AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Background

Tapeworms are long, segmented worms of the class Cestoda, which comprise 1 of 3 classes of parasitic worms (worms that require a host within which to mature). The other classes are Nematoda and Trematoda. These worms lack an intestinal tract and instead are able to absorb nutrients through their integument. The adult consists of a head (scolex), where the worms attach to the mucosa of the intestine; a neck; and a segmented body that contains both male gonads and female gonads (proglottids).

Cestodes include the following:

• Taenia solium
• Taenia saginata
• Diphyllobothrium
• Hymenolepis
• Dipylidium caninum
• Echinococcus
• Spirometra
• Taenia multiceps

Pathophysiology

Typically, a cestode requires one or more intermediate hosts in their life cycle. The life cycle is as follows:

• The eggs are passed into the soil from the primary host.
• The fertile eggs are ingested by an intermediate host in which they hatch.
• The larvae enter the tissues and encyst.
• The primary host ingests the cysts in the flesh of the intermediate host.

When humans are the primary host, the adult cestode is limited to the intestinal tract. When humans are the intermediate hosts, the larvae are within the tissues, migrating through the different organ systems.

Typically, the cestode requires one or more intermediate hosts in its life cycle. Eggs are passed into the environment from the primary host. An intermediate host ingests the fertile eggs, and they hatch inside this second host. Next, the larvae enter the tissue and encyst. Finally, the primary host ingests the cysts by ingesting the flesh of the intermediate host.

In most cestode infestations (ie, T solium, T saginata, Diphyllobothrium species, Hymenolepis species, and D caninum), humans are the primary hosts. Adult worms survive inside their human hosts, where they are limited to the intestinal tract. Human fecal contamination of the environment is needed to sustain these life cycles.

In the remaining cestodes (ie, Echinococcus species, Spirometra species, and T multiceps), humans function as the intermediate hosts. Larvae exist within the tissues and migrate through different organ systems.

Hymenolepis species and T solium are the only cestodes for which humans can function as both primary hosts and intermediate hosts. Hymenolepis diminuta is primarily a parasite of rodents, although humans can be a rare and accidental host in the life cycle. Humans are infected by swallowing insects that contain cysticercoid larvae, most often by ingesting mealworms or grain beetles that infest dried grains, cereals, flour, and dried fruit.

Cestodes and Their Hosts

Cestode	Primary Host	Intermediate Host
T solium	Humans	Pigs, humans, dogs, cats, sheep
T saginata	Humans	Cattle
Diphyllobothrium	Humans	Fish
Hymenolepis	Humans	Hymenolepis nana: None; Hymenolepis diminuta: Rodents
D caninum	Humans, dogs, cats	Fleas on dogs/cats
Echinococcus	Dogs	Humans, sheep, cattle, goats, horses, camel
Spirometra	Humans
T multiceps		Hares, rabbits, squirrels, humans (rarely)

Frequency

United States

Although many cestode infestations occur worldwide, only a few are common in the United States.

Diphyllobothriasis is an infection that occurs from eating raw or undercooked fish infected with Diphyllobothrium species. Diphyllobothrium organisms are present in lakes, rivers, and deltas of freshwaters. Eskimos in western Alaska and the West Coast of the United States are frequent hosts.

Echinococcus multilocularis causes alveolar echinococcosis, which occurs only in the northern hemisphere. In the United States, it occurs particularly in Alaska. Echinococcus granulosis causes hydatid disease, which occurs worldwide.

Although infection with T saginata (obtained from raw or undercooked beef) occurs worldwide, the prevalence in the United States is less than 1% because most cattle in the United States are free of the parasite. Infection with T solium is rare, but with the growing number of immigrants from endemic areas, the frequency is changing.

Infection with H nana is the most frequently diagnosed cestode infection in the United States.

Spirometra species cause sparganosis, which occurs accidentally in humans who ingest polluted water or raw or inadequately cooked flesh of snakes or frogs. It has been reported mainly in the southeastern region of the United States.

International

T saginata has a high endemicity in Latin America, Africa, Middle East, and central Asia and has a moderate endemicity in Europe, south Asia, Japan, and the Philippines.

T solium is prevalent in Latin America, the Slavic countries, Africa, southeast Asia, India, and China. The prevalence of T solium infection is low in northwestern Europe and is rare or absent in Canada.

Cysticercosis, caused by infection with the larvae stage of the tapeworm, is endemic in all Latin American countries (except Chile, Argentina, and Uruguay).

