Trichinosis, or trichinellosis, is caused by a parasitic nematode from the genus Trichinella. This disease, often unrecognized and underreported, has affected humans for thousands of years, with an estimated 10,000 cases occurring worldwide annually.[1, 2] Although virtually all mammals can be infected, humans are particularly susceptible to clinical disease through foodborne transmission.[3] Infection occurs when individuals consume inadequately cooked meat containing Trichinella larvae, primarily found in wild game and pork. Symptoms of trichinosis include diarrhea, myositis, fever, and periorbital edema, which arise when a significant number of larvae are ingested.[4]
The earliest documented human infection was found in an Egyptian mummy dating back to approximately 1300 BCE[5] ; this suggests an early cultural awareness of the link between human and animal infections, as reflected in religious prohibitions against pork consumption.[6]
The first modern scientific observations of human Trichinella infection were made by medical student James Paget, who reported findings from an autopsy of a man with a "sandy diaphragm." These observations were published by his lecturer, Sir Richard Owen, at the Royal College of Surgeons.[5] The life cycle of Trichinella was elucidated by Rudolf Virchow and his associates between 1850 and 1870.[6] Trichinella species are widely distributed across various geographic regions, including the Arctic, temperate lands, and tropics.[7]
Table 1. Biologic and Zoogeographic Features of Trichinella Species
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See Table
Reprinted from Adv Parasitol, Vol 63, Murrell KD, Pozio E, Systematics and epidemiology of Trichinella, pg 367, 2006, with permission from Elsevier.[8]
Trichinella species require two hosts to sustain their life cycles, spreading through the ingestion of infected flesh rather than relying on traditional arthropod intermediate hosts. There are three major life cycles in nature: pig-to-pig, rat-to-rat, and transmission among carnivorous or omnivorous animals. Although rats and pigs are the most commonly associated with trichinosis, other animals such as walruses, seals, bears, polar bears, cats, raccoons, wolves, and foxes also may be infected, depending on the region.
The life cycle of Trichinella is maintained by animals that consume other animals containing encysted infective larvae in their striated muscles, such as pigs, horses, and predators such as bears, foxes, and boars. Humans can become infected by eating raw, undercooked, or inadequately processed meat from infected sources, primarily pigs, wild boar, or bear. After ingestion, the larvae excyst in the small intestine, penetrate the mucosal lining, and develop into adults within 6 to 8 days, with females measuring about 2.2 mm and males around 1.2 mm.
Mature females release live larvae for 4 to 6 weeks before dying or being expelled. The newborn larvae migrate through the bloodstream and lymphatic system, ultimately residing in striated skeletal muscle cells. They fully encyst within 1 to 2 months and can remain viable as intracellular parasites for several years. Dead larvae may be resorbed or calcify over time. The cycle continues only if another carnivore ingests the encysted larvae.
The life cycle of Trichinella species parasite is depicted in the image below.
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Life cycle of Trichinella in humans. Courtesy of Dickson Despommier, PhD, and Daniel Griffin, MD, PhD, Parasitic Diseases, 6th Ed, published by Parasi....
The life cycle of Trichinella as a foodborne illness begins when raw or inadequately cooked meat containing viable larvae within cyst walls (nurse cells) is consumed. The acidic environment of the host's stomach releases the larvae from the cysts. The free larvae then migrate to the small intestine, where they attach to and penetrate the mucosal lining at the base of the villi. After undergoing four molts over 30 to 36 hours, they develop into adult worms, becoming obligate intracellular organisms. Adult males measure approximately 1.5 mm by 0.05 mm, whereas females measure about 3.5 mm by 0.06 mm. Around 5 days post-infection, females begin shedding live newborn larvae, measuring 80 µm by 7 µm (L1 stage). The female remains in the intestine for 4 weeks, releasing up to 1,500 larvae before being expelled in feces due to an adequate inflammatory response.
The newborn larvae enter the lymphatic and circulatory systems, migrating to well-vascularized striated skeletal muscle. The parasite preferentially targets metabolically active muscle groups, including the tongue, diaphragm, masseter, intercostal, laryngeal, extraocular, nuchal, pectoral, deltoid, gluteus, biceps, and gastrocnemius muscles. In tissues other than skeletal muscle, such as the myocardium and brain, the parasites disintegrate, causing intense inflammation and subsequent reabsorption.
During the next 2 to 3 weeks, the larvae grow until they reach the fully developed L1 infective stage, increasing in size by up to tenfold. The adult worms are viviparous, and the larvae encyst, coiling and developing a surrounding cyst wall or nurse cell to survive harsher conditions, except for Trichinella pseudospiralis, which does not encyst. The complete life cycle takes 17 to 21 days, with larvae within the cyst wall averaging 400 µm by 260 µm, although lengths of 800 to 1,000 µm have been reported. The nurse cell–L1 complex can persist for 6 months to several years before calcification and death occur. The Trichinella life cycle is completed when a compatible host ingests the infected muscle (see images below).
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Trichinella nurse cell. Courtesy of Dickson Despommier, PhD, and Daniel Griffin, MD, PhD, Parasitic Diseases, 6th Ed, published by Parasites Without B....
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Encysted larvae of Trichinella species in muscle tissue, stained with hematoxylin and eosin (H&E). The image was captured at 400X magnification. Court....
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Trichinella larvae, in pressed bear meat, partially digested with pepsin. Courtesy of the US Centers for Disease Control and Prevention ((http://www.d....
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Larvae of Trichinella from bear meat. Courtesy of the US Centers for Disease Control and Prevention (http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.h....
The intensity and frequency of exposure to infected meat determine the severity of the disease. The degree of infection is categorized as light (0-10 larvae ingested), moderate (50-500 larvae ingested), and severe (>1000 larvae ingested).
National surveillance data indicate a significant decline in reported trichinosis cases in the United States since 1947, the inaugural year of systematic data collection. Between 2011 and 2015, there were 80 reported cases across 24 states and the District of Columbia. Of these cases, 57 (71%) had a confirmed or suspected source, with 25 cases (44%) linked to bear meat, 13 cases (23%) to wild boar meat, and 9 cases (16%) linked to unspecified pork.[1] Notably, one case was associated with the consumption of residual larvae on a preparation table,[9] reinforcing the classification of trichinosis as a foodborne illness.
