Updated: Apr 18, 2018
Author: L Kristian Arnold, MD, MPH; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD 



Trichinellosis, formerly called trichinosis or trichiniasis (Trich from Greek thrix meaning hair), is an infection caused by nematodes of the genus Trichinella, most commonly T spiralis in humans. Through historical, paleopathologic, and, most recently, genomic studies, the complex intertwined history of humans, their food, and this worm has become better defined. Genomic evidence suggests the presence of Trichinella as a distinct species since some time in the mid to latter Miocene period (around 20 million years ago).[1] To date, 8 distinct species and 3 genotypes in 2 clads, encapsulated and nonencapsulated, have been found to infect mammals, birds, and reptiles around the globe.[2] Not all of these have been identified in humans.

The earliest human infection is reported to have been documented in an Egyptian mummy that dates to approximately 1300 BCE.[3] Religious injunctions on the consumption of pork may reflect early cultural awareness of this human-animal infection link.[4]

The first modern scientific observations of human Trichinella infection, from the autopsy of a man with "sandy diaphragm, were reported by medical student James Paget (of Paget disease) to a medical student society and published by his lecturer in clinical anatomy, Sir Richard Owen, then assistant curator at the Royal College of Surgeons.[3] The initial life cycle was worked out by Rudolf Virchow and associates over the years 1850-1870.[5]

By the 1860s, trichinellosis was well-recognized as a disorder spread through infected pigs, leading to a cultural aversion to certain pork products, particularly German and Dutch sausage.[6]

Geopolitical and cultural factors, such as increases in global movement of food products and persons, evolving into the 21st century are leading to a resurgence of human infections in areas that have been free of infection for decades.[7] This resurgence has particular relevance to emergency medicine because people may present to EDs in areas with little or no presence of trichinellosis locally, as they may have contracted it while travelling and because early diagnosis is associated with improved treatment outcomes.

Early diagnosis depends on clinician awareness and uncovering relevant patient history since the initial clinical presentation may be nonspecific.


Infection is initiated by ingestion of viable larvae in raw or undercooked meat. Digestive action liberates the larvae. The liberated larvae develop into adults in the duodenum and jejunum, where they mate and bear offspring. The adult worms are expelled in the stool.

Newborn larvae penetrate the intestinal wall, enter the lymphatic system, and move via the bloodstream to areas of implantation. Although the exact mechanism has not been elucidated, the newborn larvae have been implicated in cardiac and neurologic aspects of the disease. The life cycle is completed with the larvae invading a striated muscle cell.

Although the presence of larvae provokes an eosinophilia, they are generally resistant to any immunologic reaction from the host as they migrate out of the capillaries and penetrate muscle cells. Once in the cell, they alter cellular activity to turn the individual cells into "nurse cells." To nourish themselves in the nurse cell, the larvae stimulate angiogenesis leading to formation of a capillary rete around the invaded muscle cell.[8] Additionally, the normal cell life cycle of the invaded muscle cell enters a permanent arrest, with nuclear DNA remaining for the remainder of the life of the host at the G2/M phase transition.[9] Nurse cell formation has also been demonstrated to have many features analogous to muscle cell repair.[10]

A distinguishing feature between two general subclassifications (clads) of Trichinella species is whether the nurse cell forms a collagen capsule.[11]

Patients who develop neurologic and cardiac dysfunctions have marked hypereosinophilia associated with arteriolar microthrombi, often simply from numbers of larvae, leading to areas of cerebral and myocardial infarction.[12] Immunologic reactions are also deemed responsible for one of the hallmark clinical findings—palpebral edema.

The direct trauma of the larva encysting in muscle cells, coupled with the immunologic response, is responsible for other clinical features (eg, fever, myalgias). Typically, the intramuscular cysts eventually calcify. See the image below.

Life cycle of Trichinella species parasite. Image Life cycle of Trichinella species parasite. Image courtesy of the Centers for Disease Control and Prevention.



