Tapeworm Infestation 

Updated: Dec 06, 2018
Author: Lisandro Irizarry, MD, MPH, FACEP; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD 

Overview

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 can 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).

See the image below.

Adult tapeworm of Dipylidium caninum. Image courte Adult tapeworm of Dipylidium caninum. Image courtesy of the Centers for Disease Control and Prevention (CDC).

Cestodes include the following:

  • Taenia solium

  • Taenia saginata

  • Taenia asiatica[1]

  • 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 environment from the primary host.

  • The eggs are ingested by an intermediate host in which they hatch.

  • The larvae enter the tissues of the intermediate host and encyst.

  • The primary host ingests the cysts in the flesh of the intermediate host.

When humans are the primary hosts, 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.

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 cestode of rodents, although humans can be a rare and accidental hosts 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.

Table 1. Cestodes and Their Hosts (Open Table in a new window)

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)

 

Diagram of the Echinococcus life cycle. Image cour Diagram of the Echinococcus life cycle. Image courtesy of the Centers for Disease Control and Prevention.

Epidemiology

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 water containing infected cyclops, eating raw or inadequately cooked flesh of snakes, frogs, or birds. 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.[2, 3] 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.

The first study to systematically collect data on the frequency of neurocysticercosis worldwide found that one third of patients with epilepsy living in endemic communities showed neurocysticercosis brain lesions.[4]

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 hydatid cysts may rupture into the bronchial tree produce cough, dyspnea, chest pain, or hemoptysis. Pulmonary cysts rupture into the pleural space can result in 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.

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.

 

Presentation

History

Many cestode infestations are asymptomatic. The organisms may be discovered by patients during defecation with the fecal passage of proglottids. 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, cramps, anorexia, nausea, diarrhea, 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, revised diagnostic criteria were proposed as follows:[5]

Absolute criteria

  • Histologic demonstration of the parasite from biopsy

  • Direct visualization of subretinal parasite on funduscopic examination

  • Evidence of cystic lesions showing the scolex on CT scan or MRI

Major criteria

  • Lesions highly suggestive of neurocysticercosis on neuroimaging studies (cystic lesions without scolex, ring or nodular enhancing lesion and parenchymal round calcifications)

  • Positive enzyme-linked immunotransfer blot assay (EITB) for the detection of anticysticercal antibodies

  • Spontaneous resolution of small single enhancing lesions

  • Resolution of intracranial cystic lesions after therapy with albendazole or praziquantel

Minor criteria

  • Lesions compatible with neurocysticercosis on neuroimaging studies (CT or MRI showing hydrocephalus, abnormal enhancement of the leptomeninges, and myelograms showing multiple filling defects)

  • Clinical manifestations suggestive of neurocysticercosis (seizures, focal neurological deficits, increased intracranial pressure, intellectual deterioration)

  • Positive CSF ELISA for detection of anticysticercal antibodies or antigen

  • Cysticercosis outside the CNS

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

Diagnosis is definitive in patients with either (1) one absolute criterion or (2) a combination of two major criteria, one minor criterion, and one epidemiologic criterion. Diagnosis is probable in patients who meet these criteria (1) one major criterion plus two minor criteria; or (2) one major criterion plus one minor criterion and one epidemiologic criterion; or (3) three minor criteria plus one epidemiologic criterion.

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

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

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.

 

DDx

Differential Diagnoses

 

Workup

Laboratory 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

Neurocysticercosis

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. Also see Cysticercosis and Cysticercosis, CNS.

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.

Ultrasonographic appearance of echinococcal cysts Ultrasonographic appearance of echinococcal cysts (Gharbi type I, World Health Organization [WHO] standardized classification CE1).

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.

Polymerase chain reaction

Polymerase chain reaction (PCR) of stool tests are also available for the detection of Echinococcus infection.[6]

Procedures

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

 

Treatment

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 such as seizure, anaphylaxis, or organ failure is essential.

Intestinal tapeworm infestation

Recent reviews summarize that most intestinal tapeworm infections can be effectively treated with praziquantel or niclosamide.[7, 8] These antihelminthic agents have effective rates of 85-98%.[9] Praziquantel was found to be 100% effective in the treatment of Taenia and H nana infection.[10]

Administer parenteral vitamin B-12 if evidence of vitamin B-12 deficiency occurs with Diphyllobothrium infections.

Cysticercosis

In neurocysticercosis, neurologic manifestations indicate the need for antihelminthic agents and antiepileptics. The recommended antihelminthic agent is albendazole. In a meta-analysis of comparative trials, albendazole provides better seizure control and resolution of cysts or granuloma as compared with praziquantel.[11, 12] In trials of nonviable lesions, seizure recurrence is substantially lower with albendazole.[13]

Antihelminthic treatment may provoke an inflammatory response in the central nervous system. Steroids affect this inflammatory response and may influence outcomes such as headache, but further research is needed to test this.[13]

Effectiveness of therapy can be monitored via radiographic imaging. The size of the active lesions should decrease within 3-6 months.

Neurosurgical interventions should be considered for patients with mass effect, cerebral spinal fluid obstruction, and fourth ventricular cysts.[14] Endoscopic approaches provide better outcomes than the traditional open approaches for intraventricular neurocysticercosis with hydrocephalus.[14] Among patients who had undergone surgical resection of a single intraventricular lesion, those who received postoperative antihelminthic therapy, most commonly albendazole, had significantly lower risk of developing delayed hydrocephalus.[15]

Echinococcosis

Echinococcosis is treated with albendazole and surgery or albendazole and PAIR (puncture, aspiration, injection, re-aspiration). Albendazole is recommended for 1-3 months before surgical intervention.[16]

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.

