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Trichinosis

  • Author: Darvin Scott Smith, MD, MSc, DTM&H; Chief Editor: Burke A Cunha, MD  more...
 
Updated: Nov 16, 2015
 

Background

Trichinosis (trichinellosis) is the result of infection by a parasitic nematode belonging to the genus Trichinella. Trichinosis, although often unrecognized and underreported, has been an important disease for thousands of years. Virtually all mammals are susceptible to infection; however, humans are especially prone to developing clinical disease.[1] Humans are incidentally infected when they ingest inadequately cooked meat that contains larvae of Trichinella species. Symptomatic infections characterized by diarrhea, myositis, fever, and periorbital edema develop when large numbers of larvae are ingested.[2]

Species of Trichinella responsible for the infection are widely geographically distributed (see table), with habitats including the Arctic, temperate lands, and the tropics.[3]

Table 1. Biologic and Zoogeographic Features of Trichinella Species (Open Table in a new window)

Species Distribution Major Hosts Reported from Humans
T spiralis Cosmopolitan Domestic pigs, wild mammals Yes
T britovi Eurasia/Africa Wild mammals Yes
T murrelli North America Wild mammals Yes
T nativa Arctic/subarctic, Palaearctic Bears, foxes Yes
T nelsoni Equatorial Africa Hyenas, felids Yes
T pseudospiralis * Cosmopolitan Wild mammals, birds Yes
T papuae * Papua New Guinea, Thailand Pigs, crocodiles Yes
T zimbabwensis * East and South Africa Crocodiles, lizards, lions No
* Nonencapsulating types      

Reprinted from Adv Parasitol, Vol 63, Murrell KD, Pozio E, Systematics and epidemiology of Trichinella, pg 367, 2006, with permission from Elsevier.

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Pathophysiology

Trichinella species require 2 hosts to maintain their life cycles. After development in a first 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.

Trichinellosis is acquired by ingesting meat conta Trichinellosis is acquired by ingesting meat containing cysts (encysted larvae) of Trichinella. After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa, where they develop into adult worms (females, 2.2 mm in length; males, 1.2 mm; 4-week life span in the small bowel). After 1 week, the females release larvae that migrate to the striated muscles, where they encyst. Trichinella pseudospiralis, however, does not encyst. Encystment is completed in 4-5 weeks, and the encysted larvae may remain viable for several years. Ingestion of the encysted larvae perpetuates the cycle. Rats and rodents are primarily responsible for maintaining the endemicity of this infection. Carnivorous/omnivorous animals, such as pigs or bears, feed on infected rodents or meat from other animals. Different animal hosts are implicated in the life cycle of the different species of Trichinella. Humans are accidentally infected when eating improperly processed meat of these carnivorous animals (or eating food contaminated with such meat). Life cycle image and information courtesy of DPDx.

The life cycle begins when raw or inadequately cooked meat that contains viable larvae housed inside a cyst wall (nurse cells) is consumed. 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 Trichinella life cycle is complete when a compatible host ingests the infected muscle (see images below).

Encysted larvae of Trichinella species in muscle t Encysted larvae of Trichinella species in muscle tissue, stained with hematoxylin and eosin (H&E). The image was captured at 400X magnification. Courtesy of the US Centers for Disease Control and Prevention (http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.htm).
Trichinella larvae, in pressed bear meat, partiall Trichinella larvae, in pressed bear meat, partially digested with pepsin. Courtesy of the US Centers for Disease Control and Prevention ((http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.htm).
Larvae of Trichinella from bear meat. Courtesy of Larvae of Trichinella from bear meat. Courtesy of the US Centers for Disease Control and Prevention (http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.htm).

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).

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Epidemiology

Frequency

United States

National surveillance has documented a decline in the reported incidence of trichinellosis in the United States since 1947, the first year nationwide data were collected systematically. Between 2002 and 2007, 66 cases of trichinosis were reported to the Centers for Disease Control and Prevention (CDC).[4] Those cases for which a supplementary case report form was not submitted or that did not meet the case definition were excluded from analysis.