Hunters and individuals consuming carnivorous game remain at heightened risk, with the majority of cases since approximately the 1980s occurring among those who ingested lightly cooked wild game, particularly bear and wild boar.[10, 11, 12] The prevalence of infected domestic swine in the United States is approximately 0.001%; however, an autopsy study revealed a 4% incidence of historical infections.[11, 12, 13] A notable outbreak in 2008 in Northern California involved 38 individuals who consumed black bear infected with Trichinella murrelli, which also has been detected in raccoons and coyotes.
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Epidemiology of trichinellosis in the US. Courtesy of Centers for Disease Control and Prevention (CDC) (https://www.cdc.gov/parasites/trichinellosis/r....
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Reported cases of trichinellosis 2011-2015. Courtesy of Centers for Disease Control and Prevention (CDC) (https://www.cdc.gov/parasites/trichinellosis....
International
In Europe, where mandatory pork inspection is enforced, the majority of trichinosis cases are associated with horse or wild boar meat. In contrast, domestic pork is the primary source of infection in Latin America and Asia, with Trichinella infection rates in swine in China reported as high as 20%. Increased rates of trichinosis have been observed in former Eastern European countries, such as Romania and Hungary, attributed to political changes and evolving regional dietary practices.[14, 15] The European Centre for Disease Prevention and Control reported 779 human cases of trichinosis in the European Union in 2007, predominantly linked to farm and wild animal sources.[16]
Despite a substantial decline in the global incidence of trichinosis, outbreaks continue to occur frequently, particularly in developing nations.[17, 18] An estimated 10,000 cases are reported annually, with a mortality rate of approximately 0.2%.[1, 19] The international movement of processed food ingredients has introduced new challenges for control efforts. For instance, two clusters of cases in Germany in 1998 were traced to commercially produced sausage made from meat sourced from multiple European countries. A 2007 outbreak in Poland, involving over 180 confirmed cases, was linked to a single manufacturer of low-cost sausage, which subsequently spread to Germany through cross-border shoppers.
Travelers to regions with prevalent small-farm pig raising should exercise caution regarding pork products and avoid consuming any pork sausage.[13] An outbreak in Turkey was attributed to a producer who incorporated pork from unverified sources into beef meatballs. Whereas trichinosis primarily is associated with omnivorous or carnivorous animals, herbivores also can become infected, likely through feed contaminated with remnants of infected animals. In France, imported horse meat was implicated in over a dozen outbreaks, affecting more than 3,000 individuals between 1975 and 2005.
China reports some of the highest global case numbers, with serologic surveys indicating prevalence rates ranging from 0.66% to 12%, depending on regional dietary habits. The Yunnan province is particularly affected, with pigs serving as the primary vector and prevalence rates reaching 50% in certain slaughterhouse surveys. The Western Region Development strategy of the 1990s facilitated the migration of infected livestock to previously low-incidence areas, compounded by increased demand from the tourism sector.
Arctic and subarctic mammals, including polar bears, walruses, and seals, are recognized vectors for Trichinella nativa, which also can infect humans. This species exhibits resistance to freezing, with infection rates in polar bears in Nunavik reaching up to 60%. Some Inuit populations have modified their dietary practices to avoid older male walruses, which are primarily scavengers, whereas younger walruses feed predominantly on shellfish.
Consumption of wild boar sausage in Spain has resulted in human infections with T britovi, and wild boar have been identified as a source of infection in various Mediterranean regions, Southeast Asia, and Pacific Islands. This comprehensive overview underscores the clinical significance of trichinosis and highlights the importance of dietary and travel history in patients presenting with gastroenteritis, particularly when accompanied by eosinophilia or palpebral edema.
Mortality/Morbidity
Although Trichinella infections most likely are underreported in the United States, fewer than 25 cases are documented per year, with a very low mortality rate.
Specific death rate information is not established. Death is rare in the absence of neurologic or cardiac involvement.
Patients with light infection usually are asymptomatic. Those with mild symptoms improve in 2-3 weeks. Symptoms associated with heavy infections may persist for 2-3 months.
Factors that may affect morbidity include the quantity of larvae ingested, the species of Trichinella (most notably T spiralis), and the immune status of the host. Patients succumb to exhaustion, pneumonia, pulmonary embolism, encephalitis, or cardiac failure and/or arrhythmia. Death from trichinosis usually occurs in 4-8 weeks but may occur as early as in 2-3 weeks.
Although most patients with muscle involvement have resolution of pain and associated disability, some may experience persistent myalgia and fatigue. In severe infections (very high larval load) muscle weakness may be enough to significantly impair mobility.
Following neurologic or cardiac involvement, persistent variable dysfunction of either system may develop, depending upon the distribution of lesions.
Race
Although Trichinella infections may be related to cultural differences in food cooking and storing methods (eg, the inadequate cooking or freezing of meat), outcomes do not vary based on race among infected individuals.
Culture
A 2017 outbreak involved the consumption of walrus meat in Alaska.[9] The first point of healthcare contact included village healthcare centers, which are primarily used by Alaskan Native populations. Traditional cultural practices, including the hunting of polar bear and walrus, may lead to differential infection rates with Trichinella within Alaska Native communities.
Some studies have found that cultural practices, such as avoidance of pork consumption in Jewish and Muslim communities, may serve as a protective factor against Trichinella infection.[20]
Sex
No differences in trichinosis rates between males and females are reported. Incidence is equal in males and females unless particular culinary habits lead to higher exposure for one group.[21]
Pregnant individuals have milder trichinosis symptoms than nonpregnant persons; however, abortions and stillbirths have been reported. There is evidence that pregnancy may offer some protection against infection.[22]
Symptoms of trichinosis typically are worse in lactating individuals compared with nonlactating persons.
Age
Children seem to be more resistant to Trichinella infection, although their symptoms can be more severe. They generally experience fewer complications and tend to recover more quickly. The figure below illustrates the cumulative number of trichinosis cases reported in the United States from 2011 to 2015, categorized by sex and age group. During this period, a total of 80 cases were reported among individuals with known ages, whereas age data was unavailable for one patient and sex data for another. Of the 80 cases, 51 were in males and 29 in females. Among the 53 patients with known ages, the median age was 37 years, with a range from 1 to 71 years.
