Epidemiology

Trichinella occurs worldwide with the cycle maintained in several different mammalian species. The mammal serves as the definitive host for the adult worm and the intermediate host for the encysted larvae. Humans acquire the infection by eating undercooked meat that contains the infective encysted larvae. Although this is typically transmitted in pork, human cases have been associated with ingestion of bear, walrus, horsemeat, and other mammals.

The encysted larvae are ingested. When the undercooked meat is digested in the stomach, the larvae are resistant to the gastric pH and pass to the intestine, where they invade the mucosa. In about 1.5 days, the larvae mature and mate, and the female worm begins to release motile larvae. These larvae then migrate to the lymphatic system or mesenteric venules and become distributed throughout the body. The larvae then deposit in the striated muscle tissue, where they can continue development, coil, and encyst, becoming infective. The larvae encyst in the active striated muscle including the diaphragm, larynx, tongue, jaws, neck, ribs, biceps, and gastrocnemius. The generalized life cycle is depicted in Figure 52-1. The larvae may remain viable within the cyst for several years. The larvae eventually die and the encysted capsules become calcified.

Pathogenesis and Spectrum of Disease

Trichinosis is a disease of the muscle caused by infection with the encysted larval form of Trichinella spp. (Figure 52-2). The adult stages reside in the human intestine. The disease ranges from mild to severe dependent on the number of parasites present. The intestinal stage lasts approximately 1 week and typically includes mild symptoms of nausea, abdominal discomfort, diarrhea, and/or constipation. Diarrhea may last as long as 14 weeks with no apparent muscle involvement. The migration of the larvae results in an intense inflammatory response causing periorbital edema, fever, muscle pain or tenderness, headache, and myalgia. A marked peripheral eosinophilia is often present. If the parasitic infection is low, eosinophilia may be the only diagnostic sign evident. Occasionally, splinter hemorrhages may be present below the nails.

In addition to the typical infection of the active striated muscle as previously indicated, occasionally larvae will migrate into the brain, meninges, and myocardium. However, the larvae will not encyst in these tissues. Brain and meningeal infections will result in neurologic symptoms, and infection of the myocardium may result in myocarditis and dysrhythmias leading to sudden death.

Laboratory Diagnosis

Diagnosis may be difficult, because the symptoms may resemble a variety of flulike illnesses. A thorough patient history is required to assist the physician in diagnosing the condition in a timely fashion. Identification of encysted larvae through muscle biopsy provides definitive diagnosis. However, based on location, some tissues may be difficult to access and therefore the condition may not be diagnosed until the postmortem examination. Histologic examination of formalin-fixed or paraffin-imbedded tissue may be used to visualize encysted larvae. Occasionally, dependent on the length of infection, calcified larvae may be seen in x-rays.

Serologic diagnosis is sufficient in most cases. Patients will present with a specific antibody response in 3 to 5 weeks following acute illness. A negative serologic test followed by a positive seroconversion is considered definitive diagnosis.

Molecular species–specific polymerase chain reaction (PCR) has been developed. Various techniques including RFLP (restriction fragment length polymorphism) and RAPD (rapid amplification of polymorphic DNA) have been investigated. Currently, these methods are predominantly used in animal epidemiologic studies and have not been implemented within the diagnostic laboratory.

Therapy

Thiabendazole is used during the intestinal phase to reduce the number of potentially infective larvae, and although the encysted larvae cannot be removed, albendazole is used to limit the continued pathologic development of the organism. Supportive measures including analgesics and steroids may be administered to lessen the effects of the generalized inflammatory response.

Prevention

Most effective prevention relies on eating only thoroughly cooked meat as well as maintaining good animal husbandry for domestic swine.

Epidemiology

Toxocariasis is a zoonotic disease with worldwide distribution. Humans become infected with the accidental ingestion of eggs (Figure 52-3). The definitive hosts, dogs (T. canis) and cats (T. cati), pass the larvae transplacentally or lactogenically to their offspring and pass unembryonated eggs in the feces. The eggs mature in 10 to 20 days, and then become infective. Once the eggs are ingested, the larvae are released in the small intestine, penetrate the mucosa, and migrate to the liver, lungs, or other body sites. The larvae migrate up the respiratory tract and are swallowed, returning to the intestinal tract where they mature into adult worms. The adult worms are unable to mature in a human host and therefore wander throughout the body causing the migratory syndromes.

Pathogenesis and Spectrum of Disease

Typically the infections are mild but may be severe. Severe life-threatening infections occur when there is involvement in the heart, brain, or other vital organs. Disease is frequently found in young children and may persist for long periods with minimal pathologic manifestations. Larvae that remain in the liver or lungs may become encapsulated in fibrous tissue. Visceral (tissue) larva migrans (VLM) may result in a high degree of eosinophilia; however, this may be absent in ocular larva migrans (OLM). Symptoms may include fever, hepatomegaly, hyperglobulinemia, pulmonary infiltration, cough, neurologic symptoms, and endophthalmitis. OLM may result in the development of a granulomatous reaction in the retina of the eye.

