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Pediatrics: General Medicine > Parasitology
Trichinosis
Article Last Updated: Jan 29, 2008
AUTHOR AND EDITOR INFORMATION
Section 1 of 10
Author: Robert W Tolan Jr, MD, Chief 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, 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
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
Editors: Ashir Kumar, MBBS, MD, FAAP, Professor, Department of Pediatrics and Human Development, College of Human Medicine, Michigan State University; Consulting Staff, Department of Pediatrics, EW Sparrow Hospital; Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc; Leslie L Barton, MD, Professor, Program Director, Department of Pediatrics, University of Arizona School of Medicine; Daniel Rauch, MD, FAAP, Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine; Russell W Steele, MD, Professor and Vice Chairman, Department of Pediatrics, Head, Division of Infectious Diseases, Louisiana State University Health Sciences Center
Author and Editor Disclosure
Synonyms and related keywords:
food-borne illnesses, parasitic infections, Trichinella britovi, T britovi, Trichinella nativa, T nativa, Trichinella nelsoni, T nelsoni, Trichinella pseudospiralis, T pseudospiralis, Trichinella spiralis, T spiralis, trichinelliasis, trichinellosis, trichiniasis, trichinosis, pulmonary tuberculosis, myalgia, periorbital edema, myocarditis, gastroenteritis, vasculitis, pericarditis, myocarditis, pneumonitis, encephalopathy
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.
History
Most infections 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).
Acute Poststreptococcal Glomerulonephritis
Angioedema
Fascioliasis
Food Poisoning
Gastroenteritis
Influenza
Myocarditis, Nonviral
Myocarditis, Viral
Rheumatic Fever
Sinusitis
Toxocariasis
Other Problems to be Considered
- Diagnosis is particularly difficult in sporadic cases or in cases with atypical presentation.
- Myalgias are also common in dermatomyositis and typhoid fever.
- Periorbital swelling can be mistaken for allergic reactions.
- Eosinophilia, in the absence of other typical symptoms, can be mistaken for numerous parasitic infections.
- CNS symptomatology may mimic encephalitis.
- Glomerulonephritis should be considered.
Lab Studies
- CBC count
- Eosinophilia is almost universal and is among the earliest laboratory findings. Eosinophilia begins approximately 10 days after ingestion and may reach a peak of 5000/µL by 3-4 weeks after ingestion.
- Counts remain elevated during the acute stage of infection, regress slowly, and may remain elevated at lower levels for 3 months postinfection.
- An extremely severe course of trichinosis is accompanied by eosinopenia, a manifestation of immunosuppression.
- Leukocytosis is also typical and appears early in infection. The condition subsides before eosinophil counts return to the reference range.
- Serologic studies
- The anterior half of the larva presents stichosomes with discoid cells (ie, stichocytes), which are secretory, and their product is highly antigenic. Antigen preparations may be crude homogenates of T spiralis muscle larvae or excretory-secretory products produced by cultured larvae. The T spiralis larvae group 1 of larval secretory antigens are common in all Trichinella species and can be used to detect infection with any species.4
- These test results are not positive until at least 2 weeks after ingestion. Larger numbers of infecting larvae cause faster antibody response in patients.
- Immunoglobulin E (IgE)–class antibodies appear first and are typical for the acute stage of the disease, but they are seldom detected during the acute stage because their half-life in serum is relatively short.
- Tests based on immunoglobulin G (IgG)–specific antibodies are most sensitive (100% 50 d after ingestion). However, IgG antibodies can persist for years after infection, even if the disease has been benign or asymptomatic; therefore, a rising titer is needed to establish the diagnosis of acute infection.
- Antibodies can be detected using enzyme immunoassay (EIA) or the bentonite flocculation (BF) test. An EIA detects antibodies earlier than the BF test, and results also remain positive for longer periods than the BF test. However, EIA results are less specific than those of the BF test.
- EIA is used for routine screening. Test all EIA-positive specimens using the BF test for confirmation. A positive result by both tests indicates a Trichinella infection within the last several years.
