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Trichinosis Medication

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

Medication Summary

It is difficult to differentiate the efficacy of drug therapy from natural recovery of infection in mild-to-moderate cases. Factors such as the Trichinella species involved, intensity and length of infection, and host response can aid in deciding on the treatment course.[17] The mainstays of therapy include bed rest, antipyretics, and analgesics. Anthelmintic medications and steroids have a limited role in therapy. If anthelmintic medications are used, the drug of choice is albendazole, because it appears to have the best adverse-effect profile and efficacy.



Class Summary

The benzimidazole drugs albendazole, mebendazole, and thiabendazole are the available medications. These drugs bind helminthic beta-tubulin, which prevents microtubule assembly and inhibits glucose uptake, resulting in parasite immobilization and death.

Albendazole (Albenza)


Decreases ATP production in worms, causing energy depletion, immobilization, and death. To avoid inflammatory response in CNS, administer with anticonvulsants and high-dose glucocorticoids. Available as 200-mg tabs. Practically insoluble in water; absorption enhanced if taken with fatty meal. Good penetration into CNS and better tolerated than thiabendazole.

Mebendazole (Vermox)


Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible intestine, where helminths dwell. Available as 100-mg chewable tabs.

Thiabendazole (Mintezol)


For mixed helminthic infections; inhibits helminth-specific mitochondrial fumarate reductase; alleviates symptoms of trichinosis during invasive phase. Little value in disease that spreads beyond lumen of intestines; absorption from GI tract is poor. Use limited because of adverse-effect profile. Available in 500-mg tab and 500-mg/5-mL susp. Administer with meals.



Class Summary

Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients with pain.

Acetaminophen (Aspirin-Free Anacin, Tylenol, Feverall)


DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, upper GI disease, or current therapy with oral anticoagulants. Reduces fever by acting directly on hypothalamic heat-regulating centers, which increases dissipation of body-heat via vasodilation and sweating.



Class Summary

Steroids decrease inflammatory response in the host.

Prednisone (Sterapred)


Use in severe infections with signs of shock or significant pulmonary, CNS, or cardiac involvement. Steroids reduce number of worms expelled from GI tract, which may increase number of larvae produced.

Contributor Information and Disclosures

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.


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.


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 (
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 (
Trichinella larvae, in pressed bear meat, partially digested with pepsin. Courtesy of the US Centers for Disease Control and Prevention ((
Larvae of Trichinella from bear meat. Courtesy of the US Centers for Disease Control and Prevention (
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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