All age groups have been affected by trichinellosis; however, it most commonly occurs in individuals aged 20 to 49 years, primarily due to dietary habits related to wild game consumption.
Serologic evidence suggests potential transplacental migration of larvae, although direct evidence of larvae presence only has been documented in various animals and in one case report involving a fetus from a therapeutic abortion of an infected individual.[22, 23, 24]
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The number of cases of trichinellosis by age. Courtesy of Centers for Disease Control and Prevention (CDC) (https://www.cdc.gov/parasites/trichinellos....
Severe disease occurs in only 5-20% of patients during epidemics.
Individuals who receive treatment with anthelmintics and, when necessary, corticosteroids typically make a full recovery, unless they have ingested a very high load of larvae, which increases the risk for cardiac and neurologic complications.
The likelihood of complete recovery is less certain if there is cardiac or neurologic involvement.
Adequate cooking and freezing methods prevent trichinosis.
The most effective measure to eradicate Trichinella species is by adequate cooking to kill the parasite. The current recommendation for heating is 160°F (71°C) for all food-borne disease. Trichinella species typically can be killed by adequate cooking to 140°F (60°C) for 2 minutes or 131°F (55°C) for 6 minutes. If no trace of pink in fluid or flesh is found, these temperatures have been reached.
Freezing also is an effective method for killing most species of Trichinella. For a 6-inch piece of meat, the recommended temperatures to kill larvae are as follows:
5°F (-15°C) for 20 days
-10°F (-23°C) for 10 days
-20°F (-29°C) for 6 days
Salting, smoking, or drying the meat does not kill cysts.
The European Center for Disease Control has established definitions and algorithms for diagnosing acute trichinosis in humans.[19] These guidelines emphasize clinical, laboratory, and epidemiologic criteria, along with a range of symptoms. The criteria can help differentiate between very unlikely, suspected, probable, highly probable, and confirmed cases (see Staging). Understanding the incubation period is essential for identifying the source of infection in both individual cases and outbreaks.
The typical incubation period for trichinellosis is 8 to 15 days following ingestion. As the newly released juvenile larvae invade the intestinal wall, most individuals experience some degree of gastroenteritis.[25] This gastrointestinal distress may persist for up to 2 weeks until all ingested larvae have either been expelled or died, and the intestinal mucosa has healed.
As the newborn larvae enter the bloodstream and migrate through various tissues, symptoms can vary widely, ranging from allergic-like reactions to various neurologic or cardiac symptoms. Much of the cardiac and neurologic pathophysiology arises from larvae passing through individual capillaries, leading to symptoms that may present as localized dysfunction without clear vascular patterns or as diffuse processes such as encephalopathy.
Once the muscle phase begins, individuals may report muscle pain and weakness. Trichinosis typically progresses from an enteric (intestinal) phase to a parenteral (invasive) phase, followed by a period of convalescence.
Trichinosis may progress from an enteric (ie, intestinal) phase to a parenteral (ie, invasive) phase to a period of convalescence.
Intestinal phase
The intestinal phase of trichinosis typically presents symptoms within the first week of illness.
Diarrhea is the most prevalent symptom, whereas constipation, anorexia, and generalized weakness also may occur. In some cases, severe enteritis can result from a high inoculum of Trichinella species.
Symptoms generally last between 2 to 7 days but can persist for several weeks. In certain populations and geographic regions, as well as with specific Trichinella species, the disease may remain confined to the intestinal stage.
Nausea is reported in 15% of patients, vomiting in 3%, and diarrhea in 16%. Additionally, dyspnea may occur with exertion, and individuals may experience abdominal discomfort and cramps.
Invasive phase
The invasive phase of trichinosis is characterized by the migration of larvae from the intestine into the circulatory system and subsequently to striated muscles. This phase is associated with a higher incidence of symptoms compared to the intestinal stage.
Common symptoms during the invasive phase include the following:
Myalgia is reported in 75% of patients, with severe pain often affecting the masseter, diaphragm, intercostal muscles, and, in some cases, the extremities and neck/shoulder girdle. Pain can be severe enough to hinder ambulation or basic tasks such as feeding or sitting upright.
Fever occurs in 60-75% of patients, typically ranging from 38.5 to 40.5°C.
Weakness is experienced by 75% of patients.
Diarrhea is reported in 40-60% of cases, usually occurring during the acute intestinal proliferative and penetration phases, but may persist for weeks depending on the presence of adult worms in the intestinal wall.
Facial edema is seen in 40-64% of patients, particularly localized to the eyelids (palpebral edema), which is considered a hallmark feature.
Headache is reported in 50-60% of patients.
Fatigue/malaise affect up to 95% of patients.
Arthralgia (joint pain) also may be present.
Cardioneurologic syndrome
Additionally, some patients may experience a cardioneurologic syndrome, which typically manifests within days of the onset of general symptoms and before muscle invasion. This syndrome can include the following:
Encephalopathy
Focal neurologic deficits
Acute myocardial injury, such as myocarditis, sinus and atrial nodal dysfunction, congestive heart failure, and infarction
Hypereosinophilia, defined as ≥4000 granulocytes/mm³
Rash (which can take various forms) may occur, including urticaria (most common), petechiae, splinter hemorrhages, and palmar rash, which may involve peripheral palmar and volar digital edema and erythema; desquamation occurs in about 10% of cases.
The duration of symptoms can vary from weeks to months. Severe myalgia develops in 89% of patients, and central nervous system (CNS) involvement occurs in 10-24% of cases, with a mortality rate of 50%. Headaches are reported in approximately 52% of patients, along with other symptoms such as deafness, ocular disturbances, weakness, and monoparesis.
Cardiac involvement typically arises during the third week of infection; it has a mortality rate of 0.1% and often occurs between the fourth and eighth weeks. Death may result from congestive heart failure and/or arrhythmias. Pulmonary involvement is noted in 33% of patients; symptoms last up to 5 days and include dyspnea, cough, and hoarseness.
Overall, although there are variations in symptom presentation and severity, the information from both sources aligns on the key symptoms and complications associated with the invasive phase of trichinosis.
Convalescent phase
The convalescent phase, characterized by encystment and tissue repair, can last for months to years following infection.
The encystment of larvae may result in cachexia, edema, and severe dehydration.