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.

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. 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. The recurrence rate is between 3% and 10% after open surgery for patients with hepatic hydatid cyst. Special laparoscopic surgery technique for liver hydatid cysts has been described, with a result of 0% recurrence rate.[17]

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 of sparganosis and coenurosis is surgical excision of the localized infections.

 

Medication

Medication Summary

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.

Anthelmintics

Class Summary

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

Albendazole (Albenza)

Decreases ATP production in worm, causing energy depletion, immobilization, and finally death. To avoid inflammatory response in CNS, patient also must be started on anticonvulsants and high-dose glucocorticoids. DOC for some of the potentially fatal cestode infections, namely cysticercosis (for T solium) and hydatid cyst disease (from Echinococcus).

Patients with cysticercotic encephalitis develop intracranial hypertension with antihelmintic use and, thus, require a ventricular shunt prior to drug therapy.

Paromomycin (Humatin)

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.

Praziquantel (Biltricide)

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.

Niclosamide (Niclocide)

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.

Mebendazole (Vermox)

Causes worm death by selectively and irreversibly blocking uptake of glucose and other nutrients in susceptible adult intestine where helminths dwell.

Anticonvulsants

Class Summary

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

Diazepam (Valium)

Depresses all levels of CNS, including limbic and reticular formation, possibly by increasing activity of GABA, which is a major inhibitory neurotransmitter.

Individualize dosage and increase it cautiously to avoid adverse effects.

Glucocorticoids

Class Summary

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.

Prednisone (Deltasone, Sterapred, Orasone)

Useful in treatment of inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation.

If a safer alternative therapy is available, do not administer glucocorticoids.

Methylprednisolone (Solu-Medrol, Depo-Medrol, Medrol)

Decreases inflammation by suppressing migration of PMNs and reversing increased capillary permeability.

Vitamins

Class Summary

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

Cyanocobalamin (Cobex, Berubigen, Crystamine)

Deoxyadenosylcobalamin and hydroxocobalamin are active forms of vitamin B-12 in humans. Vitamin B-12 synthesized by microbes but not humans or plants.

 

Follow-up

Complications

Potential complications of tapeworm infestation include the following:

  • Systemic cysticercosis

  • Cyst rupture (hydatid cyst rupture rare[18] )

  • 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 (rare case report[19] )

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

This includes the following:

  • 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

 

Questions & Answers

Overview

What is a tapeworm?

What types of cestode (tapeworm) infestations affect humans?

What is the life cycle of a cestode in tapeworm infestation?

What is the pathophysiology of tapeworm infestation?

How common is tapeworm infestation in the US?

What is the international prevalence of tapeworm infestation?

What is the mortality/morbidity of tapeworm infestation?

What is the racial predilection of tapeworm infestation?

Is tapeworm infestation more common in males or females?

What are the age-related demographics of tapeworm infestation?

Presentation

What is the clinical history of tapeworm infestation?

What is the clinical history of cystic echinococcosis (tapeworm infestation)?

What is the clinical history of alveolar hydatid disease (tapeworm infestation)?

What is the clinical presentation of T solium infection (tapeworm infestation)?

What are the diagnostic criteria for neurocysticercosis (tapeworm infestation)?

What are the requirements for a definitive diagnosis of T solium infection (tapeworm infestation)?

What is the clinical presentation of diphyllobothrium (tapeworm) infestation?

What is the clinical presentation of hepatic echinococcosis (tapeworm infestation)?

What is the clinical presentation of sparganosis (tapeworm infestation)?

What is the clinical presentation of coenurosis (tapeworm infestation)?

What causes tapeworm infestation?

DDX

What are the differential diagnoses for Tapeworm Infestation?

Workup

Which lab studies are indicated in the workup of tapeworm infestation?

Which imaging studies are indicated in the workup of neurocysticercosis (tapeworm infestation)?

Which imaging studies are indicated in the workup of echinococcosis (tapeworm infestation)?

What is the role of immunologic testing in the workup of tapeworm infestation?

What is the role of polymerase chain reaction (PCR) in the workup of tapeworm infestation?

Which clinical procedures are indicated in the workup of tapeworm infestation?

Treatment

What is the scope of emergency care in the treatment of tapeworm infestation?

What emergency department treatment is indicated in intestinal tapeworm infestation?

What emergency care is indicated in the treatment of cysticercosis (tapeworm infestation)?

What emergency care is indicated in the treatment of echinococcosis (tapeworm infestation)?

Which specialist consultations are indicated in the treatment of tapeworm infestation?

Medications

Which medications are indicated in the treatment of tapeworm infestation?

Which medications in the drug class Vitamins are used in the treatment of Tapeworm Infestation?

Which medications in the drug class Glucocorticoids are used in the treatment of Tapeworm Infestation?

Which medications in the drug class Anticonvulsants are used in the treatment of Tapeworm Infestation?

Which medications in the drug class Anthelmintics are used in the treatment of Tapeworm Infestation?

Follow-up

What are the potential complications of tapeworm infestation?

What is the prognosis of tapeworm infestation?

What educational information should be provided to patients with tapeworm infestation?