United States

Documented occurrence in the United States is now largely limited to sporadic cases or small clusters related to consumption of home-processed meats from noncommercial farm-raised pigs and wild game.[13] Trichinellosis has been a reportable disease since 1966. The Centers for Disease Control and Prevention (CDC) surveillance system has data as far back as 1947 demonstrating a significant decrease in cases from a peak of nearly 500 in 1948 to a total of 74 from 1997-2001, the most recent reporting cycle.[14] Human migratory patterns risk to upset this improvement as demonstrated by a report of a Laotian immigrant to the US developing trichinellosis after consuming lightly cooked commercially purchased pork.[15]

The US national surveillance system has been a passive system with links to state and local levels without active sampling of pork carcasses, an expensive practice used in some countries.[16, 17] The US Department of Agriculture has, however, used periodic surveillance of farm-raised pigs. In a 1999 study, the major risk factor for seropositivity in tested pigs was access to live wildlife or wildlife carcasses.[18] Rats, raccoons, skunks, and opossums have been shown to be wild sources of domestic pork contamination.

The decrease in infection of domestic pork in the United States has been associated with federal laws regarding commercial pork feeding practices directed at other pathogens, voluntary preharvest programs to control other risk factors such as exposure to rats in commercial herds, and attention to preparation guidelines.[19]

The USDA and the National Pork Board, an industry group, have developed the US Trichinae Certification Program. Based on principles proposed by the International Commission on Trichinellosis, this program relies on inspections of pork production sites with spot audits.[20]

Hunters and others who eat carnivorous game continue to be at risk.[20]


Reliable data on the incidence of trichinellosis varies around the world for several reasons. Initial clinical features of the disease overlap with other, more benign disorders, such as simple gastroenteritis. Characteristic signs of palpebral edema may not be recognized as representative of illness. Muscle pains from encysting of larvae may be delayed. In many parts of the world, for reasons ranging from difficult access to health care to poor public health reporting systems, presence of trichinosis may not be well documented unless occurring in clusters of cases.[21]

Since the 1980s, in spite of much awareness of both the presence of this infection and the efforts in many countries to control it, an increasing number of outbreaks have occurred throughout developed as well as developing countries.[22] Some authorities believe that trichinellosis should be classified as an emerging/reemerging disease, particularly because of increasing reports of cases from some previously unaffected areas.[23] Changes in ecosystem utilization, international trade of meats, and rising affluence in countries without well-established monitoring systems have all contributed to the increasing incidence.[24]

Although rare in countries with laws limiting the feeding of raw garbage or animal byproducts to commercially raised pigs and well-managed slaughterhouse surveillance systems, many countries have passed laws but fallen short on the implementation and quality assurance of the programs.[25] The cost of surveillance programs can be high and complex to install because of education and cultural issues.[16] An international commission with representation from more than 40 countries has developed a set of guidelines and holds quadrennial scientific and policy meetings.[26]

Home raising of pigs, with feeding of raw garbage instead of grain, is still a common practice in a large part of the world at all levels of development. In many countries, pigs roam freely, leading to contact with sylvatic sources of infection. Celebration of the Thai New Year has been associated with 200-600 cases in a single year and is a known annual source of multiple cases.[27, 28] Group tourist travel has also been associated with cluster outbreaks.[29] In several Southeast Asian countries, raw pork sausage and other dishes are considered delicacies and are regularly associated with outbreaks.

Trichinellosis must be considered a risk when eating the flesh of any animal that might have fed on uncooked animal flesh. Many animals generally not considered carnivorous will eat meat products when presented in a form they can chew, that is, usually chopped, or ground and combined with vegetable matter. This most commonly occurs on small farms when animals are fed table scraps or the scraps from butchering another farm animal. Rats also represent a reservoir in settings where raw animal scraps are left out for domestic animals to eat.

Market changes with international movement of processed food ingredients through either commercial channels or individual transport of products have presented a new source of difficulty in control. Two case clusters from Germany in 1998 were related to commercially produced sausage produced from meat transported from several different countries in Europe.[30] A 2007 outbreak in Poland with more than 180 confirmed cases was linked to one manufacturer of low price sausage. This outbreak even spread to Germany as cross-border shoppers returned with lower price sausage from the same Polish region.[31] Other clusters have occurred in relation to immigrant families bringing home-country delicacies back from vacation to their new countries of residence.[32, 33, 34]

The breakdown of state supported systems for farming, inspection and slaughter of meat products in the former Soviet Union countries of Eastern Europe, combined with culinary traditions, has been implicated in increasing presence of trichinellosis in these countries.[35]

The World Health Organization (WHO) reported that swine herds in some countries had a 50% prevalence of trichinellosis, and thousands of human cases had been documented. The report correlates this increase in prevalence with a breakdown in social structure in these countries (state veterinary services, state farms), coupled with economic hardship and war.[32]