Diphyllobothrium infection is prevalent in northern Europe (Finland, east Prussia, Russian Karelia), Canada, Africa, Japan, Taiwan, Manchuria, Siberia, Papua New Guinea, Australia, and South America.

H nana infection is the most common cestode of humans. It is prevalent in areas of poor hygiene and sanitation, especially in the warm and arid countries of the Mediterranean, Indian subcontinent, and South America. The prevalence in children in these areas may reach 20%. Infection rates are highest among children.

E multilocularis infection occurs only in the northern hemisphere, especially in central Europe, Russia, China, Japan, Canada, and north Africa. Few regions in the world are completely free from E granulosis. Echinococcus vogeli and Echinococcus oligarthrus infections occur in Central America and South America.

Infection with Spirometra species has been reported worldwide but especially in east Asia (China, Japan, and Korea) and southeast Asia (Malaysia, India, and the Philippines).

Mortality/Morbidity

Many cestode infestations are asymptomatic. However, once symptoms occur, they are usually vague GI complaints such as abdominal pain, anorexia, weight loss, or malaise.

Some of the more serious infestations result in symptoms from mass effects on vital organs, inflammatory responses, nutritional deficiencies, and the potential of fatal anaphylaxis.

• Cysticercosis is a clinical syndrome of expanding embryonal cysts that occurs with T solium. The cysticerci that develop with T solium infestations can be found anywhere in the body, but they mainly occur in the central nervous system (neurocysticercosis) and skeletal muscles, causing local inflammatory responses and mass effects from the cystic growth. Cysticercosis is a common parasitic disease of the CNS. One of the most common manifestations is seizure. In endemic areas, it is a major cause of epilepsy. Neurocysticercosis may be the cause of death in many of these affected areas and may leave infected persons with irreversible brain damage.
• Diphyllobothrium species absorb a large amount of vitamin B-12 and interfere with vitamin B-12 absorption from the ileum, resulting in vitamin B-12 deficiency (this can also occur with Taenia species). Severity depends on the proximity of the worm to the ileum, where vitamin B-12 is mainly absorbed in humans. Clinically, it resembles pernicious anemia (ie, hyperchromic, macrocytic, megaloblastic anemia) that responds well to vitamin supplementation therapy without long-term sequelae.
• In Echinococcus infestations, humans ingest the eggs and the embryos escape, penetrate intestinal mucosa, and enter the portal circulation to invade other organs, mainly the liver (60%) and lungs (25%). The patient remains asymptomatic until the cysts cause a mass effect on the organ, which can be 5-20 years after the initial infestation.
  • Rupture or leakage of an Echinococcus cyst produces symptoms of fever, pruritus, urticaria, eosinophilia, and potentially fatal anaphylaxis.
  • Pulmonary cyst rupture can be associated with abscess formation and pneumothorax, with or without pleural effusion. In addition, fever and acute hypersensitivity reactions ranging from wheezing to anaphylaxis can occur following cyst rupture.
  • If alveolar hydatid disease is left untreated, more than 90% of patients will die within 10 years from the onset of symptoms and almost 100% by 15 years.
• Currently, no effective treatment for sparganosis is known.

Race

No racial risks or protections regarding cestode infestations are known.

Sex

Gender differences neither protect nor increase the risk of cestode infections.

Age

Many cestode infections are common in children as a result of their youthful habits and relatively less adequate hygiene. For instance, D caninum, one of the most common parasites of domestic dogs and cats, is typically obtained from fleas that live in the fur of these animals. Although infection of D caninum is rare, children, especially those who enjoy handling animals, are affected more frequently than adults.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

