Pediatric Trichinosis 

  • Author: Robert W Tolan Jr, MD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Jan 10, 2012
 

Background

In 1835, James Paget, a 21-year-old first-year medical student at Bartholomew's Hospital in London, observed the postmortem examination of a middle-aged man. The autopsy reported extensive pulmonary tuberculosis. Apart from the obvious, Paget noted numerous miniscule chalky spots in the corpse's muscles. He borrowed a scalpel and verified the bony texture of these lesions, which the professors deemed irrelevant. After borrowing a microscope from the nearby British Museum, and after diligent dissection, Paget concluded that the lesion consisted of a tiny calcified cyst surrounding a coiled threadlike worm. A pathologist at the medical school verified Paget's findings and gave it the genus name Trichina, from the Greek term for hair, and the species name spiralis.

Trichinosis is caused by ingestion of raw or undercooked meat infected with viable larvae of the tissue nematode Trichinella. Trichinella species occur widely in nature among approximately 150 species of mammals; however, pigs are the most commonly consumed reservoir hosts throughout the world. Humans are incidental hosts.

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Pathophysiology

Larvae gain access to the human host when raw or undercooked meat that harbors the infective larvae is ingested. Larvae excyst in the human stomach by acid-pepsin digestion. Upon reaching the upper small intestine, larvae invade the columnar epithelium and develop into adult worms in approximately 30 hours. These tiny obligate intracellular parasites occupy the cytoplasm of a row of enterocytes.

Males are approximately 1-1.5 mm long; females measure approximately 2-4 mm in length. As with most helminths, adult worms do not multiply within the human host. Worm load and disease severity depend on the number of larvae ingested. Starting approximately 6 days after ingestion, the female worms release large numbers of newborn larvae that penetrate the gut wall, enter the systemic circulation, and migrate to various tissues in the host. However, the larvae usually persist only in striated skeletal muscle cells and prefer active muscle groups such as the diaphragm, the tongue, and the masticatory, intercostal, and pectoral muscles. The larvae burrow into individual muscle fibers, which are transformed into nurse cells. The nurse cell–larva complex develops completely during the next 3 weeks.

After this period, the larvae, which are now approximately 1 mm in length, are infective to another host. In humans, the larvae at this stage have reached a dead end. Larvae may remain viable for years but usually die and calcify within the first year after formation. The presence of larvae in the circulation causes increased capillary permeability and vasculitis with fine intravascular thrombi. When the larval load is significant, these microvasculature changes lead to cardiovascular, lung, and CNS involvement.

A single fertilized Trichinella spiralis female produces approximately 500-1500 larvae over a period of 2-4 weeks; the female is then expelled in the feces because of the immune response of the host. In nature, the parasite's life cycle is maintained by carnivores that ingest infected meat and also by noncarnivorous animals that ingest food containing carcasses of infected animals.

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Epidemiology

Frequency

United States

Trichinosis is a disease that should be reported. The Centers for Disease Control and Prevention (CDC) case definition for trichinosis is " Trichinella –positive muscle biopsy or a positive serologic test for trichinosis in a patient with one or more clinical symptoms compatible with trichinosis such as eosinophilia, fever, myalgia, or periorbital edema."

In the 1940s, an average of 400 cases and 10-15 deaths were annually reported. The incidence has significantly decreased since then. From 1991-1996, 230 cases and 3 deaths were reported.[1] From 2002-2007, 66 cases were reported.[2] In approximately 60% of these cases, information on the suspected food product was available. The frequency of implicated meat was 60% pork, 23% bear meat, 10% walrus meat, and 7% cougar meat. Sausage was the most frequently implicated pork product. Sampling uncooked spiced pork used to prepare sausages is a common way to acquire infection. The vast majority of swine in the United States are grain-fed and uninfected. The small proportion fed raw meat garbage may become infected if the garbage contains trichinous scraps.

International

Trichinosis usually occurs as point-source outbreaks in all areas of the world except Australia and some South Pacific islands.[3, 4] Incidence in Europe is low because of mandatory inspection of pork for Trichinella species, although outbreaks have been reported.[5, 6] In Arctic regions, the main source of infection is meat from walrus, seal, and polar bear;[7] in Africa, the main source of infection is meat from wild canids and felids.

Mortality/Morbidity

The severity of the clinical course depends on such factors as the number of living larvae ingested and the number of newborn larvae produced per female.

  • Most infections are subclinical. When symptoms do occur, the illness is usually self-limited and is characterized by fever, myalgias, and periorbital edema. Rarely, the illness causes death.
  • With improved therapy, the mortality rate has decreased to approximately 0.3%. Death is usually due to myocarditis or CNS involvement, usually 3-5 weeks after ingestion.
  • Infection may have long-lasting sequelae (eg, muscle aches, headaches, eye disturbances, cardiac symptoms), especially in patients with severe or moderately severe acute infection.

Race

This infection has no racial predilection.

Sex

Both sexes are equally susceptible. Differential rates of infection between sexes may reflect differences in behavior related to food preparation.

Age

People of all age groups are susceptible.

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Contributor Information and Disclosures
Author

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Coauthor(s)

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.

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.

Specialty Editor Board

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

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

Disclosure: Nothing to disclose.

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.

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.

Daniel Rauch, MD, FAAP  Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine

Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine

Disclosure: Baxter Honoraria Consulting

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

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, and Southern Medical Association

Disclosure: Nothing to disclose.

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