In Eastern Europe, for example, following the break-up of the Soviet Union, large collective pig production facilities were replaced by smaller farms with free-ranging pigs, leading to increased contact with vectors such as rats.[36] Despite these socioeconomic-political forces, awareness and education have likely been the basis for decreasing caseloads over the ensuing years in some areas.[37] More recently, the economic strains on farmers in countries heavily impacted by a global recession in 2008 have increased the possibility of small farmers not adhering to safety practices involving extra cost.[38]

Travelers to regions with significant amounts of small-farm pig raising are strongly advised to consider any pork products to be suspect and to avoid consumption of any pork sausage. If eating pork or unidentified meat, adequate cooking should be personally verified. An outbreak in Turkey, a largely Muslim country, was attributed to an unscrupulous producer of meatballs adding pork from unverified farms to the beef and selling the meatballs as pure beef.[39]

Although generally thought of as a disease of omnivorous or carnivorous animals, herbivores have demonstrated infection, most likely from prepared feed that contained remnants of infected animals. In France, horse meat, largely imported, has become the most common source with more than a dozen outbreaks involving more than 3000 human victims since 1976. Interestingly, the same meat exporting countries supply various other European Union countries that have no human trichinellosis; unlike the French and Italians, those countries do not have the culinary habit of eating meat raw or minimally cooked.[40] Mutton and goat have become a recognized vector in countries where pig consumption is restricted for religious or economic reasons.

China has some of the highest recorded case numbers globally.[41] Serologic population surveys have revealed prevalence rates of between 0.66 and 12%, varying somewhat from among regions depending on eating habits. Yunan province was found to be the most significantly affected province. Pigs are the primary vector with prevalence rates as high as 50% in slaughterhouse surveys in some provinces.[42] The Western Region Development strategy of the 1990s led to many people from the endemic regions of central and eastern China migrating with infected livestock to regions with previously very low incidence. An increased demand from tourist industry development has led to an increase in small producers using uncooked swill to feed pigs and not confining the pigs from wild vectors with a concomitant increase in pig prevalence to as high as 100% reported in one region.[43]

Arctic and subarctic mammals (polar bear, walrus, seal) have been identified as being vectors for Trichinella nativa.[44, 45] T nativa is resistant to freezing, even for months at -20o C. Up to 60% of polar bears in Nunavik are infected.[46] Some Inuit have adjusted eating habits to avoid old male walruses as they are primarily scavengers, whereas the young feed primarily on shellfish.[47]

Consumption of wild boar prepared into sausage in Spain has led to human infection with T britovi in Spain and Sweden.[48] Wild boar have also been identified as a source of human infection in other areas in the Mediterranean basin, southeast Asia, and Pacific Islands.[49]

In recent years, the effect of consumer trends such as greater interest in "free ranging" and "antibiotic free" meats has been associated with an increase in trichinellosis among pigs destined to commercial markets in the United States.[50] and Europe.[51] The European Union has implemented a Trichinella monitoring program and the United States has developed a pilot program for Trichinell -free pig production.[52]

This rather extensive listing of international incidence of animal and human infection has been presented to offer some direct information regarding areas of particular concern as well as to further make the point of the importance of dietary and travel history in patients with diarrhea, particularly with associated myalgias and eosinophilia.


Specific death rate information is not established. Death is rare without development of neurologic and cardiac involvement.

The primary morbidity is persistent myalgia and fatigue in cases that do not develop neurocardiac involvement.

Following neurocardiac involvement, persistent variable dysfunction of either system may develop, depending upon the distribution of lesions.


Trichinella infection does not vary among different races. Variations in disease presence are based more on cultural food preparation and consumption practices.


Incidence is equal in males and females unless particular culinary habits lead to higher exposure for one group.[53] Serological evaluation of a small case series of pregnant women suggests that transplacental migration of larvae is possible in humans.[54]


All age groups reportedly have been affected; however, trichinellosis most commonly occurs in persons aged 20-49 years.

Although no good epidemiologic studies exist, there is evidence for potential transplacental infection of the fetus as it has been reported in different animals and in a fetus from a therapeutic abortion of an infected mother.[55, 56]




The usual incubation period of trichinellosis is 8-15 days. Following intestinal incubation, initial symptoms most commonly are gastrointestinal due to the invasion of the intestinal wall by the juvenile larvae.[57] Diagnosis depends heavily upon a suspicion and obtaining the history of ingesting potentially infected meat that was not cooked enough to kill the larvae. With increasing global migration, global exotic food transport and exotic tourism, the emergency physician should be aware of this diagnosis and include appropriate travel and dietary questions in the history of patients with gastroenteritis or unexplained myalgias.

