occurs during the third week of infection, with a mortality rate of 0.1%, often during the fourth to eighth week of infection. Death may result from congestive heart failure and/or arrhythmias.
- Pulmonary system involvement occurs in 33% of patients, with symptoms lasting up to 5 days. Patients present with dyspnea, a cough, and hoarseness.
- The convalescent phase, which corresponds to encystment and repair, may be present for months to years after infection.
- The encystment of larvae can lead to cachexia, edema, and extreme dehydration.
- Symptoms usually decrease around the second month, except in the case of T pseudospiralis infection , which may cause symptoms for several months.
Physical
- Intestinal phase
- Abdominal distention may be present.
- Macular or petechial rashes affect 20% of patients.
- Diarrhea may occur.
- Invasive phase
- After 2 weeks, 91% of patients have a fever that peaks around the fourth week. This degree of fever is unique among helminthic infections. Temperatures can reach 104°F (40°C).
- Weakness and/or myositis occur in 82% of patients. Muscles become stiff, hard, and edematous. Muscles with increased blood flow (eg, extraocular muscles, masseters, larynx, tongue, neck muscles, diaphragm, intercostals, limb flexors, lumbar muscles) are most frequently involved. Involvement of the diaphragm may result in dyspnea.
- Periorbital edema is reported in 77% of patients.
- Rash (macular or petechial) is reported in 15%-65% of patients.
- Ocular findings include subconjunctival hemorrhages in 9% of patients, conjunctivitis in 55%, and incidences of chemosis and retinal hemorrhage.
- The CNS is involved in 10%-24% of patients. Of these, 53%-96% exhibit meningoencephalitis, 40%-73% exhibit focal paralysis and/or paresis, 39%-71% exhibit delirium, 20% exhibit decreased or absent deep-tendon reflexes, 17% exhibit meningitis, and 2% exhibit evidence of psychosis.
- Signs of cardiac system involvement include hypertension, increased venous pressure, and, in 18% of patients, peripheral edema.
- Subungual splinter hemorrhages occur in 8% of patients.
- Convalescent phase
- Edema is present in 18% of patients.
- Patients are easily fatigued.
- Weakness may occur.
- Weight loss may occur.
- Myalgia may occur.
- Ocular signs with chronic headaches may be present.
Causes
- Trichinella species develop in a single host and are spread from that host to the next without an arthropod intermediate. The intensity and frequency of exposure to infected meat determine the severity of the disease.
- Infections are related to cultural differences in food cooking and storing methods, specifically the inadequate cooking or freezing of meat.
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References
Gottstein B, Pozio E, Nöckler K. Epidemiology, diagnosis, treatment, and control of trichinellosis. Clin Microbiol Rev. Jan 2009;22(1):127-45, Table of Contents. [Medline].
Pozio E, Hoberg E, La Rosa G, Zarlenga DS. Molecular taxonomy, phylogeny and biogeography of nematodes belonging to the Trichinella genus. Infect Genet Evol. Jul 2009;9(4):606-16. [Medline].
Roy SL, Lopez AS, Schantz PM. Trichinellosis surveillance--United States, 1997-2001. MMWR Surveill Summ. Jul 25 2003;52(6):1-8. [Medline].
Hill DE, Samuel MD, Nolden CA, Sundar N, Zarlenga DS, Dubey JP. Trichinella murrelli in scavenging mammals from south-central Wisconsin, USA. J Wildl Dis. Jul 2008;44(3):629-35. [Medline].
Blaga R, Durand B, Antoniu S, Gherman C, Cretu CM, Cozma V. A dramatic increase in the incidence of human trichinellosis in Romania over the past 25 years: impact of political changes and regional food habits. Am J Trop Med Hyg. May 2007;76(5):983-6. [Medline].
Westrell T, Ciampa N, Boelaert F, Helwigh B, Korsgaard H, Chríel M. Zoonotic infections in Europe in 2007: a summary of the EFSA-ECDC annual report. Euro Surveill. Jan 22 2009;14(3):[Medline].
Tassi C, Materazzi L, Pozio E, Bruschi F. Creatine kinase isoenzymes in human trichinellosis. Clin Chim Acta. Aug 14 1995;239(2):197-202. [Medline].
Dupouy-Camet J, Kociecka W, Bruschi F, et al. Opinion on the diagnosis and treatment of human trichinellosis. Expert Opin Pharmacother. Aug 2002;3(8):1117-30. [Medline].
Fourestie V, Bougnoux ME, Ancelle T, et al. Randomized trial of albendazole versus tiabendazole plus flubendazole during an outbreak of human trichinellosis. Parasitol Res. 1988;75(1):36-41. [Medline].
Med Lett Drugs Ther. Drugs for parasitic infections. Med Lett Drugs Ther. Jan 2 1998;40(1017):1-12. [Medline].
