Trichinosis

Jan 8, 1998

Trichinosis is caused by the nematode parasite Trichinella. Five species of Trichinella are currently recognized to infect humans [1]:

  •  T. spiralis is found worldwide in a great variety of carnivorous and omnivorous animals

  •  T. nativa  is found in arctic regions and infects bears

  •  T. nelsoni is present in equatorial Africa where it is common in felid predators and scavenger animals, like hyenas and bush pigs

  •  T. bitovi is found in temperate areas of Europe and western Asia in carnivores but not domestic swine

  •  T. pseudospiralis is found in mammals and birds worldwide

Most human infections are acquired by eating meat containing cysts of Trichinella. Common meats include inadequately cooked pork, although walrus, bear, cougar, wild boar, and horse meat can also be sources of trichinosis. Since cattle are herbivores, they are not naturally infected, although beef can become contaminated, incidentally or deliberately, with Trichinella larvae from pork during processing.

Within the United States, about 50 cases of trichinosis occur annually with occasional deaths. Most cases are from domestically raised or commercially obtained pork. Clusters of cases tend to occur when groups have consumed meat from a common infected animal.

Trichinella larvae in meat may be rendered noninfectious by heating to a temperature of 77ºC. Freezing at -15ºC for three weeks, as in a home freezer, will also generally kill larvae, although arctic species are more resistant to freezing and may remain viable.

CLINICAL MANIFESTATIONS — The severity of infection generally correlates with the numbers of ingested larvae. Mild infections, with less than 10 larvae/gram of muscle, can be subclinical. With heavier infections, two stages may be recognized [2]:

  •  The intestinal stage occurs between the second and seventh days after ingestion, when encysted larvae are liberated from the meat by gastric juices. Larvae mature into adult worms which burrow into the intestinal mucosa. Fertilized female worms release new larvae beginning about one week after ingestion and continuing for up to five weeks, depending upon the severity of the infection. This stage may be asymptomatic or may be accompanied by intestinal symptoms, including abdominal aches, nausea, vomiting, and diarrhea. Prolonged diarrhea lasting for weeks has been attributed to repeated reinfections in previously infected and sensitized patients [3].

  •  The muscle stage develops after the first week and represents the period when adult-derived larvae in the intestines enter the bloodstream and disseminate hematogenously. Larvae then enter skeletal muscle. For all species except T. pseudospiralis, each larva becomes encysted within a host-derived cell, termed a nurse cell (show histology 1);

T. pseudospiralis larvae remain in the muscle without forming cysts. Both encysted and free Trichinella larvae remain viable for years.

During the muscle phase of infection, the cardinal clinical findings of trichinosis develop. These include subungual splinter hemorrhages (show picture 1),

conjunctival and retinal hemorrhages, periorbital edema and chemosis (show picture 2).

As larvae enter skeletal muscles, muscle pain, tenderness, swelling, and weakness occur. Less common manifestations include macular or urticarial rashes, headache, cough, dyspnea, and dysphagia may develop.

Laboratory findings — During the early intestinal stage there are no specific laboratory abnormalities. However, leukocytosis and eosinophilia appear during the second week of the muscle stage. The proportion of eosinophils rises to a maximum of 20 to 90 percent in the third or fourth week. Eosinophilia may disappear in some heavily infected patients and is considered to be a poor prognostic sign. The eosinopenia in this setting is probably due to superimposed bacterial infections and inflammation. Nonspecific findings include elevated serum muscle enzymes (creatine kinase and lactate dehydrogenase) and hypergammaglobulinemia. (See "Muscle enzymes in the evaluation of neuromuscular diseases").

Although larvae encyst only in skeletal muscle, there may be pulmonary, cardiac or central nervous system involvement in serious infections. A fatal outcome in acute trichinosis usually results from myocarditis, encephalitis, or pneumonia.