History

• Many cestode infestations are asymptomatic. The organisms may be discovered by patients during defecation. Tapeworms may migrate from the rectum (possibly causing itching) and may be seen on toilet paper or undergarments. However, once symptoms occur, they are usually vague GI complaints of abdominal pain, anorexia, weight loss, or malaise.
• T solium infections are usually asymptomatic; however, infected patients may have generalized complaints include epigastric or periumbilical discomfort; nausea; hunger; and weight loss, anorexia, or increased appetite. The cysticerci that develop with T solium infestations can be found anywhere in the body, but they mainly occur in the central nervous system and skeletal muscles, causing local inflammatory responses and mass effects from the cystic growth. If neurocysticercosis develops, seizure is the most common form of presentation, occurring in up to 80% of patients with parenchymal brain cysts or calcifications.
• With T saginata infection, usually, the patient becomes aware of infection when worm segments are passed in the stool. Some patients complain of epigastric pain, diarrhea, and weight loss. Similar to T solium infection, the presence of cysticerci in T saginata infection can result in symptoms of obstruction of the appendix, biliary duct, and pancreatic duct.
• Diphyllobothrium infestations may result in intestinal discomfort, diarrhea, vomiting, weakness, and weight loss.
• • The cestode is not invasive, but it does absorb a large amount of vitamin B-12 and interferes with vitamin B-12 absorption from the ileum, producing a megaloblastic anemia that resembles pernicious anemia (clinically and hematologically). The tapeworm must thus be in a proximal portion of the intestine, and probably intrinsic factor secretion is defective in the host (allowing for diminished capacity to absorb vitamin B-12).
  • Patients may complain of neurologic symptoms resembling pernicious anemia (eg, paresthesias, difficulty with balance, dementia or confusional states).
• Hymenolepis typically produces asymptomatic infections; however, in patients who may have a number of parasites present, the patient can have vague symptoms of anorexia, abdominal pain, and diarrhea (the developing cysticercoids destroy their housing villi, thus with a number of parasites, significant enteritis may develop). The number of worms is regulated by the hosts nutritional and immunity states.
• D caninum infections are mostly asymptomatic with some symptoms of abdominal pain, diarrhea, anal pruritus, and urticaria.
• Echinococcosis infections are potentially dangerous because they typically remain asymptomatic until the cysts cause a mass effect on an organ, which can occur 5-20 years after the initial infestation.
• • Cystic echinococcosis
    • The larvae develop into the fluid-filled hydatid cysts that are implanted after being carried in the bloodstream and expand slowly over several years.
    • The liver is the most common site, followed by the lungs (10-30%) (mostly the right lobe (60%) and the lower lobes (60%); however, almost any tissue may be involved. In children, the lungs may be the most common site of cyst formation. Up to 40% of patients with lung cyst will have liver cysts as well.
    • Most patients have single organ involvement (85-90%), and most will have a solitary cyst (>70%).
    • These cysts do not metastasize, but they may be disseminated by accidental spillage.
    • Pulmonary cystic rupture may result in clinically impressive and misleading symptoms of cough, chest pain, and hemoptysis.
  • Alveolar hydatid disease
    • A lesion in the liver does not appear as a cyst but is a firm, solid, cancerlike mass that is primarily in the liver. Approximately 60-80% of the cysts are located in the right lobe of the liver. Single or multiple foci may be present.
    • Hepatic echinococcosis can cause epigastric pain and dyspepsia (up to 35%) and can mimic cholelithiasis or jaundice (up to 45%) from compression in the bile duct. In one third of the cases, the disease is found incidentally during the checkup for nonspecific symptoms (fatigue, weight loss, hepatomegaly).
    • The disease spreads from the liver by direct extension, by lymphatic or hematologic metastasis, or by peritoneal seeding.
    • Compression of the bile duct can occur, resulting in biliary colic or jaundice.

Physical

• T solium infections
• • The cysticerci that develop with T solium infestations can cause mass effects from the cystic growth leaving the physical findings dependent on the location and the size of the growth.
  • Although most patients have normal neurologic examinations, the most common presentation of neurocysticercosis is the neurologic manifestations of seizures and focal neurologic deficits, along with possible hydrocephalus, meningitis, and dementia. Predictably, signs of increased intracranial pressure occur, as well as headaches, visual changes, vomiting, ataxia, and confusion.
  • Clinical manifestations of spinal neurocysticercosis are nonspecific and dependent on the size and the location of the cysts.
  • To homogenize the diagnosis of neurocysticercosis, diagnostic criteria were proposed in 2001:
    • Absolute criteria
    • Histologic demonstration of the parasite
    • Direct visualization of the parasite on funduscopic examination
    • Evidence of cystic lesions showing the scolex on CT scan or MRI

      Major criteria

    • Evidence of lesions suggestive of neurocysticercosis on neuroimaging studies
    • Positive immunologic tests for the detection of anticysticercal antibodies
    • Plain radiographs showing cigar-shaped calcifications in the thigh and calf muscles

      Minor criteria

    • Presence of subcutaneous nodules (without histologic confirmation)
    • Evidence of punctate soft tissue or intracranial calcifications on plain radiographs
    • Presence of clinical manifestations suggestive of neurocysticercosis
    • Disappearance of intracranial lesions after a trial with anticysticercal drugs