- Muscle enzymes
- Muscle enzyme, creatine kinase (CK), and lactate dehydrogenase (LDH) levels are elevated in approximately 75-90% of cases.
- CK levels may increase as much as 10-fold, whereas the rise in LDH levels is less. Neither serum level correlates with the severity of clinical disease.
- Serum albumin: Hypoalbuminemia is a marker for severe trichinosis.
Imaging Studies
- 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.
Other Tests
- 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: In cases in which the diagnosis is questionable (eg, atypical presentations or patients who are immunosuppressed) or in early stages of infection when other test results are negative (eg, serologic studies), polymerase chain reaction testing used to detect Trichinella-specific DNA in muscle biopsy and blood specimens is valuable.
Procedures
- Muscle biopsy is usually unnecessary. However, in cases in which the diagnosis is in question, a sample obtained from a tender swollen muscle may confirm the diagnosis using parasitologic or histologic studies.
- Electromyography 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.
Histologic Findings
- Basophilic transformation of muscle fibers occurs within 4-5 days after larval penetration and is a valuable diagnostic criterion, even in cases in which no larvae can be demonstrated.
- Basophilic transformation affects only a portion of the affected muscle fiber, which becomes the so-called 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.
- Attempting diagnosis before larvae begin to coil (ie, <2 wk after larvae enter the muscle cell) creates a risk of confusing the worm with fragments of muscle tissue.
- Encapsulation begins approximately 2 weeks after ingestion. The capsule contains the larva and fragments of basophilically transformed sarcoplasm that directly surround the larva.
- Infiltration by eosinophils and mononuclear cells also occurs.
- The absence of a capsule and the presence of a straight larva in the complex indicate ongoing infection.
Medical Care
Attention to basic and advanced life support is mandatory in patients who present with severe cardiopulmonary or neurologic embarrassment.
Surgical Care
Surgery is unnecessary unless a biopsy is required.
Consultations
Consultation with an infectious diseases specialist is often helpful. Consultation with a neurologist or cardiologist may be appropriate for patients who present with corresponding organ involvement.
Diet
Avoidance of under-cooked meat is appropriate.
Activity
Patient tolerance determines activity restrictions; myalgias are most common in association with activity during the acute stage.
Useful drugs in the management of trichinosis include anthelminthics to eradicate adult worms, corticosteroids for anti-inflammatory effects, and nonsteroidal anti-inflammatory drugs or salicylates for analgesia. Salicylates are best avoided in children and teenaged patients with febrile illness.
Drug Category: Anthelminthics
Mebendazole and albendazole effectively eliminate adult worms from the GI tract. Thiabendazole is not recommended because of higher incidence of adverse effects. Evidence of these drugs' efficacy against tissue larvae is not well established. Because most patients continue to harbor adult worms in the gut during the acute phase of infection, treat all patients with confirmed or suspected trichinosis to prevent continued production of newborn larvae. A double-blind placebo-controlled treatment trial of Trichinella myositis in adults showed that mebendazole and thiabendazole improve muscle tenderness compared with placebo.5
| Drug Name | Albendazole (Albenza) |
| Description | Not approved by the FDA to treat trichinosis. Inhibits microtubule polymerization by binding to cytoplasmic beta-tubulin. Prevents use of nutrients by the parasite by affecting intestinal cells of the parasite, essentially starving it to death. Selectively toxic to parasites at indicated dose because binding to parasite beta-tubulin occurs at a much lower concentration than binding to mammalian protein. |
| Adult Dose | 400 mg PO bid for 8-14 d |
| Pediatric Dose | <6 years: Not established >6 years: Administer as in adults |
| Contraindications | Documented hypersensitivity |
| Interactions | Coadministration with carbamazepine may decrease efficacy; dexamethasone, cimetidine, and praziquantel may increase toxicity |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | Information on precautions is based on use treating patients with hydatid disease and neurocysticercosis, for which the drug is used for prolonged periods (ie, 8-30 d for neurocysticercosis, 3 mo for hydatid disease); embryo-toxic and teratogenic in pregnant rats and rabbits; no adequate studies have been conducted in pregnant women; no deleterious effects were recorded among 10 women who were accidentally exposed to high doses of albendazole (for systemic infection) during first trimester and monitored to term; excreted in animal milk; not known whether it is excreted in human milk; carefully evaluate patients with abnormal liver function test results prior to commencing therapy; most common adverse effect is reversible increase in serum aminotransferases (16%); abdominal pain, diarrhea, nausea, dizziness, and headache sometimes occur; reversible reductions in total WBC count in <1% of patients |
