eMedicine Specialties > Pediatrics: General Medicine > Parasitology

Trichinosis

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
Coauthor(s): Swati Garekar, MBBS, Staff Physician, Department of Pediatrics, Children's Hospital of Michigan; 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
Contributor Information and Disclosures

Updated: Jan 27, 2009

Introduction

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.

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.

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 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. Incidence in Europe is low because of mandatory inspection of pork for Trichinella species. In Arctic regions, the main source of infection is meat from walrus, seal, and polar bear; 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.

Clinical

History

Most cases of trichinosis are subclinical. Symptoms appear only in heavily infected individuals. The predominant type of symptoms (ie, GI or systemic) varies according to the Trichinella species ingested. The incubation period varies from a few days to 2 months and is generally shorter when the disease follows a more severe course.

• Early (enteral) stage
  • During the first week after ingestion, GI symptoms such as diarrhea (most common) and abdominal discomfort develop. These symptoms are often mistaken for food poisoning or viral gastroenteritis.
  • GI symptoms are absent in mildly infected patients, who ingest only a few larvae. In such patients, symptoms related to the migratory and invasive phases are usually clinically detected first.
• Acute stage
  • The acute stage, caused by larval invasion of host tissues, starts approximately 10-14 days after ingestion and lasts approximately 2 months.
  • Hallmarks of this stage are fever (in approximately 90% of patients), myalgias (in approximately 90% of patients), and periorbital edema (in approximately 80% of patients).
  • Myalgias are common in the masseters, diaphragm, and intercostal muscles. Pain is usually during exertion. Pain at rest usually occurs only in patients with severe disease.
  • Less frequent symptoms during the tissue invasion phase include headache (in approximately 50% of patients) and skin rash (in approximately 20% of patients).
• Late stage
  • The late stage usually begins 5-7 weeks after the disease is contracted and is characterized by the disappearance of most of the early signs and symptoms.
  • Myalgias and fatigue frequently persist. In one prospective study, they persisted in 98% of patients at 2 years and in 25% of patients after 10 years.²
• Patients with Trichinella nativa infection experience symptoms related only to the enteral phase; onset is delayed compared to that of infection with T spiralis, although T nativa infections may be fatal.³
• Trichinella nelsoni and Trichinella britovi both have low pathogenicity in their enteral and parenteral phases.

Physical

• Fever exhibits variable intensity and duration, lasting for a few days in mild infection and up to 3-6 weeks in severe infections. Despite the fever, patients appear to be in good condition.
• Symptoms due to increased interstitial fluid include the following:
  • Periorbital edema is symmetrical and produces a characteristic aspect, making patients unrecognizable. For this reason, trichinosis is often called the disease of big heads.
  • Muscle tenderness and weakness are secondary to pain.
• Symptoms due to vasculitis include subconjunctival and nailbed hemorrhages.
• If the heart, lungs, or nervous system is involved, findings can suggest pericarditis, myocarditis, pneumonitis, or encephalopathy.

Causes

• Most human infections involve T spiralis, the only Trichinella species that commonly infects pigs and rats.
• T spiralis and Trichinella pseudospiralis are found worldwide in many carnivorous and omnivorous animals. T pseudospiralis is the only species that does not encyst. Only one case of human infection with T pseudospiralis has been reported.
• T britovi is found in carnivores of Europe and western Asia (eg, boars, foxes). T nativa infects Arctic bears; T nelsoni is common in African predators and scavengers (eg, hyenas, lions, panthers).

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