Typically, symptoms begin to diminish around the second month, although infections caused by T pseudospiralis may lead to prolonged symptoms lasting several months.
The clinical presentation of trichinosis encompasses a range of symptoms, with abdominal distention being a potential finding. Macular or petechial rashes are observed in 15-65% of patients, and diarrhea also may be present.
Fever typically develops around 2 weeks post-infection and affects 91% of patients, with peak temperatures reaching 104°F (40°C) around the fourth week. This degree of fever notably is distinctive among helminthic infections. Weakness and/or myositis occur in 82% of patients, with affected muscles becoming stiff, hard, and edematous. Muscles with increased blood flow, such as the extraocular muscles, masseters, larynx, tongue, neck muscles, diaphragm, intercostals, and limb flexors, most frequently are involved. Diaphragmatic involvement may lead to dyspnea.
Periorbital edema is reported in 50-60% of patients; ocular findings include subconjunctival hemorrhages in 9% and conjunctivitis in 55%, and there are instances of chemosis and retinal hemorrhage. Central nervous system (CNS) involvement occurs in 10-24% of patients, with 53-96% exhibiting meningoencephalitis, 40-73% showing focal paralysis and/or paresis, and 39-71% experiencing delirium. Additional neurologic symptoms may include decreased or absent deep tendon reflexes (20%), meningitis (17%), and rare cases of psychosis (2%).
Cardiac involvement may manifest as hypertension, increased venous pressure, and peripheral edema in 18% of patients. Subungual splinter hemorrhages are noted in 8% of cases, and generalized edema is present in 18%. Patients frequently report fatigue, weakness, weight loss, and myalgia, with chronic headaches potentially accompanying ocular signs.
A comprehensive physical examination is critical, focusing on the skin for signs of rash and assessing for palpebral or recent-onset edema in other areas. Key physical examination findings may include the following:
Fever (71%)
Palpebral edema (50-60%), often considered a hallmark finding, which may be associated with chemosis and proptosis[26]
Generalized edema
Muscle weakness and tenderness, which may not indicate true neurologic weakness but rather pain related to muscle involvement; respiratory difficulties may arise in cases of significant diaphragmatic infestation
Neurologic findings consistent with encephalopathy or focal deficits
Cardiac findings indicative of myocarditis, pericarditis, or ischemia
Trichinella species develop in a single host and then are spread from that host to the next without an arthropod intermediate. The intensity and frequency of exposure to infected meat determine the severity of the disease.
Infections are related to cultural differences in food cooking and storing methods, specifically the inadequate cooking or freezing of meat.
Complications from trichinosis generally are rare, except in cases of severe infestation. In such instances, Trichinella larvae may migrate to vital organs of the host, leading to serious and potentially fatal complications, including the following:
Myocarditis[28]
Pneumonia[28]
Meningitis[29]
Encephalitis[29]
Long-term neurologic sequelae may include diminished cognitive function, numbness in the hands and feet, reduced stress tolerance, loss of motivation, and depression.
Typically, full recovery is achievable following cardiac or pulmonary involvement. However, some individuals may experience prolonged weakness and myalgia. Additionally, adrenal gland insufficiency and vascular obstruction may occur.
The clinical identification of trichinellosis presents challenges due to the absence of definitive clinical manifestations, making epidemiologic data crucial for diagnosis. During the acute phase, trichinellosis may manifest with eyelid or facial edema and myalgia, and may be complicated by myocarditis, thromboembolic disease, and encephalitis. Laboratory findings commonly include elevated eosinophil counts and increased serum creatine phosphokinase (CPK) levels. Confirmation of the diagnosis is achieved through parasitological analysis of muscle biopsy specimens and detection of specific circulating antibodies.[6]
Early diagnosis of trichinosis relies on clinician awareness and thorough exploration of the patient's history, as the initial clinical presentation can be nonspecific.
No readily available definitive laboratory test for emergency physicians exists. Although the presence of larvae can trigger eosinophilia, the larvae generally are resistant to the host's immunologic response as they migrate out of capillaries and penetrate muscle cells using a stylet.
Once inside the muscle cell, the larvae modify cellular activity, transforming the individual cells into "nurse cells." To sustain themselves within these nurse cells, the larvae promote angiogenesis, resulting in the formation of a capillary network around the affected muscle cell.[30] Additionally, the normal life cycle of the invaded muscle cell is permanently halted, with its nuclear DNA remaining in the G2/M phase transition for the duration of the host's life.[31] The process of nurse cell formation also exhibits several characteristics similar to muscle cell repair.[32]
CBC count
A complete blood count (CBC) should be obtained for patients suspected of trichinosis.
Leukocytosis is observed in 65% of patients, with white blood cell counts reaching up to 24,000/µL. Eosinophilia typically develops around 10 days after infection, with total eosinophil counts rising to as high as 8,700/µL (40-80% of total WBC). Eosinophil counts peak between 3 to 4 weeks post-infection and may take several months to resolve. Eosinophilia is present in nearly all patients; however, it may not manifest until 2 to 6 weeks after ingestion of infected meat, as larvae exit the intestines.[27]
It is important to note that eosinopenia has been associated with more severe infections, and an early decline in eosinophils correlates with poorer outcomes. Eosinophilia can persist for up to 3 months.
Additionally, creatine phosphokinase and lactic dehydrogenase levels are elevated in 90% of patients once the muscle invasion phase begins. Most patients with trichinosis, whether symptomatic or asymptomatic, exhibit eosinophilia, except in severe cases in which eosinophil counts may be significantly depressed. A low eosinophil count is indicative of an increased mortality rate.
Erythrocyte sedimentation rate
Erythrocyte sedimentation rates usually are within the reference range.
Creatine kinase
Obtain creatine kinase (CK) levels.[33]
Creatine kinase levels are elevated to 17,000 U/L.
Creatine kinase (isoenz me myocardial band [MB]) elevations may indicate myocardial involvement; however, as many as 35% of patients without cardiac involvement may have elevated CK-MB levels.
Lactate dehydrogenase
Levels of lactate dehydrogenase isoenzymatic forms (ie, lactate dehydrogenase fraction 4 [LD4] and lactate dehydrogenase fraction 5 [LD5]) are elevated in 50% of patients.
