Trichinosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Danitza Lukac

Trichinosis, also called trichinellosis or trichiniasis, is a parasitic disease caused by eating raw or undercooked pork and wild game products infected with the larvae of Trichinella species. Based on the severity of signs and larval density, trichinosis may be classified into asymptomatic, abortive, mild, pronounced, and severe.^[1] Trichinella spp. is usually transmitted to the human host by eating undercooked meat containing cysts of Trichinella spp. Following ingestion, exposure to gastric acid and pepsin release the larvae from the cysts and invade the small bowel mucosa. When an individual eats meat from an infected animal, Trichinella cysts break open in the intestines and grow into adult roundworms. These organisms tend to invade muscle tissues, including the heart and diaphragm. They can also affect the lungs and brain.^[2] Trichinosis must be differentiated from influenza virus, salmonella, shigella, eosinophilia-myalgia syndromes, tissular parasitosis, glomerulonephritis, serum sickness, infectious meningitis and encephalitis, leptospirosis, bacterial endocarditis and typhus exanthematicus.^[3] Worldwide, an estimated 10,000 cases of trichinosis occur every year.^[4] Common risk factors in the development of trichinosis disease are consuming raw or undercooked meat, informal meat transportation, age, antimicrobial free/organic pork and hunting practices.^{[1][4][5][6][7]} If left untreated, infected patients develop manifestations within 1-2 days of infection. Infected patients with trichinosis may progress to develop periorbital edema, muscle pain, and fever.^{[1] [2]} Complications of trichinosis affect the cardiovascular, neurological, ocular, respiratory, and digestive systems.^[3] Most people with trichinosis have no symptoms, the infection is usually self-limited. The prognosis of trichinosis is good with adequate treatment.^[8] The diagnosis of trichinosis is based on the European Center for Disease Control criteria, which include a combination of clinical, laboratory and epidemiological criteria.^[1][3] The mainstay of therapy for trichinosis are anthelmintics drugs, such as albendazole or mebendazole.^[9] The optimal way to prevent trichinosis is to cook meat to safe temperatures. Using food thermometers can make sure the temperature inside the meat is high enough to kill the parasites.^[2]

Trichinella spiralis was first discovered by James Paget, an English first-year medical student, in 1835.^[4] In 1846, Joseph Leidy, an American paleontologist, was the first to discover the association between undercooked meat and development of trichinosis.^[10] There have been several outbreaks of trichinosis, most of them for consuming infected pork, wild boar and bear.

Based on the severity of signs and larval density, trichinosis may be classified into asymptomatic, abortive, mild, pronounced, and severe. ^[1]

Trichinella spp. is usually transmitted to the human host by eating undercooked meat containing cysts of Trichinella spp. Following ingestion, exposure to gastric acid and pepsin release the larvae from the cysts and invade the small bowel mucosa. When an individual eats meat from an infected animal, Trichinella cysts break open in the intestines and grow into adult roundworms. Females are approximately 2.2 mm in length; males 1.2 mm. The life span in the small intestine is approximately four weeks. After 1 week, the females release more larvae that migrate through the bloodstream to voluntarily controlled muscles where they encyst. These organisms tend to invade muscle tissues, including the heart and diaphragm. They can also affect the lungs and brain.^[2] Characteristic findings on microscopic histopathological analysis of the muscle, the nurse cell has a collagen capsule with larvae inside and is surrounded by cellular infiltrates.^[1]

Common cause of trichinosis include Trichinella spiralis. Less common causes of trichinosis include T. britovi, T. nativa, T. pseudospiralis, T. papuae, T. nelsoni, T. murrelli, and T. zimbabwensis.^[4]

Trichinosis must be differentiated from influenza virus, salmonella, shigella, eosinophilia-myalgia syndromes, tissular parasitosis, glomerulonephritis, serum sickness, infectious meningitis and encephalitis, leptospirosis, bacterial endocarditis and typhus exanthematicus.^[3]

Worldwide, an estimated 10,000 cases of trichinosis occur every year.^[4] Trichinosis is rare in developed countries, but it is still common in developing countries.

