Updated: Dec 21, 2020
Author: Harbir Singh Arora, MD; Chief Editor: Russell W Steele, MD 



Hymenolepiasis is the most common intestinal tapeworm infection of humans caused by worm of family cestoda, genus Hymenolepis and species nana. This infection does not require an intermediate host and infection can occur directly from one infected person to another by fecal-oral transmission. H nana is commonly known as the dwarf tapeworm. Another less frequent zoonotic intestinal tapeworm infection is caused by H diminuta, commonly known as the rat tapeworm, in which humans are incidental hosts.[1]


The life cycles consist of adult (tapeworm) stages in the small bowel of humans and rodents, and also larval tissue stages in insects (cysticercoid). In addition, the cysticer­coid stages of H nana can also invade and develop in the human intestine thus is capable of completing its entire life cycle in the human host. H nana can also be transmitted through autoinfection without having to pass through the insect host.

Life cycle and mode of transmission of H nana:[1]

Life cycle of Hymenolepis nana. Courtesy of the Ce Life cycle of Hymenolepis nana. Courtesy of the Centers for Disease Control and Prevention (CDC at http://www.cdc.gov/dpdx/hymenolepiasis/index.html).

Eggs of Hymenolepis nana are immediately infective when passed with the stool and cannot survive more than 10 days in the external environment (1). When eggs are ingested by an arthropod intermediate host (2) (various species of beetles and fleas may serve as intermediate hosts), they develop into cysticercoids, which can infect humans or rodents upon ingestion (3) and develop into adults in the small intestine. A morphologically identical variant, H. nana var. fraterna, infects rodents and uses arthropods as intermediate hosts. When eggs are ingested (4) (in contaminated food or water or from hands contaminated with feces), the oncospheres contained in the eggs are released. The oncospheres (hexacanth larvae) penetrate the intestinal villus and develop into cysticercoid larvae (5). Upon rupture of the villus, the cysticercoids return to the intestinal lumen, evaginate their scoleces (6), attach to the intestinal mucosa and develop into adults that reside in the ileal portion ofthesmallintestine producing gravid proglottids (7). Eggs are passed in the stool when released from proglottids through its genital atrium or when proglottids disintegrate in the small intestine (8). An alternate mode of infection consists of internal autoinfection, where the eggs release their hexacanth embryo, which penetrates the villus continuing the infective cycle without passage through the external environment (9). The life span of adult worms is 4 to 6 weeks, but internal autoinfection allows the infection to persist for years.[1]

Life cycle and mode of transmission of H. dimunita:[1]

Life cycle of Hymenolepis dimunita. Courtesy of th Life cycle of Hymenolepis dimunita. Courtesy of the Centers for Disease Control and Prevention (CDC at http://www.cdc.gov/dpdx/hymenolepiasis/index.html).

Eggs of Hymenolepis diminuta are passed out in the feces of the infected definitive host (rodents, man) (1). The mature eggs are ingested by an intermediate host (various arthropod adults or larvae) (2), and oncospheres are released from the eggs and penetrate the intestinal wall of the host (3), which develop into cysticercoid larvae. Species from the genus Tribolium are common intermediate hosts for H. diminuta. The cysticercoid larvae persist through the arthropod's morphogenesis to adulthood. H. diminuta infection is acquired by the mammalian host after ingestion of an intermediate host carrying the cysticercoid larvae (4). Humans can be accidentally infected through the ingestion of insects in precooked cereals, or other food items, and directly from the environment (e.g., oral exploration of the environment by children). After ingestion, the tissue of the infected arthropod is digested releasing the cysticercoid larvae in the stomach and small intestine. Eversion of thescoleces (5) occurs shortly after the cysticercoid larvae are released. Using the four suckers on the scolex, the parasite attaches to the small intestine wall. Maturation of the parasites occurs within 20 days and the adult worms can reach an average of 30 cm in length (6). Eggs are released in the small intestine from gravid proglottids (7) that disintegrate after breaking off from the adult worms. The eggs are expelled to the environment in the mammalian host's feces (1).


United States data

Infection is most common in the Southeast (1% of school children in one study) and among institutionalized children. Among the 216,275 stool specimens tested in the year of 1987, 0.4% tested positive for H nana.[2] In a study done in western states of Colorado, Utah, New Mexico and Montana; only 1 out of 795 stool samples tested in spring season were positive for H. nana (0.1%), as compared to 33% positive stools for Blastocystis hominis.[3]

The infection rates were found to be higher among Southeast Asian refugees (4.7% and 5.2%) in the Unites States in two different studies.[4, 5] In a large study of internationally adopted children in the USA, H nana was found in the stools of 1% of the 1042 children screened.[6]

International data

Infection is most common in children aged 4-10 years, in dry, warm regions of the developing world. H nana infection affects millions of people, primarily children, worldwide. Estimated rates of infection in various regions range from 0.1-58%. It is estimated to have 50-75 million carriers of H. nana with 5 to 25% prevalence in children worldwide, which can be as high as 50% in children between 1-4 years of age.[7] Regions with high reported infection rates include Sicily (46%), Argentina (34% of school children), and southern areas of the former Soviet Union (26%). In contrast, only 0.1% of stools examined at a children's hospital in Calgary were positive for H nana. Most cases with associated neurologic symptoms have been reported from the former Soviet Union.