Laboratory Diagnosis

Toxocariasis must be differentiated from other migratory helmintic diseases including A. lumbricoides, S. stercoralis, and Trichinella spp. A history of exposure to dogs and cats is of importance when considering an infection with Toxocara spp. Because humans are an insufficient host for completion of the organism’s life cycle, eggs are not passed in the stool. Diagnosis typically requires biopsy of tissue.

Serologic diagnosis has proven effective, particularly in OLM. Aqueous humor–elevated antibody titer specific for Toxocara spp., in comparison to serum levels, is considered diagnostic. Although serologic testing has been useful, it is important to note that antibody titers may vary depending on the location of the infection. A serum titer of 1 : 8 is considered significant for OLM; 1 : 32 is significant for VLM.

Therapy

Effective therapy depends on the location of infection but several anthelmintic medications have been used including thiabendazole, ivermectin, albendazole, and diethylcarbamazine. Antiinflammatory medications including corticosteroids may be used to reduce the pathology associated with inflammation. Photocoagulation has been used to treat OLM. The prognosis is good, even in cases of OLM, with prompt diagnosis and proper treatment.

Prevention

Small children should be kept out of sandboxes and playgrounds frequented by dogs and cats. Sandboxes should be covered when not in use. Encouraging regular hand washing and teaching children to keep dirt out of their mouths will decrease the potential for infection. In addition, regular deworming of dogs and cats will reduce the spread of infective eggs.

Epidemiology

The organisms are found in warm climates within the Southeastern United States. Dogs and cats are the natural definitive host for Ancylostoma spp. The infective larvae penetrate the skin of the host and migrate in the circulation. The adult worms reside in the intestine. The eggs are shed in the feces of dogs and cats. The eggs undergo maturation in moist, sandy soil in areas protected from desiccation, such as under shady trees and houses. Children are often infected when playing in sandboxes that have been contaminated with dog and cat feces.

Pathogenesis and Spectrum of Disease

The infective larvae penetrate the skin of the human host and migrate through the subcutaneous tissue. The host develops pruritic papules at the site of penetration, followed by serpiginous, vesicular, elevated linear tracks. The larvae will migrate several millimeters each day, forming these continued tracks. The area surrounding the tracks becomes inflamed with marked edema. The patient may present with a peripheral eosinophilia. Infection is typically self-limiting. As the larvae migrate, the host may scratch and scar the tissue, subjecting the host to potential secondary bacterial infections. The signs and symptoms resemble those of infection with similar insect larvae, Strongyloides stercoralis, and other animal hookworms.

Systemic involvement is rare; however, cases of pneumonitis resulting from larvae migration into the lungs have been identified. In addition, gastrointestinal discomfort including abdominal pain, diarrhea, and weight loss has been associated with Ancylostoma spp. infections. This condition is referred to as eosinophilic enteritis.

See Table 52-1 for a summarized detail of associated diseases.

  Trichinella spp. Worm burden may be small to several hundred
Migration and deposition of larvae in tissue depends on tissue involved in infection Ingestion of poorly cooked meat, particularly domestic swine, but may be found in several mammalian species including bear, walrus, horse Toxocara canis and Toxocara cati Migration in host tissue and immune response Accidental ingestion of eggs
Mild to severe disease dependent on tissue Ancylostoma braziliense or A. caninum Migration, inflammation, and edema
Secondary bacterial infections Penetrate skin and migrate in circulation
Pneumonitis may occur
Systemic involvement is rare Dracunculus medinensis Larvae migration, inflammation, and secondary bacterial infections Ingestion of infected copepods
Blisters develop where female exits the skin Parastrongylus cantonensis Migration to central nervous system Ingestion of infected shrimp, fish, crabs, and frogs
Often self-limiting, but may cause meningoencephalitis or meningitis Parastrongylus costaricensis Migration resulting in inflammation and lesions in bowel Ingestion of salad contaminated with infected slugs or snails Gnathostoma spinigerum Migration resulting in inflammation Ingestion of contaminated fish
Tissue damage based on worm burden and migration pattern

Epidemiology

The parasite was once known to have a worldwide distribution affecting millions of people. In 2008, the World Health Organization in collaboration with governmental groups and other organizations attempted to eradicate the organism. Efforts have reduced the incidence of infection, confining the remaining endemic area to Africa.