Common risk factors in the development of trichinosis disease are consuming raw or undercooked meat, informal meat transportation, age, antimicrobial free/organic pork, and hunting practices.^{[1][4][5][6][7]}

If left untreated, infected patients develop manifestations within 1-2 days of infection. Infected patients with trichinosis may progress to develop periorbital edema, muscle pain, and fever.^{[1] [2]} Complications of trichinosis affect the cardiovascular, neurological, ocular, respiratory, and digestive systems.^[3] Most people with trichinosis have no symptoms, the infection is usually self-limited. The prognosis of trichinosis is good with adequate treatment.^[8]

The diagnosis of trichinosis is based on the European Center for Disease Control criteria, which include a combination of clinical, laboratory and epidemiological criteria.^[1][3]

Trichinosis initially involves the intestines. Symptoms include nausea, heartburn, dyspepsia, and diarrhea. The severity of symptoms depends on the number of worms ingested. As the worms encyst in different parts of the human body, other manifestations may occur, such as headache, fever, chills, cough, eye swelling, joint pain and muscle pain, and itching. A positive history of gastroenteritis symptoms, muscle pain and fever and recent ingestion of undercooked meat such as pork, wild boar or bear is suggestive of trichinosis.^[1][2][4]

Common physical examination findings of trichinosis include periorbital edema and splinter hemorrhage.^[1][2]

Laboratory findings suggestive of trichinosis include eosinophilia, elevated muscle enzymes and anti trichinella IgG. Muscle biopsy is diagnostic of trichinosis.^[1][2]

The mainstay of therapy for trichinosis are anthelmintics drugs such as albendazole or mebendazole.^[9]

The optimal way to prevent trichinosis is to cook meat to safe temperatures. Using food thermometers can make sure the temperature inside the meat is high enough to kill the parasites.^[2]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Danitza Lukac

Trichinella spiralis was first discovered by James Paget, an English first-year medical student, in 1835.^[1] In 1846, Joseph Leidy, an American paleontologist, was the first to discover the association between undercooked meat and development of trichinosis.^[2] There have been several outbreaks of trichinosis, most of them for consuming infected pork, wild boar and bear.

• Trichinella spiralis was first discovered by James Paget, a English first-year medical student, in 1835 while witnessing and autopsy at St. Bartholomew’s Hospital in London.
• Paget took special interest in the presentation of muscle with white flecks, described as a “sandy diaphragm”.
• Although Paget is most likely the first person to have noticed and recorded these findings, the parasite was named and published in a report by his professor, Richard Owen, who is now credited for the discovery of the T. spiralis larval form.
• Trichinosis was known as early as 1835 to have been caused by a parasite, but the mechanism of infection was unclear at the time.
• It was not until a decade later that the American scientist Joseph Leidy pinpointed undercooked meat as the primary vector for the parasite, and not until two decades afterwards that this hypothesis was fully accepted by the scientific community.^[3]

• The kashrut and halal dietary laws of Judaism and Islam prohibit eating pork.
  • In the 19th century, when the association between trichinosis and under-cooked pork was first established, it was suggested that this association was the reason for the prohibition, reminiscent of the earlier opinion of the medieval Jewish philosopher Maimonides that food forbidden by Jewish law was “unwholesome”.
  • This theory was controversial and eventually fell out of favor.^[3]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Danitza Lukac

Based on the severity of signs and larval density, trichinosis may be classified into asymptomatic, abortive, mild, pronounced, and severe. ^[1]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Danitza Lukac

Trichinella spp. is usually transmitted to the human host by eating undercooked meat containing cysts of Trichinella spp. Following ingestion, exposure to gastric acid and pepsin release the larvae from the cysts and invade the small bowel mucosa. When an individual eats meat from an infected animal, Trichinella cysts break open in the intestines and grow into adult roundworms. Females are approximately 2.2 mm in length; males 1.2 mm. The life span in the small intestine is approximately four weeks. After 1 week, the females release more larvae that migrate through the bloodstream to voluntarily controlled muscles where they encyst. These organisms tend to invade muscle tissues, including the heart and diaphragm. They can also affect the lungs and brain.^[1] Characteristic findings on microscopic histopathological analysis of the muscle, the nurse cell has a collagen capsule with larvae inside and is surrounded by cellular infiltrates.^[2]

• Trichinosis is acquired by ingesting meat containing cysts (encysted larvae) (life cycle stage: 1) of Trichinella.

• After exposure to gastric acid and pepsin, the larvae are released (life cycle stage: 2) from the cysts and invade the small bowel mucosa.
• Thirty to 34 hours after the cysts were originally ingested, they develop into adult worms (life cycle stage: 3) (female approximately 2.2 mm in length, males 1.2 mm); life span in the small bowel is approximately 4 weeks.
• The adults worms mate. The production of larvae generally occurs within 5 days.
• The worms can only reproduce for a limited time. The immune system will eventually expel them from the small intestine.
• After 1 week, the females release larvae (life cycle stage: 4).
• The newborn larvae then use their piercing mouthpart (called the “stylet”) to pass through the intestinal mucosa.