Immunoglobulin E
Immunoglobulin E levels typically are elevated.
Serology
Serology results typically do not become positive until 2 to 3 weeks after infection, peaking around the third month and potentially persisting for years. The serology ratios do not correlate with disease severity or clinical course; however, a strong positive test result generally indicates an early infection.
Testing methods include indirect hemagglutination and indirect immunofluorescence. Bentonites flocculation and latex agglutination results usually remain negative for more than 1 year post-infection.
The enzyme-linked immunosorbent assay (ELISA) demonstrates 100% sensitivity by day 50, with 88% of results remaining positive 2 years after infection.
Hypersensitivity skin test
The immediate hypersensitivity skin test no longer is commercially available. Reactions results are positive (5 mm) at approximately day 17 and remain positive for life.
Molecular techniques
Molecular techniques are being developed but have not been validated.
In patients with CNS involvement, CT scanning and MRI with contrast enhancement may reveal 3- to 8-mm nodular or ringlike lesions.
Plain radiographs of the extremities
Calcified densities in the muscles, which indicate a previous Trichinella infection, may be the only positive findings observed on radiographs. However, radiographic imaging is not useful for assessing acute infestations.
Computerized tomographic (CT) scanning of the brain
CT scanning can be beneficial for patients exhibiting neurologic symptoms. The scan may reveal focal deficits along with small hypodensities in the cortex and white matter.[34]
In patients without neurologic symptoms, abnormal findings are unlikely. Additionally, CT imaging of the orbits is recommended for patients with chemosis to exclude other potential causes of proptosis.[26]
Magnetic resonance imaging (MRI) of the brain
Diffusion-weighted (DW) MRI can be useful for characterizing lesions identified on standard MRI.[35] DW MRI reveals multifocal small lesions distributed across different regions of the brain, especially at the border zone between white and gray matter. These lesions have been described with varying characteristics, often resembling those of infarcts.[35]
Electrocardiography (ECG) may reveal signs of ischemia, pericarditis, or myocarditis, including the following:
Premature contractions
Prolongation of PR intervals
Small QRS complexes with intraventricular block
Flattening or inversion of T waves, particularly in lead II and precordial leads[36]
Cardiac ultrasound (ECHO) can demonstrate pericardial fluid or wall motion abnormalities.[36]
Polymerase chain reaction (PCR) is a valuable tool for isolating the parasite and performing genetic typing, primarily used in research settings. PCR evaluation of biopsy tissue for Trichinella-specific DNA is highly sensitive and specific, allowing for the detection of worms even when initial microscopic assessments of the biopsy are negative.
Urinalysis (UA) may indicate myoglobinuria once muscle invasion occurs. In severe cases, casts and proteinuria may be present, reflecting renal damage likely caused by the inflammatory response to the larvae as they invade muscle tissue.
Parasite-specific indirect immunoglobulin G (IgG) enzyme-linked immunosorbent assay (ELISA) titers reach 100% sensitivity, and anti-newborn larvae antibodies appear in 30% of cases within 2 weeks of infection. However, these tests may not be positive initially and can exhibit cross-reactivity with other parasitic disorders, reducing their specificity when results are weakly positive.[37] ELISA results should be confirmed with Western blot analysis.[38]
Electromyography may be helpful in diagnosing moderate-to-severe infection, but no pathognomonic findings exist. The test result may reveal acute myositis or diffuse myopathic dysfunction.
Changes usually resolve 2-3 months after infection but may persist for 1-8 years.
Lumbar puncture
Lumbar puncture is used to evaluate for suspected neurologic disease.
Results are normal in 50-75% of patients.
Larvae are found in 8-24% of patients.
Eosinophilic meningitis may be present.
Muscle biopsy
Muscle biopsy provides a definitive diagnosis; however, it is rarely recommended except in difficult cases when serology tests are unhelpful.
Obtain a 0.5- to 1-g muscle biopsy specimen from the deltoid or gastrocnemius muscle because these are most easily accessible. The yield increases if the biopsy site is swollen or tender. Stain the specimen with hematoxylin and eosin (H&E) and examine multiple sections. Occasionally, larvae can be found after the muscle has been digested enzymatically.
If a biopsy is performed prior to larvae coiling (beyond day 17 of infection), worm tissue can be confused with muscle tissue.
A negative result does not necessarily exclude infection.
The presence of larvae in muscle tissue is pathognomonic. These generally are encysted, though they may not be if the patient has ingested one of the forms of Trichinella that does not form cysts. Identification of round worms in other tissue than muscle depends on knowledge of the shape and size of different round worms.
A histologic examination may reveal destruction of skeletal muscles, including a basophilic degeneration of the fibers observed on H&E-stained sections. Dead, nonencapsulated parasites can be observed. Muscle cells contain small hemorrhages and an accumulation of inflammatory cells (eg, eosinophils, lymphocytes, macrophages).
The results of a histologic examination in myocardial muscle are consistent with an immune-mediated reaction. Parasites migrate through the myocardium but do not encyst; however, a strong inflammatory reaction occurs, with numerous eosinophils, erythrocytes, fibrin deposits, and foci of necrotic myocardium. A mild-to-moderate pericardial effusion may be present. Perivascular collections of eosinophils, lymphocytes, macrophages, and polymorphonuclear leukocytes develop in the CNS and are associated with areas of ischemia. Larvae may be surrounded by astrocytes and microglial cells.
Case definitions for human trichinosis include possible cases (not applicable), probable cases (patients who meet the clinical criteria and with an epidemiological link [below]), and confirmed cases (patients who meet the laboratory criteria and clinical criteria within the past 2 months).[19]
Clinical criteria - At least 3 of the following: (1) fever, (2) muscle soreness and pain, (3) gastrointestinal symptoms, (4) facial edema, (5) eosinophilia, or (6) subconjunctival, subungual, and retinal hemorrhages
Laboratory criteria - At least 1 of the following: (1) demonstration of Trichinella larvae in tissue obtained by muscle biopsy or (2) demonstration of Trichinella-specific antibody response by indirect immunofluorescence, ELISA, or Western blot
Epidemiologic criteria - At least 1 of the following: (1) consumption of laboratory-confirmed parasitized meat, (2) consumption of potentially parasitized products from a laboratory-confirmed infected animal, or (3) epidemiologic link to a laboratory-confirmed human case by exposure to the same common source
The therapeutic regimen for this condition includes anthelmintics (mebendazole or albendazole) and glucocorticosteroids.