Consider the following:

  • Myalgia (75%) - Classically reported as most common in masseter, diaphragm, and intercostal muscles, though high percent reported in extremities and neck/shoulder girdle in one cohort from a large outbreak in Turkey[58] ; may be severe to point of inability to ambulate or perform simple upper extremity or truncal tasks like feeding or sitting upright

  • Fever (60-75%) - 38.5-40.5°C

  • Weakness (75%)

  • Diarrhea (40-60%) - Usually only in the acute intestinal proliferative and penetration phases of nematode infestation

  • Facial edema (40-64%) - Usually considered one of the hallmark features, particularly when localized to the eyelids

  • Headache (50-60%)

  • Fatigue/malaise (up to 95%)

  • Arthralgia

  • Cardioneurologic syndrome - Onset of these symptoms has usually been reported to occur early following onset of general symptoms and prior to muscle invasion.[59, 12] The syndrome includes varying combinations of the following:

    • Encephalopathy

    • Focal neurologic deficits

    • Acute myocardial injury (eg, myocarditis, sinus and atrial nodal dysfunction, congestive heart failure, infarction)

    • Hypereosinophilia (≥4000 granulocytes/mm3)

  • Rash - This may occur in several forms, as follows:

    • Urticaria (most common)

    • Petechiae

    • Splinter hemorrhages

    • Palmar rash - Peripheral palmar and volar digital edema and erythema; desquamation occurs (10% in one study[60] )


Physical examination findings may include the following:

  • Fever (71%)

  • Palpebral edema (50-60%) - Usually considered one of the hallmark findings; may be associated with chemosis and proptosis.[61]

  • Generalized edema

  • Muscle weakness and tenderness - Usually not true neurologic weakness but pain related

  • Neurologic findings consistent with encephalopathy or focal deficits

  • Cardiac findings of myocarditis, pericarditis, or ischemia


Trichinellosis is a completely preventable infestation. The single most important causative factor is the consumption of inadequately cooked meat. Although most developed countries have some form of trichosis control program, these controls have been documented to fail.

Trichinella species of nematodes: Of the 11 recognized genotypes, the following are the most clinically significant, although others may not yet have been identified:

  • T spiralis is the primary cause associated with domesticated animals.

  • T britovi is seen frequently in wild boar, horses, and free-ranging swine. It has also been reported in bear in Japan where it has been given a separate classification, T9, because of minor genetic variations from the European T britova.[14]

  • T murrelli has been identified in wild and domestic animals other than pigs only in North America.[49]

  • T nelsoni is seen in various large carnivores of sub-Saharan Africa.[24]

  • T nativa has been documented in almost all land and marine mammalian carnivores in the arctic and periarctic regions around the globe. In humans, it has been associated with more prolonged diarrhea and fewer muscle symptoms. It is also more resistant to freezing than other species, having been documented to not be killed by prolonged freezing at -18o C.[49]

  • T9, closely related to T britovi is isolated to Japan, existing in bear, fox, and raccoon dog.[49]

  • T pseudospiralis has been documented in birds and does not form a capsule in the muscle, thus leading to less muscle inflammation and pain. Conversely, the muscle phase seems to remain actively infective for a longer period, probably since, without cyst formation, ultimate calcification does not occur.[62]

  • T papuae in wild pigs has been identified in Papua-New Guinea as a source of infection among forest-dwelling hunters. It is a nonencapsulating form of Trichinella.[53]

  • T zimbabwensis has been identified as infecting reptiles in southern Africa. Particularly concerning for increasing human risk is their presence in farm-raised crocodiles.[63] More recent reports indicate a presence in sylvatic reptiles as well.[64]





Laboratory Studies

There is no definitive laboratory test with easy availability to the emergency physician.

CBC reveals eosinophilia in virtually all patients, though it does not develop until 2-6 weeks following ingestion of infected meat when larvae pass out of the intestines. Of note, eosinopenia has been noted to be associated with more severe infections and an early fall in eosinophils with a poorer outcomes.[65] Eosinophilia may persist for up to 3 months.