Of the 66 cases reported between 2002 and 2007, a total of 12 (18%) cases were excluded from analysis. Associated meat products were classified as either pork or meat products other than pork and were identified for 43 (80%) cases. Meat products other than pork were associated with 27 (50%) cases: 21 with bear meat, 1 with either bear or deer meat, 1 with cougar meat, 1 with deer meat, 1 with walrus or seal meat, and 2 with commercial beef. Pork was associated with 10 (19%) cases: 7 with commercial pork, 2 with noncommercial pork, and 1 with an unspecified type of pork. Of the 7 cases associated with consumption of commercial pork, 5 were linked to US commercial pork and 2 were attributed to pork ingested during travel in Asia.[4]

Trichinella is also tied to geopolitical factors, including movement of persons, livestock, and food (especially including 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. In 2008, an outbreak in Northern California affected 38 individuals who ate black bear infected with T murrelli.[5] Data have also shown the presence of T murrelli in raccoons and coyotes.[6]

Table 2. Number of Trichinellosis Cases and Outbreak Cases, by Reporting State -- United States, 2002--2007[4] (Open Table in a new window)

State 2002 2003 2004 2005 2006 2007 Total Outbreak cases
Alaska 7 0 0 3 0 0 10 8
California 0 2 1 2 4 1 10 2
Florida 0 0 0 1 1 0 2 0
Illinois 1 0 0 0 0 0 1 0
Maryland 0 0 0 0 1 0 1 0
Massachusetts 0 0 0 1 0 0 1 0
Michigan 0 0 0 3 0 0 3 0
Minnesota 0 0 0 0 3 0 3 2
New Hampshire 0 1 0 0 0 0 1 0
New Jersey 0 0 0 0 2 1 3 0
New York 0 1 0 0 0 3 4 2
North Dakota 0 0 2 0 0 0 2 0
Ohio 0 0 0 1 0 0 1 0
Pennsylvania 1 0 1 3 0 0 5 0
Rhode Island 0 0 1 1 0 0 2 0
Tennessee 0 2 0 0 1 0 3 2
Vermont 1 0 0 0 0 0 1 0
Washington 0 0 0 0 1 0 1 0
Total 10 6 5 15 13 5 54 16

 

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 and Hungary due to political changes and regional food habits.[7, 8] 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.[9] Studies are underway to determine the incidence of trichinosis in sub-Saharan Africa and developing countries.[10, 11]

The worldwide incidence of trichinosis has declined substantially during the past few decades, but outbreaks are still frequent, especially in developing countries.[12]

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

Although Trichinella infections are related to cultural differences in food cooking and storing methods (eg, the inadequate cooking or freezing of meat), outcomes do not vary based on race among infected individuals.

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. The figure below shows the cumulative number of patients with trichinellosis in the United States between 2002 and 2007, displayed by sex and age group. During this time period, a total of 52 cases were reported for persons whose age was known. Age was unknown for an additional patient, and sex was unknown for another patient. Of the 54 cases, 35 occurred in males and 19 in females. For the 53 patients whose age was known, the median age was 39 years (range: 2-73 years).

Cumulative number* of patients with trichinellosis Cumulative number* of patients with trichinellosis, by sex and age group, in the United States 2002-2007. (*N = 52 years. Age was unknown for one patient, and sex was unknown for another patient.) Courtesy of the US Centers for Disease Control and Prevention (http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5809a1.htm).

For more information on the specific epidemiology of trichinosis in children, see Pediatric Trichinosis.

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Contributor Information and Disclosures
Author

Darvin Scott Smith, MD, MSc, DTM&H Adjunct Associate Clinical Professor, Department of Microbiology and Immunology, Stanford University School of Medicine; Chief of Infectious Diseases and Geographic Medicine, Department of Internal Medicine, Kaiser Redwood City Hospital

Darvin Scott Smith, MD, MSc, DTM&H is a member of the following medical societies: American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society of Travel Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Lauren E Wedekind Stanford University

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

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, 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, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Stephanie A Nevins Research Assistant, Department of Genetics, Snyder Lab, Stanford University School of Medicine

Disclosure: Nothing to disclose.