Cardiac disease — Cardiac complications are the most frequent cause of death in severe trichinosis [2,4]. Although larvae do not encyst in cardiac muscle, larvae elicit an eosinophil-enriched inflammatory response and myocarditis [2,5]. Arrhythmias are the likely causes of death in many patients with trichinella myocarditis.

Neurologic manifestations — Neurologic manifestations, which may include signs of meningitis or encephalitis, develop in 10 to 24 percent of patients with severe trichinosis [2,5,6]. Neurologic disease may develop early or late, and can be diffuse or focal in nature. Pathologic findings can include edema, hemorrhage, emboli, and perivascular infiltrates in fatal cases.

Pulmonary disease — Serious pulmonary involvement in trichinosis is infrequent, being recorded in only 6.5 percent of 856 hospitalized patients with acute trichinosis [7]. Pulmonary involvement may result from direct larval invasion of pulmonary tissues, myositis involving respiratory muscles, or secondary pyogenic pneumonia. Respiratory symptoms can also be caused by congestive heart failure due to myocarditis.

  •  Direct pulmonary involvement — Early in the stage of muscle invasion, when intravascular larvae are passing through the lungs, a dry, nonproductive cough is a common symptom. Chest x-ray at this time may reveal patchy basilar infiltrates, small micronodular lesions, or pleural effusions. These radiographic findings resolve spontaneously over one to two weeks.

Bronchitis is common between the third and fifth weeks of infection. As an example, bronchitis was observed in 40 percent of patients in one epidemic [2]. The mucoid sputum commonly seen in these patients may contain many eosinophils.

  •  Respiratory myositis — Myositis develops in response to encysted trichinella larvae. The diaphragm usually has a relatively high density of encysted larvae compared to other skeletal muscles. Diaphragmatic involvement can result in lower thoracic or epigastric pain and can produce sufficient weakness of the diaphragm to compromise respiratory function [4]. Painful intercostal myositis may further impair respiratory function [8]. These symptoms are often most prominent in the second and third weeks of severe infection.

Symptomatic involvement of the upper airway muscular can also occur. Affected patients may present with hoarseness or dysphagia due to involvement of the laryngeal muscles or the muscles of deglutition, respectively.

  •  Secondary pneumonia — Superimposed bacterial pneumonia due to prolonged bed rest and impaired pulmonary toilet may develop in hospitalized patients with trichinosis in the later stages of infection. In one large series of patients hospitalized with trichinosis, bronchopneumonia occurred in about 1 percent [7].

Course — With most Trichinella infections, progressive muscle encystment is associated with resolution of clinical manifestations even though the encysted larvae remain viable. An exception to this general rule occurs with T. pseudospiralis infections. These larvae do not encyst and early experience with human infection suggests that the manifestations of T. pseudospiralis may include fatigue, postexercise weakness, and myositis that persist for several years [9].

DIAGNOSIS — The diagnosis of trichinosis should be considered in patients with periorbital edema, myositis, and eosinophilia. Trichinosis should be particularly suspected in individuals with these symptoms and a history of ingesting inadequately cooked meat, particularly pork, or meat ingested by other symptomatic individuals.

Serologic tests, including enzyme-linked immunosorbent assays, are available and reliable. However, antibody levels are not detectable until after three or more weeks of infection and are therefore not useful for early diagnosis.

The definitive diagnosis is made by finding larvae in biopsied muscle (show histology 1). The yield of muscle biopsy is highest in symptomatic muscles and near a tendinous insertion. In addition to routine histopathologic examination, the muscle should be examined after enzymatic digestion to free larvae. The specimen can also be examined undigested in a preparation of unfixed muscle compressed between microscope slides (show histology 2).

TREATMENT — The clinical course of most Trichinella infections is uncomplicated and self-limited. As a result, specific therapy is usually not required. Corticosteroids with mebendazole or albendazole are used for symptomatic Trichinella infection involving the central nervous system, myocardium, or respiratory muscles [10]. Mebendazole is given at 200 to 400 mg TID for three days, then 400 to 500 mg TID for ten days. Albendazole has been effective in the treatment of T. pseudospiralis infection [9].