Watt G, Saisorn S, Jongsakul K, et al. Blinded, placebo-controlled trial of antiparasitic drugs for trichinosis myositis. J Infect Dis. Jul 2000;182(1):371-4. [Medline].
Al-Sherbiny MM, Farrag AA, Fayad MH, et al. Application and assessment of a dipstick assay in the diagnosis of hydatidosis and trichinosis. Parasitol Res. Jun 2004;93(2):87-95. [Medline].
Cleri DJ, Ricketti AJ, Ramos-Bonner LS, Vernalco JR. Trichinosis (Part I and II). Infect Dis Pract. 2005;29:439-444 and 451-459.
Compton SJ, Celum CL, Lee C, et al. Trichinosis with ventilatory failure and persistent myocarditis. Clin Infect Dis. Apr 1993;16(4):500-4. [Medline].
Dalessio DJ, Wolff HG. Trichinella spiralis infection of the central nervous system. Report of a case and review of the literature. Arch Neurol. Apr 1961;4:407-17. [Medline].
Froscher W, Gullotta F, Saathoff M, Tackmann W. Chronic trichinosis. Clinical, bioptic, serological and electromyographic observations. Eur Neurol. 1988;28(4):221-6. [Medline].
Gottstein B, Pozio E, Nöckler K. Epidemiology, diagnosis, treatment, and control of trichinellosis. Clin Microbiol Rev. Jan 2009;22(1):127-45, Table of Contents. [Medline].
Harms G, Binz P, Feldmeier H, et al. Trichinosis: a prospective controlled study of patients ten years after acute infection. Clin Infect Dis. Oct 1993;17(4):637-43. [Medline].
Jongwutiwes S, Chantachum N, Kraivichian P, et al. First outbreak of human trichinellosis caused by Trichinella pseudospiralis. Clin Infect Dis. Jan 1998;26(1):111-5. [Medline].
Kozar Z, Kozar M. Dynamics and persistence of antibodies in trichinellosis. Wiad Parazytol. 1968;14(2):171-85. [Medline].
Louthrenoo W, Mahanuphab P, Sanguanmitra P, Thamprasert K. Trichinosis mimicking polymyositis in a patient with human immunodeficiency virus infection. Br J Rheumatol. 32(11):1025-6. [Medline].
MacLean JD, Viallet J, Law C, Staudt M. Trichinosis in the Canadian Arctic: report of five outbreaks and a new clinical syndrome. J Infect Dis. Sep 1989;160(3):513-20. [Medline].
Mawhorter SD, Kazura JW. Trichinosis of the central nervous system. Semin Neurol. Jun 1993;13(2):148-52. [Medline].
McAuley JB, Michelson MK, Hightower AW, et al. A trichinosis outbreak among Southeast Asian refugees. Am J Epidemiol. Jun 15 1992;135(12):1404-10. [Medline].
McAuley JB, Michelson MK, Schantz PM. Trichinella infection in travelers. J Infect Dis. Nov 1991;164(5):1013-6. [Medline].
Pozio E, Darwin Murrell K. Systematics and epidemiology of trichinella. Adv Parasitol. 2006;63:367-439. [Medline].
Pozio E, La Rosa G, Murrell KD, Lichtenfels JR. Taxonomic revision of the genus Trichinella. J Parasitol. Aug 1992;78(4):654-9. [Medline].
Rosenblatt JE. Laboratory diagnosis of infections due to blood and tissue parasites. Clin Infect Dis. Oct 1 2009;49(7):1103-8. [Medline].
Taylor WR, Tran GV, Nguyen TQ, Dang DV, Nguyen VK, Nguyen CT, et al. Acute febrile myalgia in Vietnam due to trichinellosis following the consumption of raw pork. Clin Infect Dis. Oct 1 2009;49(7):e79-83. [Medline].
Tint D, Cocuz ME, Ortan OF, Niculescu MD, Radoi M. Cardiac involvement in trichinellosis: a case of left ventricular thrombosis. Am J Trop Med Hyg. Aug 2009;81(2):313-6. [Medline].
Viallet J, MacLean JD, Goresky CA, et al. Arctic trichinosis presenting as prolonged diarrhea. Gastroenterology. Oct 1986;91(4):938-46. [Medline].
Further Reading
Keywords
trichinosis, trichinellosis, trichinelliasis, trichinellosis, trichiniasis, Trichinella, Trichinella infection, trichinellosis infection, Trichinella species, Trichinella spiralis, T spiralis, Trichinella nativa, T nativa, Trichinella britovi, T britovi, Trichinella pseudospiralis, T pseudospiralis, Trichinella nelsoni, T nelsoni, undercooked meat, larval infection, obligate intracellular organism, food-borne infection


Overview: Trichinosis