eMedicine Specialties > Infectious Diseases > Parasitic Infections

Trichinosis

Author: Clinton Murray, MD, Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium
Contributor Information and Disclosures

Updated: Jan 4, 2010

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

Open table in new window

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.

Trichinosis. Life cycle of <em>Trichinella</em> s...

Trichinosis. Life cycle of Trichinella species parasite. (Image courtesy of the CDC)

Trichinosis. Life cycle of <em>Trichinella</em> s...

Trichinosis. Life cycle of Trichinella species parasite. (Image courtesy of the CDC)


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.

More on Trichinosis

Overview: Trichinosis
Differential Diagnoses & Workup: Trichinosis
Treatment & Medication: Trichinosis
Follow-up: Trichinosis
Multimedia: Trichinosis
References

References

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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

Contributor Information and Disclosures

Author

Clinton Murray, MD, Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium
Clinton Murray, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Association of Military Surgeons of the US, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Medical Editor

Pranatharthi Haran Chandrasekar, MD, Director of Infectious Disease Fellowship, Professor, Department of Internal Medicine, Harper Hospital, Wayne State University School of Medicine
Pranatharthi Haran Chandrasekar, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

John L Brusch, MD, FACP, Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance
John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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