Creatine phosphokinase and lactic dehydrogenase levels are elevated in 90% of patients once the muscle invasion phase begins.

Urinalysis (UA) may reveal myoglobinuria.

Parasite-specific indirect immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) titers (100%) and anti-newborn larvae antibodies (30%) begin to be positive within 2 weeks of infection. These may not be positive initially, and they also are subject to some cross-reactivity with other parasitic disorders making their specificity less when weakly positive.[66] Western-blot analysis is used as a confirmatory evaluation.[67]

Imaging Studies

Plain radiographs of the extremities

Calcified densities in the muscles, indicating an old trichinization, may be the only positive radiographic findings.

Radiographs do not help evaluate acute infestation.

Computerized tomographic (CT) scanning of the brain

CT scanning may be helpful in patients demonstrating neurologic symptoms.

CT scan reveals focal deficits with small hypodensities in the cortex and white matter.[12]

Abnormal findings are unlikely in patients without neurologic symptoms.

CT scanning of the orbits is warranted in patients with chemosis to rule out other causes of proptosis.[61]

Magnetic resonance imaging (MRI) of the brain

Diffusion-weighted MRI may be helpful in defining lesions noted on plain MRI.[68]

Other Tests

ECG may show signs of ischemia, pericarditis, or myocarditis, such as the following[69] :

  • Premature atrial or ventricular contractions

  • P-R prolongation

  • Flattened or inverted T waves

  • Conduction blocks

  • Atrial fibrillation

Cardiac ultrasound (ECHO) may demonstrate pericardial fluid or wall motion abnormalities.[69]


A muscle biopsy is the definitive diagnostic test but is not an ED procedure. It is also being replaced for treatment decisions by algorithms such as one presented below. Consider the following when performing biopsy:

  • Larvae are found free or encapsulated, depending on the species of Trichinella causing the infection.

  • At the time of biopsy, initial preparation may be made by crushing a portion of muscle tissue between 2 slides and viewing directly.

  • Biopsy may be negative in active infection due to physically missing an area of implantation if the number of larvae in muscle tissue is low enough that the biopsy misses an infected area.

  • Treatment should not be withheld in the face of a negative biopsy result and negative immunoglobulins if there is high clinical suspicion.[70]

  • Polymerase chain reaction (PCR) evaluation of biopsy tissue for Trichinella -specific DNA, because of the high sensitivity and specificity, may detect the presence of worms in cases where initial biopsy results are negative. See the image below.

    Photomicrograph depicting numbers of Trichinella s Photomicrograph depicting numbers of Trichinella spiralis cysts seen embedded in a muscle tissue specimen, in a case of trichinellosis. Image courtesy of the Centers for Disease Control and Prevention.

The Food and Agriculture Organization of the United Nations (FAO), in conjunction with the WHO and the World Organization for Animal Health (OIE), have proposed an algorithm for predicting the likelihood of being infected with Trichinella based on combinations of clinical and laboratory elements and their relative sensitivities and specificities.[4] Diagnosis of confirmed cases requires fever, facial/eyelid edema, and myalgia, along with a positive high-specificity serologic test result, seroconversion, or a positive muscle biopsy finding. Alternatively, diagnosis is confirmed with eosinophilia, elevated IgE levels, or elevated muscle enzymes; a positive high-specificity serologic test result, seroconversion, or a positive muscle biopsy finding; and at least one of the following:

  • Fever

  • Myalgia

  • Facial/eyelid edema

  • Neurological signs

  • Cardiological signs

  • Conjunctivitis

  • Subungual hemorrhages

  • Cutaneous rash

This algorithm allows for graded suspicion based on various combinations and does not always require serology or muscle biopsy. For example, high probability cases are defined by the presence of myalgia, eyelid/facial edema, and fever and at least 2 of the following:

  • Eosinophilia

  • Elevated IgE level

  • Elevated muscle enzyme level



Prehospital Care

Institute appropriate supportive therapy for patients who present with symptoms of neurologic or cardiac involvement.

Emergency Department Care

Patients with mild cases require no special care.

Patients with more severe cases of muscle involvement may need basic supportive therapy (eg, oxygen, intravenous fluids).

Cardiac monitoring is suggested for patients who present early. Cardiac findings are unlikely to develop late in the course (ie, after peripheral muscle invasion has started).