• The newborn larvae enter the lymphatic vessels and then enter the bloodstream.
• The larvae travel by capillaries to various organs, such as the retina, myocardium, or lymph nodes; however, only larvae that migrate to skeletal muscle cells survive and encyst.
• Skeletal muscle cells act as nurse cells where larvae can develop and after weeks, months or years calcify.
• Encystment is completed in 4 to 5 weeks and the encysted larvae may remain viable for several years (life cycle stage: 5).^[1][2][3]

• Males T. spiralis:
  • Measure between 1.4 and 1.6 mm long and are more flat anteriorly than posteriorly.
  • The anus can be found in the terminal (side) and they have a large copulatory pseudobursa on each side.
• Females T. spiralis:
  • Are about twice the size of the males
  • Have an anus found terminally
  • The vulva is located near the esophagus
  • The single uterus of the female is filled with developing eggs in the posterior portion, while the anterior portion contained the fully developed juveniles.^[4]
• Muscle biopsy (hematoxylin and eosin stain):
  • Nurse cell has a collagen capsule (thickness depends on Trichinella species) with larvae inside and surrounded by cellular infiltrates.^[2]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Danitza Lukac

Trichinosis is caused by Trichinella species. The most common species involved in trichinosis is T. spiralis. Less common species include T. britovi, T. nativa, T. pseudospiralis, T. papuae, T. nelsoni, T. murrelli, and T. zimbabwensis.^[1]

• Trichinosis is usually caused by T. spiralis. T. spiralis is usually found worldwide in many carnivorous and omnivorous animals,
• Other species of Trichinella include:^[1]
  • T. pseudospiralis (mammals and birds worldwide)
  • T. nativa (Arctic bears)
  • T. nelsoni (African predators and scavengers)
  • T. britovi (carnivores of Europe and western Asia)
  • T. papuae (wild and domestic pigs, Papua New Guinea and Thailand).

Species and characteristics:

• Trichinosis is acquired by ingesting meat containing cysts (encysted larvae) (life cycle stage: 1) of Trichinella.
• Sylvatic cycle: Pigs become infected when they eat infectious cysts in raw meat, often pork or rats.
• Domestic cycle: Humans become infected when they eat raw or undercooked infected pork.
• After exposure to gastric acid and pepsin, the larvae are released (life cycle stage: 2) from the cysts and invade the small bowel mucosa where they develop into adult worms (life cycle stage: 3) (female 2.2 mm in length, males 1.2 mm; life span in the small bowel: 4 weeks).
• After 1 week, the females release larvae (life cycle stage: 4) that migrate to the striated muscles where they encyst (life cycle stage: 5).
• Encystment is completed in 4 to 5 weeks and the encysted larvae may remain viable for several years.
• Ingestion of the encysted larvae perpetuates the cycle.
• Rats and rodents are primarily responsible for maintaining the endemicity of this infection.
• Carnivorous/omnivorous animals, such as pigs or bears, feed on infected rodents or meat from other animals.
• Different animal hosts are implicated in the life cycle of the different species of Trichinella.
• Humans are accidentally infected when eating improperly processed meat of these carnivorous animals (or eating food contaminated with such meat).^[1][3]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Danitza Lukac

Trichinosis must be differentiated from influenza virus, salmonella, shigella, eosinophilia-myalgia syndromes, tissular parasitosis, glomerulonephritis, serum sickness, infectious meningitis and encephalitis, leptospirosis, bacterial endocarditis and typhus exanthematicus.^[1]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Danitza Lukac

Worldwide, an estimated 10,000 cases of trichinosis occur every year.^[1] Trichinosis is rare in developed countries, but it is still common in developing countries.

• Worldwide, an estimated 10,000 cases of trichinosis occur every year.
• During 2008–2012, a total of 90 cases of trichinosis were reported in the USA.
• In the USA, the average of trichinosis is approximately 15 cases per year.^[1]

• The mortality rate of trichinosis is approximately 0.2% worldwide.^[2]

• Trichinosis most commonly affects individuals 30 to 39 years of age.^[3]
• Although infections also occur in children and adolescents, the predominance of infection in adults probably results from culture-driven food behavior.
• Improperly cooked or prepared meat dishes may be more commonly eaten at adult-oriented events, especially among alcohol consumers.^[4]

• Men are more commonly affected with trichinosis than women.^[3]

• There is no racial predilection to trichinosis.