Anthelmintics
Only three comparative studies have assessed the effectiveness of different anthelmintics for treating trichinellosis.[6] The primary drugs used are mebendazole and albendazole, whereas thiabendazole has been discontinued due to adverse effects. Pyrantel is suggested for children and pregnant women, and flubendazole has been used in some regions, though their efficacy is questionable. Anthelmintics are most effective if administered within 1 week of infection to prevent adult worms from producing new larvae and invading muscle tissue. However, treatment typically begins during the larval development stage in muscle cells. It is advised that treatment with anthelmintics be given to all infected individuals within 4 to 6 weeks of exposure. Early administration of mebendazole, within 48 hours of consuming highly infected meat, has been shown to prevent clinical disease. Delayed treatment increases the likelihood of long-term viability of larvae in the muscles, potentially causing persistent myalgia.
Mebendazole
Several studies have confirmed the effectiveness of mebendazole, a benzimidazole anthelmintic, in treating trichinellosis.[6] Mebendazole is poorly absorbed in the intestinal lumen, and plasma concentrations vary widely among individuals. Its absorption can be enhanced with the concurrent administration of cimetidine. Mebendazole typically is prescribed at a daily dose of 5 mg/kg, divided into 2 doses, for a duration of 10 to 15 days, with the option to repeat the cycle after 5 days. In some countries, higher doses of 20 mg/kg/day to 25 mg/kg/day are recommended, which are associated with more frequent adverse effects such as allergic reactions, elevated liver enzymes, alopecia, and bone marrow depression. High-dose treatments require close medical supervision, including monitoring of blood counts and liver function. The effectiveness of mebendazole against muscle larvae varies with the timing and dosage of the treatment. For instance, lower cumulative doses started 1 month post-infection have failed to eliminate muscle larvae, whereas a very high cumulative dose started 4 months post-infection showed a larvicidal effect.
Albendazole
Albendazole, a benzimidazole carbamate anthelmintic, is absorbed relatively quickly in the intestinal lumen. Peak plasma concentrations of its sulphoxide metabolite are reached 1 to 4 hours after a single 400mg dose, and these concentrations can increase two to four-fold when taken with a fatty meal. However, there is significant variability in plasma concentrations among individuals. For doses of 15mg/kg, concentrations ranged from 0.45 mg/l to 2.96 mg/l, with the metabolite's half-life between 10 and 15 hours. It's unclear if the higher concentrations of albendazole compared to mebendazole correlate with greater antiparasitic activity. Albendazole is generally well-tolerated in trichinellosis patients. High doses used in echinococcosis treatment have caused side effects such as gastrointestinal issues, dizziness, headaches, urticaria, itching, leukopenia, and elevated serum transaminases. Alopecia has also been reported. Albendazole is available in 200 mg tablets or as a suspension, and the recommended adult dosage is 800 mg/day, divided into two doses for 10 to 15 days. For children over two years, the dosage is 10 mg/kg. Treatment may be repeated after five days for severe infections, and monitoring of blood cell counts and liver function is advised.
New formulations
The effectiveness of benzimidazoles, such as mebendazole and albendazole, is hindered by their low water solubility, leading to poor bioavailability and absorption in the intestinal tract. To enhance their absorption and plasma concentration, formulations have been developed for use in animal models. These include solid dispersions with polyvinyl-pyrrolidone and liquid solutions of albendazole with absorption enhancers, crystalline cyclodextrin complexes, or arachis oil-polysorbate 80 as an excipient. Although promising, further research is necessary to confirm the potential of these approaches for human treatment.
Glucocorticosteroids
Glucocorticosteroids are commonly used by physicians to manage type I hypersensitivity symptoms, despite the lack of controlled studies validating their efficacy.[6] They should always be used alongside anthelmintics, not alone, to avoid increasing the larval burden by delaying worm expulsion from the intestines. Research indicates that combining steroids with mebendazole can significantly reduce the duration of fever and may cause prolonged eosinophilia due to delayed encapsulation of muscular larvae. Glucocorticosteroids are also beneficial in treating acute vasculitis and myositis by inhibiting eosinophil activation and preventing endothelial damage. Additionally, combining dexamethasone with albendazole can increase serum levels of albendazole sulphoxide by about 50%. Prednisolone is the most commonly used glucocorticosteroid, typically administered in doses of 30 mg to 60 mg per day over 10 to 14 days.
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 emergency care other than as indicated for their presenting symptoms of gastroenteritis or muscle pains while awaiting confirmatory laboratory test results.
Patients with more severe cases of muscle involvement may need admission for basic supportive therapy (eg, oxygen, intravenous fluids).
Cardiac management should occur as suggested by presentation. Cardiac involvement most commonly has been reported to resemble myocarditis or pericarditis.
Medical Care
In the acute setting, supportive care for gastroenteritis and muscle pain should be instituted. In patients with more severe muscle involvement that may include diaphragmatic involvement leading to respiratory insufficiency, supplemental oxygen may be needed.
In moderate-to-heavy Trichinella infections, the goal is to stop the larval invasion into the host muscle.
In a study in Romania, patients treated with corticosteroids and albendazole experienced longer hospitalizations than those treated with albendazole alone.[39] 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.[40]
Within 1 week of ingestion of contaminated meat, administer albendazole (5 mg/kg/d for 1 wk) or mebendazole (5 mg/kg/d for 8-14 d). Note that mebendazole is not commercially available in the United States but can be obtained from Expert Compound Pharmacy (expertpharmacy.org).
This drug is effective against worms limited to the intestinal lumen.
No diet limitations are indicated; however, this is an excellent opportunity to educate patients regarding the avoidance of potentially infected meats and how to properly cook and store foods. For further details, see Prevention.
For severe infections, bed rest is recommended. This is especially important upon evidence of myocardial involvement because patients may deteriorate clinically during ambulation.
After a successful course of medications, patients have experienced menstrual irregularities, hearing disorders, weight loss, hair and nail loss, skin desquamation, aphonia, muscle stiffness, and hoarseness.[41]
The following suggestions for prevention and control of trichinosis in humans have been adapted from the World Health Organization[42] :
Cook meat to safe temperatures, using a food thermometer to measure the internal temperature of the cooked meat.
