Pediatric Trichinosis Workup

  • Author: Germaine L Defendi, MD, MS, FAAP; Chief Editor: Russell W Steele, MD  more...
 
Updated: Feb 24, 2015
 

Laboratory Studies

The following studies are indicated in trichinosis:

CBC (complete blood count) with indices

Peripheral eosinophilia is almost universal and is an early laboratory finding. Eosinophilia begins approximately 10 days after ingestion and may reach a peak of 5000/µL by 3-4 weeks after ingestion (range of about 50-70% of the white cell indices).

  • Eosinophil counts remain elevated during the acute parenteral stage of infection, regress slowly, and may remain elevated (although at lower levels) for 3 months post-infection.
  • Of grave concern is the absence of eosinophilia, eosinopenia or gradual disappearance of eosinophils during the parenteral phase of the illness. This serologic finding indicates an overwhelming infection, a sign of immunosuppression and carries a very poor prognosis. [3]

Leukocytosis (elevated white cell count) is typical and appears in the early phase of infection. The elevated white cell count subsides before eosinophil counts return to the normal reference range.

Muscle enzymes

Creatine kinase (CK), and lactate dehydrogenase (LDH) levels are elevated in 75-90% of cases. CK levels may increase as much as 10-fold, whereas the rise in LDH levels is less. Neither serum levels correlate with clinical disease severity.

Serum albumin

Hypoalbuminemia is a marker of severe clinical disease.

Serologic studies [18]

In the US, immunodiagnostic tests currently available are enzyme immunoassays (EIAs). EIAs detect Trichinella -specific antibodies and use antigen preparations that may be either crude extracts prepared from homogenates of T. spiralis muscle larvae or excretory-secretory (ES) products produced by cultured larvae. The key antigenic product is secreted from stichocytes located on the anterior side of the larva. The T. spiralis larva-1 group, also named as TSL-1 group of larval secretory antigens, are conserved in all species/isolates of Trichinella and thus can be used to detect infection in animals or people infected with any of Trichinella species currently recognized.[19, 20]

Trichinella -specific antibody levels are usually not detected until 3 to 5 weeks post-infection, well after the onset of acute-stage illness. Antibody development is also affected by the infecting dose of larvae. The higher infecting dose induces a faster patient's antibody response. Repeat serum specimens should be drawn several weeks apart to demonstrate sero-conversion in patients whose initial EIA specimen was negative.[19]

EIAs with ES antigens detect antibodies earlier than bentonite flocculation (BF) test in 25% of serum specimens from patients with acute infection. The BF test typically becomes positive 3 weeks post-infection. EIAs also remain positive for longer period of time after infection than the BF, and are reactive in a larger proportion of persons with no clinical evidence of trichinosis.[19, 3]

EIA is used for routine screening. Present recommendations are to test all EIA-positive specimens using the BF test, for confirmation. Positive results by both tests indicate Trichinella infection within the last several years.

IgG, IgM, and IgE antibodies are detectable in many patients; however, tests based on IgG antibodies are most sensitive. Typically these antibody levels peak in 2 or 3 months post-infection and then decline slowly over several years.

  • Tests based on immunoglobulin G (IgG)–ELISA specific antibodies are most sensitive (100% positive on the 50th day of infection). However, IgG antibodies can persist for years after infection, even if the disease process itself was benign or asymptomatic. Morakote et al. reported that 31 months after T. spiralis infection, the diagnostic sensitivity of IgG-ELISA was 88%. [21]
  • Morakote et al. further reported that IgM-ELISA’s peak sensitivity was 93% at 57th day post-infection. IgE-ELISA was 100% positive on the 85th day of infection. At 31 months post-infection, IgE-ELISA was positive 47%, while IgM-ELISA was sensitive only to 12%. Data from the IgM-ELISA appears to be a helpful indicator of infection within a 3-year (36 month) time frame.
  • Of the three antibodies, immunoglobulin E (IgE)–class antibodies appear first and are typical positive at the parenteral phase of trichinosis; however IgE antibodies are seldom detected during this time because their serum half-life is relatively short. An IgG antibody is detectable early in patients with high-titers, cited at 23 days post infection. [21]
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Imaging Studies

See the list below:

  • Plain radiography may show calcified densities in soft tissues, indicating old infection, but is not useful in diagnosing acute infection.
  • In patients with CNS involvement, brain CT scanning using ring enhancement following intravenous contrast reveals multiple small hypodense lesions in the hemispheric white matter.
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Other Tests

See the list below:

  • Stool examination: Charcot-Leyden crystals from eosinophils may be found in stools. Ova are not found in stools; larvae are rarely found in stools.
  • Antigen detection: Circulating antigens can be detected by EIA or immunoradiometric assay and by monoclonal antibodies specific for antigens obtained from T spiralis muscle larvae, although these tests are not typically used for diagnosis.
  • Polymerase chain reaction (PCR): In cases in which the diagnosis is questioned (eg, atypical presentations or patients who are immunosuppressed) or in early stages of infection when other test results are negative (eg, serologic studies), PCR testing used to detect Trichinella- specific DNA in muscle biopsy and blood specimens can be helpful.
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Procedures

See the list below:

  • Definitive diagnosis can be made via biopsy of a tender skeletal muscle. The muscle tissue (0.2 to 0.5 grams) is best examined unfixed under low microscope power to detect whole larvae. In cases in which the diagnosis is unclear, this biopsy sample may confirm the suspected diagnosis using parasitologic or histologic studies.
  • Electromyography (EMG) reveals changes of the myopathic type during the acute stage, but these changes are not pathognomonic for trichinosis. In most patients, bioelectric disturbances correspond in severity to the clinical course.
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Histologic Findings

See the list below:

  • Basophilic transformation of muscle fibers occurs within 4-5 days after larvae penetration (about 2 weeks post-ingestion) and is a valuable diagnostic criterion, even in cases, in which no larvae can be demonstrated. Only a portion of the affected muscle fiber undergoes basophilic transformation; the area that becomes the so-called larval nurse-cell.
    • Myofibrils disappear, the sarcoplasm becomes basophilic, and the cell nucleus is displaced to the center of the cell.
    • The larva can be observed within the affected nurse cell-larva complex.
    • Infiltration by eosinophils and mononuclear cells also occurs.
  • Attempting diagnosis before larvae begin to coil (ie, < 2 wk after larvae enter the muscle cell) creates a risk of confusing the worm appearance with fragments of muscle tissue.
  • Absence of a capsule and presence of a straight larva in the nurse-cell complex indicate an ongoing infection.
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Contributor Information and Disclosures
Author

Germaine L Defendi, MD, MS, FAAP Associate Clinical Professor, Department of Pediatrics, Olive View-UCLA Medical Center

Germaine L Defendi, MD, MS, FAAP is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

Ashir Kumar, MD, MBBS FAAP, Professor Emeritus, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine

Ashir Kumar, MD, MBBS is a member of the following medical societies: Infectious Diseases Society of America, American Association of Physicians of Indian Origin

Disclosure: Nothing to disclose.

Acknowledgements

Basim Asmar, MD Director, Department of Pediatrics, Division of Infectious Diseases, Children's Hospital of Michigan; Professor, Department of Pediatrics, Wayne State University School of Medicine

Basim Asmar, MD is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Leslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Swati Garekar, MBBS Staff Physician, Department of Pediatrics, Children's Hospital of Michigan

Swati Garekar, MBBS is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

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