• In the US and EU, the overall incidence of trichinosis is low given the improved pig-raising practices in the pork industry, commercial and home freezing of pork, and public awareness of the danger of eating raw or undercooked meat products.
• The number of cases associated with raw or undercooked wild game meats has remained relatively constant over time.^[1][5][6]

• Trichinosis is common in developing countries where meat fed to pigs is either raw or undercooked.^[7]
• In South America, outbreaks in Argentina are common.
• Incidence data from developing countries are limited.
• In Asia, the majority of the outbreaks were reported from Thailand, Laos, and Vietnam, and the northern mountainous regions among the indigenous people who practice free-roaming pig husbandry.^[4]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Danitza Lukac

Common risk factors in the development of trichinosis disease are: consuming raw or undercooked meat, informal meat transportation, age, antimicrobial free/organic pork and hunting practices.^{[1][2][3][4][5]}

Common risk factors in the development of trichinosis disease are:

• Particularly wild game meat or pork^[1]
• Informal or clandestine meat transportation^[2]

• Predominance of infection in adults probably results from culture-driven food behavior. Improperly cooked or prepared meat dishes may be more commonly eaten at adult-oriented events, particularly if alcohol is consumed.^[2]

• Farmers and producers must certify the safety of the meat by using good practices.^[3][4]

• In some countries such as Papua New Guinea, hunting practices lead men to eat undercooked meat regularly.^[5]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Danitza Lukac

If left untreated, infected patients develop manifestations within 1-2 days of infection. Infected patients with trichinosis may progress to develop periorbital edema, muscle pain, and fever.^[1][2] Complications of trichinosis affect the cardiovascular, neurological, ocular, respiratory, and digestive systems.^[3] Most people with trichinosis have no symptoms, the infection is usually self-limited. The prognosis of trichinosis is good with adequate treatment.^[4]

• Trichinosis is usually self-limited, and the majority of individuals with trichinosis are asymptomatic.
• The symptoms vary depending on the phase, species of Trichinella, amount of encysted larvae ingested, age, gender, and host immunity.
• Patients infected by 10 or less larvae have either minor or no symptoms and no complications.

• From two to seven days after infection.
• The large burden of adult worms in the intestines promote symptoms such as nausea, heartburn, dyspepsia, and diarrhea.

• The parental phase starts approximately seven days after infection.
• The severity of symptoms caused by larval migration from the intestines depends on the number of larvae produced.
• As the larvae migrate through tissue and vessels, the body’s inflammatory response results in edema, muscle pain, fever, and weakness.
• A classic sign of trichinosis is periorbital edema, swelling around the eyes, which may be caused by vasculitis.
• If left untreated, the worms may cause enough damage to produce serious neurological deficits (such as ataxia or respiratory paralysis) from worms entering the central nervous system (CNS).
• The CNS is compromised by trichinosis in 10–24% of reported cases of cerebral venous sinus thrombosis, a very rare form of stroke (3-4 cases per million annual incidence in adults).
• Trichinosis can be fatal depending on the severity of the infection. Death can occur 4–6 weeks after the infection, and is usually caused by myocarditis, encephalitis, or pneumonia.^[1][2]

Common complications of trichinosis include:^[3]

• Heart failure
• Heart rhythm problems (arrhythmias) from heart inflammation (myocarditis)
• Thromboembolic disease
  • Deep thrombophlebitis
  • Intraventricular thrombi
  • Pulmonary embolism
• Paroxysmal tachycardia
• Pericardial effusion

• Encephalomyelitis
• Neuromuscular disturbances:
  • Decreased muscular strength and tendon reflexes
  • Dysphagia
  • Trismus

• Edema and vascular lesions within the conjunctiva, uvea, retina, and, in some cases, the optic nerve
• Pain when moving the eyeballs
• Muscle paralysis
• Diplopia
• Disturbed accommodation

• Dyspnea
• Pneumonia
• Obstructive bronchitis
• Löffler-type infiltrates or ventilature failures

• Hypoalbuminemia
• Acute intestinal necrosis
• Prolonged diarrhoea

• The prognosis of trichinosis is good with adequate treatment.
• Most people with trichinosis have no symptoms, the infection is usually self-limited.^[4]
• The mortality rate of trichinosis is approximately 0.2% worldwide.^[6]
• Prompt treatment with antiparasitic drugs can help prevent the progression of trichinosis by killing the adult worms and so preventing further release of larvae.
• Once the ”Trichinella” larvae have become established in skeletal muscle cells, usually by 3 to 4 weeks post infection, treatment may not completely eliminate the infection and associated symptoms.
• If trichinosis treatment is not initiated within the first several days of infection, more prolonged or repeated courses of treatment may be necessary.^[7]