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Tapeworm Infestation Clinical Presentation

  • Author: Lisandro Irizarry, MD, MPH, FACEP; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD  more...
Updated: Jul 28, 2015


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.



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 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.



See Pathophysiology.

Contributor Information and Disclosures

Lisandro Irizarry, MD, MPH, FACEP Chair, Department of Emergency Medicine, Wyckoff Heights Medical Center

Lisandro Irizarry, MD, MPH, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


Kim A Guishard, MD Vice Chairman, Department of Emergency Medicine, Wycroft Heights Medical Center

Kim A Guishard, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada

Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association of Emergency Physicians

Disclosure: Nothing to disclose.

Chief Editor

Jeter (Jay) Pritchard Taylor, III, MD Assistant Professor, Department of Surgery, University of South Carolina School of Medicine; Attending Physician, Clinical Instructor, Compliance Officer, Department of Emergency Medicine, Palmetto Richland Hospital

Jeter (Jay) Pritchard Taylor, III, MD is a member of the following medical societies: American Academy of Emergency Medicine, South Carolina Medical Association, Columbia Medical Society, South Carolina College of Emergency Physicians, American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Chief Editor for Medscape.

Additional Contributors

Richard S Krause, MD Senior Clinical Faculty/Clinical Assistant Professor, Department of Emergency Medicine, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.


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

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Adult tapeworm of Dipylidium caninum. Image courtesy of the Centers for Disease Control and Prevention (CDC).
Ultrasonographic appearance of echinococcal cysts (Gharbi type I, World Health Organization [WHO] standardized classification CE1).
Diagram of the Echinococcus life cycle. Image courtesy of the Centers for Disease Control and Prevention.
Table 1. 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)
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