      Epidemiologic criteria

    • Individuals coming from or living in an area where cysticercosis is endemic
    • History of frequent travel to cysticercosis endemic areas
    • Evidence of a household contact with T solium infection
  • Ocular cysticercosis can be seen on ophthalmologic examination of the eye. Parasites may be seen in the posterior chamber of the eye.
  • Cysticercosis of the muscle and subcutaneous tissues can be palpated or seen on plain radiographs. Almost all patients with symptomatic muscle cysticercosis are reportedly from Asia.
• Diphyllobothrium infestations
• • Megaloblastic anemia that resembles pernicious anemia (hyperchromic, macrocytic, megaloblastic anemia with thrombocytopenia and mild leukopenia) may be present. Additionally, while true pernicious anemia is associated with gastric achlorhydria, tapeworm-induced anemia is not.
  • Only D latum is associated with macrocytic anemia.
  • Of patients who are infected with this tapeworm, 40% have decreased vitamin B-12 levels, but fewer than 2% of those develop anemia, which seems to occur mainly in Scandinavian countries.
• Echinococcosis infections
• • Hepatic echinococcosis can cause signs of abdominal pain and a palpable mass in the right upper quadrant.
  • The physical examination may mimic cholelithiasis or jaundice from compression of the bile duct. Additionally, the patient may have chronic pancreatitis and signs and symptoms therein as related to the location and the size of the cystic infestation.
  • Rupture or leakage of the hydatid cyst produces fever, urticaria, and potentially fatal anaphylaxis.
  • Pulmonary cystic rupture may result in clinically impressive hemoptysis.
• Sparganosis commonly presents as subcutaneous edema and invades not only the subcutaneous tissue but also the muscles, eyes, urogenital system, abdominal viscera, and rarely the central nervous system.
• Coenurosis caused by T multiceps presents as a space-occupying cystic lesion of the central nervous system and subcutaneous tissues, leading to symptoms of mass effects and obstruction.

Causes

See Pathophysiology.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Other Problems to be Considered

Hepatocellular carcinoma
Hepatic hematoma
Peritonitis
Pernicious anemia

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Lab Studies

• Perianal and stool examinations can be performed.
• • If worm infestation is suspected, first consider a stool examination for ova and parasites.
  • This clearly is indicated for some of the cestodes that release eggs or worm segments directly into the stool (ie, T saginata, Diphyllobothrium species, D caninum). This is especially true of H nana infection, which is the most frequently diagnosed cestode infection in the United States.
  • Collecting 2-3 stool samples is necessary for detection of the parasite because eggs and parasite particles are released irregularly into the stool and may be periodically absent from stool during infection. Therefore, microscopy has been known to be relatively insensitive.
  • In T saginata infections, eggs may be observed in the perianal area and can be detected by using a cellophane tape swab. This method detects eggs in 85-90% of patients.
• Eosinophil counts are not diagnostically reliable.
• • Eosinophilia is sporadically present and does not correlate with the severity of the infection.
  • Eosinophil counts also do not help in monitoring treatment modalities.

Imaging Studies

• Imaging studies are not only useful in differential diagnosis and evaluation of neurocysticercosis, but they are important in identifying the number, the location, and the stage of the infestation.
• • The size of cysticerci varies according to location in the CNS. If located in the brain parenchyma, cysts are rarely larger than 10 mm in diameter because of physical space limitations. In contrast, cysts located in the cisterns of the cerebrospinal fluid may grow to 5 cm or greater in diameter.
  • Appearance of the cysticerci depends on the stage of development. On entering the CNS, the cysticerci are in a vesicular stage where the parasites are viable and surrounding tissue inflammatory changes are scant. After a variable time (maybe years), the host attacks immunologically and the process of degeneration occurs; this process changes the appearance of the cysticerci until ultimately complete degeneration leaves a nodular calcified cyst.
  • Generally, MRI is better than CT for the diagnosis of neurocysticercosis, detecting up to 60% of cases missed on CT. However, MRI is less sensitive than CT in identifying small calcifications, and many patients have parenchymal calcifications as the sole evidence of the disease (up to 40% of symptomatic patients). This along with cost-effectiveness lends to CT as the image study of choice and MRI for more inconclusive findings.
  • Ultrasonography may be useful in evaluation of patients with orbital infestations.
• Echinococcosis
• • As with most space-occupying lesions, imaging techniques are very useful. CT, MRI, and/or ultrasonography can assist in determining the extent and stage of the infestation and in evaluating the surrounding structures. CT is better in detecting calcified lesions, and MRI is better for visualizing necrotic or fibrotic noncalcified lesions and extrahepatic lesions of alveolar echinococcosis. Calcification occurs commonly in hepatic cysts but rarely in pulmonary cysts.
  • Radiographically, guided needle aspiration of a cyst is occasionally indicated for proper identification of cyst etiology without a need for concern of dissemination.