Humans are infected by the ingestion of freshwater from stagnant ponds containing larvae-infected copepods. The copepods are digested in the stomach, releasing the larvae. The larvae penetrate the small intestine and migrate through the thoracic musculature. Both adult male and female worms mature in approximately 2 to 3 months. The gravid female develops in approximately 10 to 14 months, migrating to the lower extremities. The gravid female produces a blister on the skin, and when the host submerges the affected area in water, the blister erupts and releases larvae into the water.

Pathogenesis and Spectrum of Disease

The blisters formed by the gravid female worm cause burning and itching. Systemic symptoms may include fever, nausea, vomiting, diarrhea, headache, urticaria and eosinophilia. Secondary bacterial infections may occur. In addition, dead worms within the host may be absorbed or may calcify, causing secondary inflammatory symptoms.

Laboratory Diagnosis

Diagnosis is by identification of larvae or adult worms.

Therapy

Treatment requires removal of the adult worms. The female worms are attached to a stick and slowly retracted from the host by gradual turning of the stick and removal of the worm. Although anthelmintic medications, such as metronidazole or thiabendazole, are not lethal, they are administered to assist with the retraction of the worms. Analgesics and antimicrobials are administered for discomfort and the prevention of secondary infections.

Epidemiology

The parasite has a worldwide distribution; however, it remains an endemic health threat in Southeast Asia and the Asian Pacific Islands. A variety of rodents serve as the definitive host. The adult worms reside in the pulmonary artery and right side of the heart. Eggs shed by the female lodge in the pulmonary capillaries, where the larvae hatch and migrate up the trachea. The larvae are swallowed and passed in the rodent feces. Once released the larvae infect the intermediate host, mollusks. The mollusks are consumed by a variety of paratenic hosts such as shrimp, fish, crabs, or frogs. The rodents then consume the paratenic hosts and the larvae penetrate the intestine, enter the circulation, and migrate to the central nervous system. Following two successive molts, the larvae then reenter the circulation and migrate to the pulmonary artery. Humans are infected by ingestion of either the intermediate or the paratenic host.

Pathogenesis and Spectrum of Disease

The pathogenesis correlates with the worm burden and the site of infection. The larvae may migrate to the central nervous system, causing meningitis or meningoencephalitis. Symptoms include headache, fever, eosinophilia, increased cerebrospinal fluid (CSF) protein, and neurologic manifestations. Occasionally, the larvae may migrate to the eye, causing blindness. Most often the disease is self-limiting.

Laboratory Diagnosis

Definitive diagnosis relies on histologic identification of the adult female worm. The adult female worm has a distinctive morphologic appearance with spiral, winding, “barber pole” appearing uterus. Highly specific serologic assays are available.

Therapy

Anthelmintic therapy may be helpful, such as mebendazole. It is important to closely monitor therapy, because the therapy may actually exacerbate the inflammatory response of the host and cause more systemic damage. If larvae are located within the eye, surgical removal is recommended.

Epidemiology

The parasite is endemic in areas of Central and South America including Mexico and Costa Rica.

Pathogenesis and Spectrum of Disease

The life cycle is very similar to that of Parastrongylus cantonensis. Human infection is typically by ingestion of salad contaminated with infected slugs or snails. The larvae create inflammatory lesions in the wall of the bowel, resulting in tissue inflammation, necrosis, vomiting, and diarrhea. The patient may experience lower right quadrant abdominal pain similar to that manifested in appendicitis.

Laboratory Diagnosis

Histologic identification of larvae or eggs in tissue sections results in definitive diagnosis. Patients often present with leukocytosis and eosinophilia. Radiologic imaging may be useful.

Therapy

Traditional anthelmintic therapy is recommended.

Epidemiology

The adult worms reside in the stomach of the definitive host where they mate and produce eggs that are passed in the feces. When the feces are deposited in water, the larvae hatch and infect copepods. The larvae mature in the copepods and are then ingested by a variety of hosts including fish, snakes, and frogs. Inside the paratenic host the larvae then migrate to the musculature and encyst until the tissue is ingested by the definitive host. Once in the definitive host, the larvae excyst and penetrate the gastric wall, migrating and maturing in the stomach. Humans act as accidental hosts when they ingest larvae in contaminated fish.

Pathogenesis and Spectrum of Disease

The worms are incapable of maturation within the human host and migrate aimlessly, causing tissue damage and inflammation. The infection is not typically fatal; however, it depends on the migration pattern and organs infected.

Laboratory Diagnosis

The identification of the larvae in tissue is definitive for diagnosis. The head contains four rows of cephalic hooklets. The body is covered with transverse rows of spines that diminish anteriorly to posteriorly.

Therapy

Supportive corticosteroid treatment is recommended. Although anthelmintics are not lethal, they are often recommended. Surgical excision of the larvae is optimal treatment.