| Drug Name | Mebendazole (Vermox) |
| Description | Inhibits microtubule polymerization by binding to cytoplasmic beta-tubulin. Prevents use of nutrients by the parasite by affecting intestinal cells of the parasite, essentially starving it to death. Selectively toxic to parasites at indicated dose because binding to parasite beta-tubulin occurs at a much lower concentration than binding to mammalian protein. The tab may be chewed, swallowed, or crushed and mixed with food. No fasting or purging is required. |
| Adult Dose | 200-400 mg PO tid for 3 d, then 400-500 mg tid for 10 d |
| Pediatric Dose | <2 years: Not established >2 years: Administer as in adults |
| Contraindications | Documented hypersensitivity |
| Interactions | Carbamazepine and phenytoin may decrease effects; cimetidine may increase levels |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
|
| Precautions | Found to be embryo-toxic and teratogenic in pregnant rats at single PO dose as low as 10 mg/kg (approximately equal to the human dose based on mg/m2); based on these findings, not recommended in pregnant women, especially in first trimester; no adequate studies of administration in pregnant women have been conducted, although postmarketing studies in 170 pregnant women who had inadvertently taken the drug did not reveal higher than usual incidence of spontaneous abortions or malformations Not known whether mebendazole is excreted in human milk; therapy may not eradicate dormant larvae residing in extraintestinal tissues because drug is poorly absorbed into the systemic circulation; abdominal pain and diarrhea may occur in massive infections and expulsion of GI worms; rare reports of neutropenia and agranulocytosis when used for prolonged periods and at higher than recommended doses; elevation of liver enzymes and hepatitis (rare) have been noted after mebendazole use for prolonged periods and when administered in dosages substantially above those recommended |
Drug Category: Corticosteroids
Many clinical features and most complications in the acute stage of trichinosis are due to the host's immune response to larval antigens in the circulation or tissues. Corticosteroids, because of their potent anti-inflammatory actions, help control systemic inflammation. They should be used in all patients with severe or moderately severe disease. Systemic symptoms (eg, fever) dramatically respond to corticosteroid therapy within a few days.
| Drug Name | Prednisone (Deltasone) |
| Description | May decrease inflammation by reversing increased capillary permeability and by suppressing polymorphonuclear cell activity. |
| Adult Dose | 5-60 mg/d PO qd or divided bid/qid; taper over 2 wk as symptoms resolve |
| Pediatric Dose | 4-5 mg/m2/d PO; alternatively, 0.5-2 mg/kg/d PO divided bid/qid; taper over 2 wk as symptoms resolve |
| Contraindications | Documented hypersensitivity; viral infection; peptic ulcer disease; hepatic dysfunction; connective tissue infections; fungal or tubercular skin infections; GI disease |
| Interactions | Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing dose) |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
|
| Precautions | Hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with use; abrupt discontinuation may cause adrenal crisis |
Drug Category: Nonsteroidal anti-inflammatory drugs
These agents have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may also be present, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.
| Drug Name | Ibuprofen (Advil, Motrin) |
| Description | DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis. |
| Adult Dose | 200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d |
| Pediatric Dose | 6 months to 12 years: 4-10 mg/kg/dose PO tid/qid; not to exceed 40 mg/kg/d or 2.4 g/d >12 years: Administer as in adults |
| Contraindications | Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding |
| Interactions | Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
|
| Precautions | Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in coagulation abnormalities or during anticoagulant therapy |
Further Inpatient Care
- Hospitalize all patients with severe and moderately severe disease and all pregnant women, regardless of disease severity, for monitoring and treatment of complications.