Ensure appropriate temperatures are reached for different types of meat.
Wash hands and other food preparation and storage equipment with warm water and soap after handling raw meat.
Ensure proper hygiene during preparation, serving, and storage of food.
Freezing does not always ensure that all of the Trichinella will be destroyed.
It is recommended that proper temperatures be maintained for at least 1 minute.[43] Trichinella infection in animal populations can be prevented by not allowing domesticated and wild animals to eat uncooked meat of any animals that may be infected with Trichinella.
In suspected cases that do not require admission, ensure early follow-up for continued monitoring and diagnostic evaluation, if needed.
Admit patients with neurologic or cardiac symptoms for initiation of therapy.
Consider patients with significant diffuse muscle involvement for hospitalization since they may have some degree of respiratory compromise due to diaphragmatic or intercostal muscle involvement.
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 their pain is reported as more persistent. Nurse cells in encapsulated species tend to eventually calcify, resulting in diminution of the painful inflammation.
Patients with CNS, cardiac, or renal involvement may have protracted courses with persistent stiffness, neurologic disorders, and heart or kidney dysfunction.
The following organizations have released guidelines for the management of trichinosis (trichinellosis). Key diagnostic and management recommendations have been reviewed and integrated throughout the article.
2007. Food and Agriculture Organization/World Health Organization/World Organization for Animal Health - Surveillance, Prevention, and Control of Trichinellosis[6]
It is difficult to differentiate the efficacy of drug therapy from natural recovery of infection in mild-to-moderate cases. Factors such as the Trichinella species involved, intensity and length of infection, and host response can aid in deciding on the treatment course.[44] The mainstays of therapy include bed rest, antipyretics, and analgesics. Anthelmintic medications and steroids have a limited role in therapy. If anthelmintic medications are used, the drug of choice is albendazole, because it appears to have the best adverse-effect profile and efficacy.
Class Overview
Benzimidazoles, specifically albendazole and mebendazole, are the primary medications for treating trichinellosis. They disrupt microtubule formation, primarily affecting glucose absorption of Trichinellae, which decreases mobility and aids in expulsion from the intestinal tract. However, these medications are poorly absorbed in the intestines, limiting their effectiveness against larvae in the muscle phase and encysted worms, which do not require mobility.[45]
Efficacy and Trials
Due to the limited number of cases in outbreaks, comparative trials at various infection stages are scarce, leading to controversy related to dosing and effectiveness during the muscle phase. One Italian trial showed that although mebendazole improved symptoms in all patients, 3-45% experienced symptom recurrence after a 10-day course.[46] A study in Thailand reported 100% resolution of myalgias in groups treated with mebendazole or thiabendazole, compared with only 50% resolution in groups treated with fluconazole and pyrantel.[47]
Thiabendazole is not recommended due to its adverse effects, including rashes and gastrointestinal upset.[48] A Romanian review indicated that children responded better to albendazole than adults, and both children and adults had better outcomes with albendazole compared with mebendazole.[39, 49]
Mechanism of Action
Benzimidazole drugs bind to helminthic beta-tubulin, preventing microtubule assembly and inhibiting glucose uptake, leading to parasite immobilization and death.
Safety Considerations
Albendazole and mebendazole are not recommended during the first trimester of pregnancy or for children under 2 years, based on animal studies.[45] However, a report involving over a thousand pregnant individuals treated with mebendazole during the second trimester found no increased risk of adverse outcomes compared with placebo.[50]
Emerging Treatments
Increasing resistance to helminths has prompted research into new treatments, including the activity of various Artemisia species, known for their effectiveness against malaria, which have shown promise against Trichinella in animal models.[51]
Controversy in Treatment
Anthelmintic therapy remains controversial due to the lack of controlled trials and the fact that many infected individuals experience mild cases without complications or long-term sequelae. Additionally, anthelmintics are considered minimally effective during the muscular phase of infection.
Clinical Context:
Decreases ATP production in worms, causing energy depletion, immobilization, and death. To avoid inflammatory response in CNS, administer with anticonvulsants and high-dose glucocorticoids. Available as 200-mg tabs. Practically insoluble in water; absorption enhanced if taken with fatty meal. Good penetration into CNS and better tolerated than thiabendazole.
Clinical Context:
Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible intestine, where helminths dwell. Available as 100-mg chewable tabs.
Clinical Context:
For mixed helminthic infections; inhibits helminth-specific mitochondrial fumarate reductase; alleviates symptoms of trichinosis during invasive phase. Little value in disease that spreads beyond lumen of intestines; absorption from GI tract is poor. Use limited because of adverse-effect profile. Available in 500-mg tab and 500-mg/5-mL susp. Administer with meals.
The benzimidazole drugs albendazole, mebendazole, and thiabendazole are the available medications. These drugs bind helminthic beta-tubulin, which prevents microtubule assembly and inhibits glucose uptake, resulting in parasite immobilization and death.
Clinical Context:
DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, upper GI disease, or current therapy with oral anticoagulants. Reduces fever by acting directly on hypothalamic heat-regulating centers, which increases dissipation of body-heat via vasodilation and sweating.
Pain control is essential to quality patient care. Analgesics ensure patient comfort and have sedating properties, which are beneficial for patients with pain.
Clinical Context:
Prednisolone is the most commonly reported corticosteroid used. It is favored over prednisone since it does not require hepatic processing which may be impaired by the anthelmintics recommended.
Use in severe infections with signs of shock or significant pulmonary, CNS, or cardiac involvement. Steroids reduce number of worms expelled from GI tract, which may increase number of larvae produced.
Steroids decrease inflammatory response in the host.
Glucocorticoids generally are administered to combat the inflammatory response generated by the larvae, though no controlled studies have been published.[5]
Corticosteroids frequently are used to decrease myalgia and to limit eosinophilia and the associated inflammatory response, particularly if neurologic or myocardial involvement is present.[5]
Darvin Scott Smith, MD, MSc, DTM&H, FIDSA, Chief of Infectious Diseases and Geographic Medicine, Department of Internal Medicine, Kaiser Permanente Medical Group
Disclosure: Nothing to disclose.
