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Trichinosis Workup

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

Laboratory Studies

CBC count

Obtain a CBC count.

Leukocytosis occurs in 65% of patients, with cell counts of up to 24,000/µL.

Eosinophilia typically rises 10 days after infection, with total eosinophil counts of up to 8700/µL (40%-80% of total WBC). The counts peak in 3-4 weeks and resolve over the next few months.

Nearly all patients with trichinosis, either symptomatic or asymptomatic, exhibit eosinophilia. The only exception is in severe cases, when the eosinophil count may be severely depressed. A low eosinophil count indicates an increased mortality rate.

Erythrocyte sedimentation rate

Erythrocyte sedimentation rates are usually within the reference range.

Creatine kinase

Obtain creatine kinase (CK) levels.[16]

CK levels are elevated to 17,000 U/L.

CK (isoenzyme myocardial band [MB]) elevations may indicate myocardial involvement; however, as many as 35% of patients without cardiac involvement may have elevated CK-MB levels.

Lactate dehydrogenase

Levels of lactate dehydrogenase isoenzymatic forms (ie, lactate dehydrogenase fraction 4 [LD4] and lactate dehydrogenase fraction 5 [LD5]) are elevated in 50% of patients.

Immunoglobulin E

Immunoglobulin E levels are typically elevated.


Serology results are not positive until 2-3 weeks after infection. They peak around the third month and may persist for years.

Serology ratios do not correlate with the severity of disease or the clinical course. However, a strong positive test result usually indicates an early infection.

Perform indirect hemagglutination.

Bentonite flocculation results are usually not positive for more than 1 year after infection.

Perform indirect immunofluorescence.

Latex agglutination results are usually not positive for more than 1 year after infection.

Enzyme-linked immunosorbent assay (ELISA) is 100% sensitive on day 50, with 88% of results remaining positive 2 years after infection.

Hypersensitivity skin test

The immediate hypersensitivity skin test is no longer commercially available. Reactions results are positive (5 mm) at approximately day 17 and remain positive for life.

Molecular techniques

Molecular techniques are being developed but have not been validated.


Imaging Studies

In patients with CNS involvement, CT scanning and MRI with contrast enhancement may reveal 3- to 8-mm nodular or ringlike lesions.


Other Tests

Electrocardiography may show the following:

  • Premature contractions
  • Prolongation of the PR intervals
  • Small QRS complexes with intraventricular block
  • Flattening or inversion of the T waves, especially lead II and precordial leads

Polymerase chain reaction is useful for isolating the parasite and subsequent genetic typing. it is used primarily as a research tool.




Electromyelography may be helpful in diagnosing moderate-to-severe infection, but no pathognomonic findings exist. The test result may reveal acute myositis or diffuse myopathic dysfunction.

Changes usually resolve 2-3 months after infection but may persist for 1-8 years.

Lumbar puncture

Lumbar puncture is used to evaluate for suspected neurologic disease.

Results are normal in 50%-75% of patients.

Larvae are found in 8%-24% in patients.

Eosinophilic meningitis may be present.

Muscle biopsy

Muscle biopsy provides a definitive diagnosis; however, it is rarely recommended except in difficult cases when serology tests are unhelpful.

Obtain a 0.5- to 1-g muscle biopsy specimen from the deltoid or gastrocnemius muscle because these are most easily accessible. The yield increases if the biopsy site is swollen or tender. Stain the specimen with hematoxylin and eosin (H&E) and examine multiple sections. Occasionally, larvae can be found after the muscle has been digested enzymatically.

If a biopsy is performed prior to larvae coiling (beyond day 17 of infection), worm tissue can be confused with muscle tissue.

A negative result does not necessarily exclude infection.


Histologic Findings

A histologic examination may reveal destruction of skeletal muscles, including a basophilic degeneration of the fibers observed on H&E-stained sections. Dead, nonencapsulated parasites can be observed. Muscle cells contain small hemorrhages and an accumulation of inflammatory cells (eg, eosinophils, lymphocytes, macrophages).

The results of a histologic examination in myocardial muscle are consistent with an immune-mediated reaction. Parasites migrate through the myocardium but do not encyst; however, a strong inflammatory reaction occurs, with numerous eosinophils, erythrocytes, fibrin deposits, and foci of necrotic myocardium. A mild-to-moderate pericardial effusion may also be present. Perivascular collections of eosinophils, lymphocytes, macrophages, and polymorphonuclear leukocytes develop in the CNS and are associated with areas of ischemia. Larvae may be surrounded by astrocytes and microglial cells.



Case definitions for human trichinosis include possible cases (not applicable), probable cases (patients who meet the clinical criteria and with an epidemiological link [below]), and confirmed cases (patients who meet the laboratory criteria and clinical criteria within the past 2 months).[13]

Clinical criteria - At least 3 of the following: (1) fever, (2) muscle soreness and pain, (3) gastrointestinal symptoms, (4) facial edema, (5) eosinophilia, or (6) subconjunctival, subungual, and retinal hemorrhages

Laboratory criteria - At least 1 of the following: (1) demonstration of Trichinella larvae in tissue obtained by muscle biopsy or (2) demonstration of Trichinella -specific antibody response by indirect immunofluorescence, ELISA, or Western blot

Epidemiological criteria - At least one of the following: (1) consumption of laboratory-confirmed parasitized meat, (2) consumption of potentially parasitized products from a laboratory-confirmed infected animal, or (3) epidemiological link to a laboratory-confirmed human case by exposure to the same common source

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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