Other Tests

• Immunologic testing
• • Although this type of testing may be useful for primary screening, it is most commonly used for confirmation testing for parasitic disease.
  • Complement fixation, hemagglutination, radioimmunoassay, enzyme-linked immunosorbent assay (ELISA), and immunoblot can be used for the detection of anticysticercal antibodies in serum, cerebrospinal fluid, and saliva.
  • The immunoblot (Western blot = enzyme-linked immunoelectrotransfer blot assay) is the most effective, with sensitivity and specificity as high as 100% and 98%, respectively; however, the sensitivity decreases to about 70% in patients with a single cyst or in those with only calcified lesions. ELISA is more reliable when performed in cerebrospinal fluid than in serum, but the accuracy depends on the viability and location of the cysticerci. Stool antigen testing detects at least 2-3 times more cases of Taenia infection than stool microscopy. In echinococcosis, ELISA is positive in only 50% of patients with pulmonary hydatidosis and in more than 90% of patients with hepatic cysts.

Procedures

• Although invasive, the subcutaneous edema of sparganosis and the space-occupying lesions of coenurosis require surgery for diagnostic and therapeutic purposes.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Emergency Department Care

Unless the parasite is detected (eg, presence of eggs, worm segments, cysts), definitive therapy in the ED is unlikely. Stabilization of any patient in the presence of a systemic disease or organ failure is essential.

• Intestinal T solium infections
• • In cysticercosis, if the patient is asymptomatic with calcified soft tissue or neural lesions, no treatment is required.
  • For symptomatic patients with neurocysticercosis, the neurologic manifestations may indicate a need for antiepileptics or antibiotics. These medications may resolve some of the symptoms or discomfort. However, once the definitive diagnosis has been confirmed, the treatment is praziquantel or albendazole. These agents can provoke an inflammatory response in the central nervous system. Thus, if either drug is given, the patient must be started on high-dose glucocorticoids.
  • Effectiveness of therapy can be monitored via radiographic imaging. The size of the active lesions should decrease within 3-6 months.
  • Ocular, ventricular, and spinal lesions are subject to irreversible drug-induced inflammation, which may require surgical treatments.
• T saginata, Diphyllobothrium, and D caninum (similar to intestinal T solium infections) infections can be treated with niclosamide or praziquantel (see Medication). Niclosamide is the drug of choice in these infections, with cure rates of 95%. Administer parenteral vitamin B-12 if evidence of vitamin B-12 deficiency occurs with Diphyllobothrium infections.
• The drug of choice against Hymenolepis is praziquantel because it is effective against both the adult and the cysticercoids in the intestinal villi. A 95% cure rate has been reported. Alternatively, consider niclosamide, which has a cure rate of 75%. Niclosamide must be given over 1 week because it is ineffective against the cysticercoids stage.
• Since determining whether all cestode tissue has been removed surgically is impossible, the World Health Organization (WHO) recommends that patients receive postoperative chemotherapy with benzimidazole derivatives (ie, mebendazole and albendazole) for 2 years after surgery.
• • Cysts with homogenously calcified cyst walls are not likely to require therapy since spontaneous inactivation of larvae tissue has probably occurred.
  • Medical therapy consists of albendazole for 28 days, repeated 1-8 times, and separated by 2-3 weeks of drug-free intervals.
  • According to the WHO, chemotherapy for these infections should be reserved for patients with inoperative disease or after incomplete surgery. Chemotherapy is also indicated to prevent secondary echinococcosis after spontaneous or traumatic (perioperative) rupture of cysts.
• Echinococcosis is treated with albendazole and surgery or albendazole and PAIR (ie, puncture, aspiration, injection of scolicidal agent, and reaspiration).
• Sparganosis and coenurosis treatment involves surgical excision for localized infections.