See the list below:

  • Infectious disease/tropical medicine/travel medicine specialists

  • Surgeons (for muscle biopsy)

  • Cardiologists



Medication Summary

Anthelminthic therapy is generally considered only effective during the intestinal phase of infection. Because of the limited number of cases in any one outbreak, comparative trials at various stages of infection are lacking, leading to controversy regarding appropriate dosing and effectiveness in the muscle phase of the disease.[71] One trial during an outbreak in Italy assessed the effectiveness of mebendazole in patients several weeks following infection.[72] All patients became better in terms of decreased myalgias and other symptoms while under treatment, but between 3 and 45% had recurrence of various symptoms following a 10-day mebendazole course. In another study in Thailand, groups treated with mebendazole or thiabendazole had 100% resolution of myalgias reported at 4 months.[28] A review of experience in Romania revealed a better response among children with albendazole than in adults and a better result in both children and adults with albendazole than mebendazole.[73, 74]

Corticosteroid treatment usually is instituted to reduce the immunologic response to the larvae. Jarisch-Herxheimer–like reactions have been described in patients with heavy larval loads following the administration of anthelmintic medications. This reaction is clinically manifested by a worsening of symptoms and is thought to be caused by a response to liberation of immunologically active components of the dying larvae. If the larval load is extremely high or in critical locations, this reaction may result in significant clinical deterioration resembling septic shock.

In the study in Romania, patients treated with corticosteroids and albendazole experienced longer hospitalizations than those treated with albendazole alone. The study does not specify what clinical parameters were used to determine timing of hospital discharge because it was a retrospective population study. A different study of an outbreak in Turkey due to T britovi reported more rapid improvement in symptoms and laboratory values in patients given prednisolone along with either mebendazole or albendazole.[75]

Increasing resistance to helminths has led to investigation of potential new treatments. Investigators have demonstrated activity of different Artemisia species, effective against malaria, on Trichinella in animal models.[76]


Class Summary

These agents are frequently used to decrease myalgia and to limit eosinophilia when neurologic or myocardial involvement is present, although their efficacy and safety has been questioned.[4]

Prednisone (Deltasone, Orasone)

Useful in treating inflammatory reactions. May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Hydrocortisone (Solu-Cortef, Westcort)

May be used in place of prednisone in patients too ill to take PO medications. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing the increased capillary permeability.


Class Summary

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

Mebendazole (Vermox)

Causes worm death by selectively and irreversibly blocking cell division and intestinal glucose uptake and in the adult.

Albendazole (Albenza)

Decreases ATP production in the worm, causing worms' energy depletion, immobilization, and death.



Further Outpatient Care

In suspected cases that do not require admission, ensure early follow-up for continued monitoring.

In suspected cases, arrange for surgical follow-up care in 1-2 days for muscle biopsy.

Further Inpatient Care

Admit patients with neurologic or cardiac symptoms for initiation of therapy.

Consider patients with significant diffuse muscle involvement for hospitalization because they are at risk for Jarisch-Herxheimer-like reactions.


Adequate cooking of all meat products is the primary deterrent to acquiring infection with the Trichinella species.

Adequate cooking refers to the point at which no red meat remains.

The US Code of Federal Regulations and the US Department of Agriculture have information regarding preparation of pork and appropriate times and temperatures needed to kill larvae. For cooking, pork must reach an internal temperature of 160°F (71°C); for freezing, it must remain at 5°F (-15°C) for 3 weeks.[19]


Potential complications of trichinellosis/trichinosis include the following:

  • Meningitis

  • Subcortical infarcts

  • Encephalitis

  • Myocarditis with congestive heart failure

  • Nephritis

  • Glomerulonephritis

  • Sinusitis

  • Pneumonia


Recovery with resolution of signs and symptoms may occur in 5-6 weeks after infestation in many patients with disease limited to enteropathic and mild muscular involvement.

More than 50% of patients with disease that progresses only to muscle involvement may experience varying degrees of persistent fatigue and myalgia despite a full course of anthelminthic treatment. Patients infected with nonencapsulating species tend to have less muscle pain, although this pain is more persistent. Nurse cells in encapsulated species tend to eventually calcify, resulting in destruction of the larva and resolution of the painful inflammation, although live larvae have been documented in lesions many years after initial infestation.

Patients with CNS, cardiac, or renal involvement may have protracted courses with persistent stiffness, neurologic disorders, and heart or kidney dysfunction.