Acknowledgements

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.

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Trichinellosis is acquired by ingesting meat containing cysts (encysted larvae) of Trichinella. After exposure to gastric acid and pepsin, the larvae are released from the cysts and invade the small bowel mucosa, where they develop into adult worms (females, 2.2 mm in length; males, 1.2 mm; 4-week life span in the small bowel). After 1 week, the females release larvae that migrate to the striated muscles, where they encyst. Trichinella pseudospiralis, however, does not encyst. Encystment is completed in 4-5 weeks, and the encysted larvae may remain viable for several years. Ingestion of the encysted larvae perpetuates the cycle. Rats and rodents are primarily responsible for maintaining the endemicity of this infection. Carnivorous/omnivorous animals, such as pigs or bears, feed on infected rodents or meat from other animals. Different animal hosts are implicated in the life cycle of the different species of Trichinella. Humans are accidentally infected when eating improperly processed meat of these carnivorous animals (or eating food contaminated with such meat). Life cycle image and information courtesy of DPDx.
Cumulative number* of patients with trichinellosis, by sex and age group, in the United States 2002-2007. (*N = 52 years. Age was unknown for one patient, and sex was unknown for another patient.) Courtesy of the US Centers for Disease Control and Prevention (http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5809a1.htm).
Encysted larvae of Trichinella species in muscle tissue, stained with hematoxylin and eosin (H&E). The image was captured at 400X magnification. Courtesy of the US Centers for Disease Control and Prevention (http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.htm).
Trichinella larvae, in pressed bear meat, partially digested with pepsin. Courtesy of the US Centers for Disease Control and Prevention ((http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.htm).
Larvae of Trichinella from bear meat. Courtesy of the US Centers for Disease Control and Prevention (http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.htm).
Table 1. Biologic and Zoogeographic Features of Trichinella Species
Species Distribution Major Hosts Reported from Humans
T spiralis Cosmopolitan Domestic pigs, wild mammals Yes
T britovi Eurasia/Africa Wild mammals Yes
T murrelli North America Wild mammals Yes
T nativa Arctic/subarctic, Palaearctic Bears, foxes Yes
T nelsoni Equatorial Africa Hyenas, felids Yes
T pseudospiralis * Cosmopolitan Wild mammals, birds Yes
T papuae * Papua New Guinea, Thailand Pigs, crocodiles Yes
T zimbabwensis * East and South Africa Crocodiles, lizards, lions No
* Nonencapsulating types      
Table 2. Number of Trichinellosis Cases and Outbreak Cases, by Reporting State -- United States, 2002--2007 [4]
State 2002 2003 2004 2005 2006 2007 Total Outbreak cases
Alaska 7 0 0 3 0 0 10 8
California 0 2 1 2 4 1 10 2
Florida 0 0 0 1 1 0 2 0
Illinois 1 0 0 0 0 0 1 0
Maryland 0 0 0 0 1 0 1 0
Massachusetts 0 0 0 1 0 0 1 0
Michigan 0 0 0 3 0 0 3 0
Minnesota 0 0 0 0 3 0 3 2
New Hampshire 0 1 0 0 0 0 1 0
New Jersey 0 0 0 0 2 1 3 0
New York 0 1 0 0 0 3 4 2
North Dakota 0 0 2 0 0 0 2 0
Ohio 0 0 0 1 0 0 1 0
Pennsylvania 1 0 1 3 0 0 5 0
Rhode Island 0 0 1 1 0 0 2 0
Tennessee 0 2 0 0 1 0 3 2
Vermont 1 0 0 0 0 0 1 0
Washington 0 0 0 0 1 0 1 0
Total 10 6 5 15 13 5 54 16
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