Consultations

• An infectious diseases specialist can secure the tracking and reporting of important epidemiologic and epidemic patterns.
• Gastroenterologist and/or primary care physician
• • Most patients' symptoms hasten the physician to notify the gastroenterologist for evaluation of their source of symptoms.
  • After treatment, the passage of segments and eggs may continue for several days. Treatment is reevaluated for success by examining the stool at intervals allowing regrowth of worms: 3 months for Taenia species and 1 month for Hymenolepis, Diphyllobothrium, and other species. The difficulty arises with H nana, which can result in reinfection through internal autoinfection, causing patients to appear as though treatment has failed. Fortunately, the medications will reduce the worm burden, and the infections in children are usually spontaneously resolved in adolescence.
• In the presence of apparent cysts in the brain, meninges, or spinal cord, consultation with a neurologist may be indicated. Aspiration may be needed for diagnostic purposes and for relief of compression that may cause severe or discomforting symptoms.
• Surgery
• • Some cestode infections require surgery not only for diagnostic purposes but also for therapy.
  • Patients with hydrocephalus due to cysticercosis require placement of a ventricular shunt. This is needed prior to any recommended drug therapies because drug therapies typically result in further increases in intracranial pressures. In patients with neurocysticercosis, the rate of shunt dysfunctions requiring frequent revisions is high. These patients high mortality rate (50% in 2 y) is directly related to the number of surgeries involving their shunt.
  • Symptomatic echinococcosis infections require surgical treatment with perioperative medical interventions. Surgical excision of the complete alveolar echinococcosis lesion is the only possible curative therapy. The surgical resections that are usually performed have an operative mortality rate that has dropped from about 7-23% before 1980 to 0-5% in more recent years. Palliative use of surgery is not indicated because most local complications can be treated by nonsurgical interventional techniques.
  • The puncture of cysts percutaneously, aspiration of fluid, introduction of protoscolicidal agent, and reaspiration method, also known as the PAIR method, has been described as an alternative treatment for hepatic cysts. Currently, however, the efficacy and safety of the PAIR method has not been confirmed. Therefore, the PAIR method cannot be regarded as an established alternative to surgery.
  • The only treatment for sparganosis and coenurosis is surgical excision of the localized infections.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Anthelmintic drugs act locally to rid the GI tract of worms or systemically to rid the body of the helminth forms that invade organs and tissues. Much of the success of development of these medications is dedicated to the efforts of veterinarians because many cestodes have animal hosts.

Drug Category: Anthelmintics

Parasite biochemical pathways are sufficiently different from the human host, which allows for selective interference by chemotherapeutic agents in relatively small doses.

Drug Name	Paromomycin (Humatin)
Description	Alternative therapy for patients infected with Diphyllobothrium species, Hymenolepis species, T solium, and T saginata. Since action is mainly in adult worms, does not reach ova. Patients with T solium infections remain at risk of cysticercosis.
Adult Dose	D latum, T saginata, T solium, D caninum infections: 1 g PO q15min for 4 doses H nana infections: 45 mg/kg/d PO for 5-7 d
Pediatric Dose	D latum, T saginata, T solium, D caninum infections: 11 mg/kg PO q15min for 4 doses H nana infections: 45 mg/kg/d PO for 5-7 d
Contraindications	Documented hypersensitivity; intestinal obstruction
Interactions	Nephrotoxic potential may increase with concurrent administration of other aminoglycosides, penicillins, cephalosporins, amphotericin B, and loop diuretics
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Because of narrow therapeutic index and toxic hazards associated with extended administration, do not use for long-term therapy; caution in renal failure, hypocalcemia, myasthenia gravis, and conditions that depress neuromuscular transmission; adjust dose in renal impairment

Drug Name	Praziquantel (Biltricide)
Description	Acylated isoquinoline that increases cell membrane permeability in susceptible worms, resulting in a loss of intracellular calcium, massive contractions, and paralysis of their musculature. In addition, produces vacuolization and disintegration of the schistosome tegument. This is followed by attachment of phagocytes to the parasite and death. Tablets should be swallowed whole with some liquid during meals. Keeping tablet in the mouth may reveal a bitter taste that can produce nausea or vomiting. Effective against cestodes (except Echinococcus species) and trematodes, but not nematodes. DOC in the treatment of hymenolepiasis. In cysticercosis, this medication has the potential to provoke an inflammatory response in the CNS. Thus, the patient must also be started on high-dose glucocorticoids. Patients with cysticercotic encephalitis develop intracranial hypertension with antihelmintic use and, thus, require a ventricular shunt prior to drug therapy.
Adult Dose	Hymenolepis: 25 mg/kg PO once Intestinal T solium, T saginata, D caninum, Diphyllobothrium species: 10-20 mg/kg PO once Cysticercosis infections: 50 mg/kg/d PO divided tid for 14 d
Pediatric Dose	<4 years: Not established >4 years: Administer as in adults
Contraindications	Documented hypersensitivity; ocular cysticercosis
Interactions	Serum praziquantel concentrations may be reduced by hydantoin, possibly leading to treatment failures; may lower serum levels of phenytoin and carbamazepine; serum levels of praziquantel decrease with concomitant steroids (unknown clinical significance)
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	May use during pregnancy if benefits outweigh risks; neurocysticercosis a possibility when convulsions observed for first time in patients from developing countries; if seizures are well controlled on antiepileptics alone, antihelmintic therapy can be withheld until postpartum; consider praziquantel in patients in whom antiepileptic drugs fail to adequately control seizures When destruction of parasite within eyes, may cause irreparable lesions (do not treat ocular cysticercosis with praziquantel); may produce drowsiness; caution while driving or performing other tasks that require alertness on day of and following treatment; minimal increases in liver enzyme levels documented in some patients; when schistosomiasis or flulike infection is associated with cerebral cysticercosis, hospitalize patient for duration of treatment