Coauthor(s)
Gianna Jamilecks Nino-Tapias, Stanford University
Disclosure: Nothing to disclose.
Jeanette Rios, Stanford University
Disclosure: Nothing to disclose.
Joyce Essuman, Stanford University
Disclosure: Nothing to disclose.
L Kristian Arnold, MD, MPH, Chief Medical Officer, ArLac Global Health Services, Lexington, MA; Medical Director, Boston Police Department; Assistant Professor (Retired), Emergency Medicine, Boston University School of Medicine
Disclosure: Nothing to disclose.
Rebecca-Ann S Jattan, Stanford University
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
John L Brusch, MD, FACP, Corresponding Faculty Member, Harvard Medical School
Disclosure: Nothing to disclose.
Additional Contributors
Lauren E Wedekind, Stanford University
Disclosure: Nothing to disclose.
Pranatharthi Haran Chandrasekar, MBBS, MD, Professor, Chief of Infectious Disease, Department of Internal Medicine, Wayne State University School of Medicine
Disclosure: Nothing to disclose.
Stephanie A Nevins, Research Assistant, Department of Genetics, Snyder Lab, Stanford University School of Medicine
Disclosure: Nothing to disclose.
Acknowledgements
Clinton Murray, MD Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium
Clinton Murray, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Association of Military Surgeons of the US, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
References
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Government of Canada. Trichinellosis - Fact Sheet. Government of Canada. Available at https://inspection.canada.ca/en/animal-health/terrestrial-animals/diseases/reportable/trichinellosis/fact-sheet. March 11, 2013; Accessed: January 23, 2025.
[Guideline] Dupuoy-Camet, Bruschi F. Management and Diagnosis of Human Trichinellosis. FAO/WHO/OIE Guidelines for the Surveillance, Prevention, and Control of Trichinellosis. Trichinellosis.org. Available at http://www.trichinellosis.org/uploads/FAO-WHO-OIE_Guidelines.pdf. 2007; Accessed: January 23, 2025.
Murrell KD, Pozio E. Systematics and epidemiology of Trichinella. Adv Parasitol. 2006. 63:367.
CDC. Surveillance for Trichinellosis — United States, 2015 Annual Summary. US Centers for Disease Control and Prevention. Available at https://stacks.cdc.gov/pdfjs/web/viewer.html?file=https://stacks.cdc.gov/view/cdc/55300/cdc_55300_DS1.pdf. 2015; Accessed: January 24, 2025.
USDA. Foodborne Illness and Disease Safe Food Handling and Preparation. US Department of Agriculture. Available at https://www.fsis.usda.gov/food-safety/safe-food-handling-and-preparation/meat-catfish/fresh-pork-farm-table. December 10, 2024; Accessed: January 24, 2025.
WHO. Foodborne parasitic infections: Trichinellosis (trichinosis). World Health Organization. Available at https://www.who.int/publications/i/item/WHO-UCN-NTD-VVE-2021.7. June 22, 2021; Accessed: January 23, 2025.
Life cycle of Trichinella in humans. Courtesy of Dickson Despommier, PhD, and Daniel Griffin, MD, PhD, Parasitic Diseases, 6th Ed, published by Parasites Without Borders (www.parasiteswithoutborders.com).
Trichinella nurse cell. Courtesy of Dickson Despommier, PhD, and Daniel Griffin, MD, PhD, Parasitic Diseases, 6th Ed, published by Parasites Without Borders (www.parasiteswithoutborders.com).
Encysted larvae of Trichinella species in muscle tissue, stained with hematoxylin and eosin (H&E). The image was captured at 400X magnification. Courtesy of the US Centers for Disease Control and Prevention (http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.htm).
Trichinella larvae, in pressed bear meat, partially digested with pepsin. Courtesy of the US Centers for Disease Control and Prevention ((http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.htm).
Larvae of Trichinella from bear meat. Courtesy of the US Centers for Disease Control and Prevention (http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.htm).
Epidemiology of trichinellosis in the US. Courtesy of Centers for Disease Control and Prevention (CDC) (https://www.cdc.gov/parasites/trichinellosis/resources/trichinellosis_surveillance_summary_2015.pdf).
Reported cases of trichinellosis 2011-2015. Courtesy of Centers for Disease Control and Prevention (CDC) (https://www.cdc.gov/parasites/trichinellosis/resources/trichinellosis_surveillance_summary_2015.pdf).
The number of cases of trichinellosis by age. Courtesy of Centers for Disease Control and Prevention (CDC) (https://www.cdc.gov/parasites/trichinellosis/resources/trichinellosis_surveillance_summary_2015.pdf).
Encysted larvae of Trichinella species in muscle tissue, stained with hematoxylin and eosin (H&E). The image was captured at 400X magnification. Courtesy of the US Centers for Disease Control and Prevention (http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.htm).
Trichinella larvae, in pressed bear meat, partially digested with pepsin. Courtesy of the US Centers for Disease Control and Prevention ((http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.htm).
Larvae of Trichinella from bear meat. Courtesy of the US Centers for Disease Control and Prevention (http://www.dpd.cdc.gov/dpdx/HTML/Trichinellosis.htm).
The number of cases of trichinellosis by age. Courtesy of Centers for Disease Control and Prevention (CDC) (https://www.cdc.gov/parasites/trichinellosis/resources/trichinellosis_surveillance_summary_2015.pdf).
Epidemiology of trichinellosis in the US. Courtesy of Centers for Disease Control and Prevention (CDC) (https://www.cdc.gov/parasites/trichinellosis/resources/trichinellosis_surveillance_summary_2015.pdf).
Reported cases of trichinellosis 2011-2015. Courtesy of Centers for Disease Control and Prevention (CDC) (https://www.cdc.gov/parasites/trichinellosis/resources/trichinellosis_surveillance_summary_2015.pdf).
Trichinella nurse cell. Courtesy of Dickson Despommier, PhD, and Daniel Griffin, MD, PhD, Parasitic Diseases, 6th Ed, published by Parasites Without Borders (www.parasiteswithoutborders.com).
Life cycle of Trichinella in humans. Courtesy of Dickson Despommier, PhD, and Daniel Griffin, MD, PhD, Parasitic Diseases, 6th Ed, published by Parasites Without Borders (www.parasiteswithoutborders.com).
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