- Hospitalization is also indicated for fluid and electrolyte management and for analgesia.
Further Outpatient Care
- Symptoms such as myalgias and headaches may persist long after the acute stage of disease has ended. Treatment with anthelminthic therapy during the acute stage has affected these late-stage symptoms.
- Treatment is entirely symptomatic.
Deterrence/Prevention
- Controlling infection in swine
- Many countries have regulations that prohibit feeding raw abattoir scraps to domesticated pigs and that require inspection of commercial meat for Trichinella species.
- Infection in pigs also results from scavenging on infected rodent populations. Controlling rodent populations decreases the prevalence of infection in pigs.
- Meat preparation
- Proper cooking of meat is the most effective method to prevent infection. Larvae are destroyed by cooking meat until no trace of pink fluid or flesh remains; this occurs at about 60°C for 10 minutes. To allow a margin of error, the recommended internal temperature of meat should be raised uniformly to about 70°C. Cooking in microwave ovens does not effectively prevent infection because it does not sufficiently heat all parts of the meat.
- Larvae in pork products are also destroyed by freezing at -30°C for 1 week or at -15°C for 3 weeks. Note, however, that the meat of some wild animals (eg, bear, fox) possesses an antifreeze molecule that protects the larvae from the killing effects of extreme cold temperatures.
- Smoked or salted meat may contain viable parasites.
Complications
- Clinical disease due to Trichinella species is classified based on the severity and likelihood of complications. The following classification also helps in management and prognosis:
- Severe disease - Full syndrome of highly pronounced systemic signs and symptoms with metabolic disturbances (eg, hypoalbuminemia) and circulatory or neurologic complications
- Moderately severe disease - Full syndrome of significant intensity, rarely with complications
- Benign disease - Full syndrome of low-intensity signs and symptoms and no complications
- Abortive disease - Signs and symptoms that appear individually and not as a syndrome
- Asymptomatic infection - A history of exposure associated with eosinophilia but without signs and symptoms
- Complications occur in the early or acute stages of severe or, occasionally, in moderately severe trichinosis and can usually be prevented if patients receive adequate treatment during early stages of the disease.
- Cardiac: Although T spiralis larvae do not become encapsulated in heart muscle tissue, focal cellular infiltrates, consisting mainly of eosinophils and mononuclear cells, are observed because of their transitory stay in the heart. The changes are more extensive 4-8 weeks after ingestion. Arrhythmias and heart failure may occur in exceptionally heavy infection. A prospective study showed cardiac involvement in 13% of patients, almost all of which consisted of nonspecific ST-T changes and minimal effusions without impairment of systolic function.
- Pulmonary: Patients with lung involvement can present with pneumonitis or bronchitis.
- CNS: In cases of very severe infection, migrating larvae may penetrate cerebral tissues from blood vessels. Patients may present with obtundation or excessive excitement. Some present with signs of meningitis.
Prognosis
- Trichinosis is usually a self-limited illness, but death sometimes occurs if the number of infective larvae ingested is large.
- Early treatment helps prevent complications during the acute stage.
- Despite adequate treatment in the acute stage, infection may have long-lasting sequelae (eg, muscle aches, headaches, eye disturbances), especially in severe cases.
Patient Education
- The key to preventing trichinosis is public education about the potential danger of eating any raw meat product, especially the meat of wild game animals.
Medical/Legal Pitfalls
- Failure to consider ingestion of meats other than pork, especially the meats of wild game species, as a source of the infection
Special Concerns
- In pregnant women, trichinosis may cause abortion or premature delivery.
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Trichinosis excerpt Article Last Updated: Jan 29, 2008
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