Drug Name	Niclosamide (Niclocide)
Description	A chlorinated salicylanilide. DOC; inhibits mitochondrial oxidative phosphorylation and glucose uptake in parasite. Cure rate of about 90% for Taenia species and a little less than 90% for Diphyllobothrium species.
Adult Dose	D latum, T saginata, T solium, D caninum infections: 2 g PO once
Pediatric Dose	D latum, T saginata, T solium, D caninum infections: <11 kg: Not established 11-34 kg: 1 g PO once >34 kg: 1.5 g PO once
Contraindications	Documented hypersensitivity
Interactions	None reported
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	Associated with GI distress, anorexia, drowsiness, dizziness, headache, and rash; not FDA approved for this indication, although generally accepted as antimicrobial of choice for treating D latum infection

Drug Name	Mebendazole (Vermox)
Description	Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell.
Adult Dose	100 mg PO bid for 3 d; second course if patient not cured in 3-4 wk
Pediatric Dose	<2 years: Not established >2 years: Administer as in adults
Contraindications	Documented hypersensitivity
Interactions	Carbamazepine and phenytoin may decrease effects; cimetidine may increase levels
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Adjust dose in hepatic impairment

Drug Category: Anticonvulsants

These agents are used to manage symptoms in patients being treated for neurocysticercosis.

Drug Category: Glucocorticoids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, they modify the body's immune response to diverse stimuli.

Drug Name	Methylprednisolone (Solu-Medrol, Depo-Medrol, Medrol)
Description	Decreases inflammation by suppressing migration of PMNs and reversing increased capillary permeability.
Adult Dose	Loading dose: 125-250 mg IV Maintenance dose: 0.5-1 mg/kg/dose IV q6h; not to exceed 5 d
Pediatric Dose	Loading dose: 2 mg/kg IV Maintenance dose: 0.5-1 mg/kg/dose IV q6h; not to exceed 5 d
Contraindications	Documented hypersensitivity; viral, fungal, or tubercular skin infections
Interactions	Coadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels of methylprednisolone; phenobarbital, phenytoin, and rifampin may decrease levels of methylprednisolone (adjust dose); monitor patients for hypokalemia when taking medication concurrently with diuretics
Pregnancy	C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions	Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use

Drug Category: Vitamins

These agents are essential for normal DNA synthesis. Indicated for use in patients with megaloblastic anemia due to deficiency in vitamin B-12.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Complications

• Systemic cysticercosis
• Cyst rupture
• Vitamin B-12 deficiency
• Obstruction of the appendix or pancreatic or bile ducts (rare)
• Intestinal obstruction (rare)
• Cholangitis (rare)
• Cholecystitis (rare)
• Pancreatitis
• Iron deficiency anemia

Prognosis

• The cure rate for tapeworm infestation is greater than 95% in patients who receive appropriate treatment.
• The prognosis for systemic cysts depends on the location of the cysts.

Patient Education

• Proper cooking of beef, pork, and fish
• Proper freezing of meat or fish
• Fecal-oral precautions with good hand washing
• Treatment of infected dogs and prevention of fleas

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Special Concerns

• Pregnancy makes treatment for cestode infections difficult.
• • An associated risk of possible teratogenic effects with the administration of antihelminthic medications exists.
  • Caution and consideration of risks and benefits are vital in the proper treatment of cestode infections during pregnancy.

ACKNOWLEDGMENTS

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Raquel Mora, MD, to the development and writing of this article.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

• Barnett K, Emder P, Day AS, Selby WS. Tapeworm infestation: a cause of iron deficiency anemia shown by capsule endoscopy. Gastrointest Endosc. Sep 2007;66(3):625-7. [Medline].
• Bildik N, Cevik A, Altintas M, Ekinci H, Canberk M, Gülmen M. Efficacy of preoperative albendazole use according to months in hydatid cyst of the liver. J Clin Gastroenterol. Mar 2007;41(3):312-6. [Medline].
• Carpio A. Neurocysticercosis: an update. Lancet Infect Dis. Dec 2002;2(12):751-62. [Medline].
• Chrieki M. Echinococcosis--an emerging parasite in the immigrant population. Am Fam Physician. Sep 1 2002;66(5):817-20. [Medline].
• Christie JD, Garcia LS. Emerging parasitic infections. Clin Lab Med. Dec 2002;24(3):737-72.
• Cox FE. History of human parasitic diseases. Infect Dis Clin North Am. Jun 2004;18(2):171-88, table of contents. [Medline].
• Craig P. Echinococcus multilocularis. Curr Opin Infect Dis. Oct 2003;16(5):437-44. [Medline].
• Craig PS, McManus DP, Lightowlers MW, Chabalgoity JA, Garcia HH, Gavidia CM. Prevention and control of cystic echinococcosis. Lancet Infect Dis. Jun 2007;7(6):385-94. [Medline].
• Falagas ME, Bliziotis IA. Albendazole for the treatment of human echinococcosis: a review of comparative clinical trials. Am J Med Sci. Sep/2007;334(3):171-9. [Medline].
• Garcia HH, Del Brutto OH,. Neurocysticercosis: updated concepts about an old disease. Lancet Neurol. Oct 2005;4(10):653-61. [Medline].
• Garcia HH, Gonzalez AE, Gilman RH. Diagnosis, treatment and control of Taenia solium cysticercosis. Curr Opin Infect Dis. Oct 2003;16(5):411-9. [Medline].
• Garcia HH, Pretell EJ, Gilman RH, Martinez SM, Moulton LH, Del Brutto OH. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med. Jan 15 2004;350(3):249-58. [Medline].
• Khuroo MS, Wani NA, Javid G, et al. Percutaneous drainage compared with surgery for hepatic hydatid cysts. N Engl J Med. Sep/1997;337(13):881-7. [Medline].
• Kolars JC, Fischer PR. Evaluation of diarrhea in the returned traveler. Prim Care. Dec 2002;29(4):931-45. [Medline].
• Kraft R. Cysticercosis: an emerging parasitic disease. Am Fam Physician. Jul 1 2007;76(1):91-6. [Medline].
• Loukas A, Hotez PJ. Chemotherapy of helminth infections. In: Brunton LL, Lazo JS, Parker KL, eds. Goodman & Gilman's Pharmacology. 11^th ed. McGraw-Hill; 2006:1121-1141.
• McAdam AJ, Sharpe AH. Infectious diseases. In: Kumar V, Abbas AK, Fausto N, eds. Kumar, Robbins, and Cotran: Pathologic Basis of Disease. 7^th ed. Philadelphia: Saunders; 2005:838-8.
• Moon TD, Oberhelman RA. Antiparasitic therapy in children. Pediatr Clin North Am. Jun 2005;52(3):917-48, viii. [Medline].
• Morar R, Feldman C. Pulmonary echinococcosis. Eur Respir J. Jun 2003;21(6):1069-77. [Medline].
• Nash TE, Singh G, White AC, Rajshekhar V, Loeb JA, Proaño JV. Treatment of neurocysticercosis: current status and future research needs. Neurology. Oct 10 2006;67(7):1120-7. [Medline].
• Ong S, Talan DA, Moran GJ, Mower W, Newdow M, Tsang VC. Neurocysticercosis in radiographically imaged seizure patients in U.S. emergency departments. Emerg Infect Dis. Jun 2002;8(6):608-13. [Medline].
• Ozturk G, Aydinli B, Yildirgan MI, Basoglu M, Atamanalp SS, Polat KY. Posttraumatic free intraperitoneal rupture of liver cystic echinococcosis: a case series and review of literature. Am J Surg. Sep 2007;194(3):313-6. [Medline].
• Romig T. Epidemiology of echinococcosis. Langenbecks Arch Surg. Sep 2003;388(4):209-17. [Medline].
• Wallin MT, Kurtzke JF. Neurocysticercosis in the United States: review of an important emerging infection. Neurology. Nov 9 2004;63(9):1559-64. [Medline].
• White AC, Weller PF. Cestodes. In: Kasper DL, Braunwald E, Fauci AS, eds. Harrison's Principles of Internal Medicine. 16^th ed. McGraw-Hill; 2005:1272-7.

Article Last Updated: Dec 21, 2007