Morbidity is uncommon, only occurring when parasite burden is very high. Death has not been reported in association with this infection.

In a study of Bolivian schoolchildren, H nana infection was associated with an increased risk of anemia (odds ratio, 2.9; 95% confidence interval: 1.5-5.7; P=.002).[8]

Race-, sex-, and age-related demographics

No racial predisposition is known for hymenolepiasis.

No gender predilection is known for hymenolepiasis.

Disease is most prevalent in school aged children, up to 50% in children between 1-4 years of age.[7]




Most of the cases infected with H. nana are asymptomatic. Several studies have reported non-specific symptoms such as abdominal pain, loss of appetite, diarrhea, flatulence, weight loss, irritable behavior, anal pruritus, nasal pruritus, delayed growth.[9, 10, 11, 12] Increased severity of symptoms has been reported in patients with higher load of infestation (>3000 parasites).[13]


Aside from rare abdominal tenderness or urticaria, physical examination is typically unrevealing.


The infection is acquired mainly by fecal-oral route. The risk factors of infection with H. nana include absence of proper sanitation, contact with environments contaminated with human feces, inadequate treatment of excreta and waste, consumption of untreated water, presence of infected person in the household, and bathing in contaminated irrigation canals.[14]





Laboratory Studies

The diagnosis of infection with Hymenolepiasis is made by direct examination of eggs in concentrated stool specimen. Multiple stool examinations increase the yield of testing.[6]

H nana egg in an unstained wet mount. Courtesy of H nana egg in an unstained wet mount. Courtesy of the Centers for Disease Control and Prevention (CDC at http://www.cdc.gov/dpdx/hymenolepiasis/index.html).


Medical Care

Supportive care is typically sufficient as an adjunct to drug therapy.


In severe cases, consultation with an infectious diseases specialist or gastroenterologist may be appropriate.


The symptomatic child with severe infection may better tolerate a bland diet.



Medication Summary

The 3 drugs that are used for the treatment of hymenolepiasis are praziquantel, nitazoxanide, and niclosamide. In a comparative study done in Peru among children 2-11 years of age, a cure rate of 89% was achieved with 3 day regimen of nitazoxanide in the treatment of 39 children with hymenolepiasis as compared to cure rate of 96% in the treatment of 49 children with a single dose (25 mg/kg) of praziquantel.[15]


Class Summary

Parasite biochemical pathways are different from the human host; thus, toxicity is directed to the parasite, egg, or larvae. The mechanism of action varies within the drug class. Antiparasitic actions may include the following:

- Inhibition of microtubules, which causes irreversible block of glucose uptake

- Tubulin polymerization inhibition

- Depolarizing neuromuscular blockade

- Cholinesterase inhibition

- Increased cell membrane permeability, resulting in intracellular calcium loss

- Vacuolization of the schistosome tegument

- Increased cell membrane permeability to chloride ions via chloride channels alteration

Praziquantel (Biltricide)

It is FDA approved in the United States for the treatment of schistosomiasis and liver flukes only and not hymenolepiasis.[16] A cure rate of 96% was obtained among 49 children aged 2-11 years with hymenolepiasis who received a single dose of praziquantel (25 mg/kg) in Peru.[14]


Nitazoxanide is available for use in USA. It is FDA approved for use in the treatment of giardiasis in both adults and children; and cryptosporidiosis in children only.[19] It is used as off label for the treatment of hymenolepiasis in the United States. The mechanism of action of Nitazoxanide against helminthes is unknown. The efficacy with nitazoxanide was found to be 75-82 % in the treatment of hymenolepiasis in studies done in Peru.[14, 17]


Niclosamide is not commercially available in the USA. It is manufactured as 500 mg tablet, is poorly absorbed and should be thoroughly chewed before swallowing for maximum efficacy. Treatment for H. nana infection requires a course of 7 days to eradicate the maturing H. nana cysts which are not affected by this drug until they are matured.[21, 20]



Further Outpatient Care

Perform follow-up stool examination for ova and parasites 2 weeks and 3 months after treatment to determine whether reinfection or treatment failure has occurred.

Further Inpatient Care

Inpatient care is rarely, if ever, necessary.


See the list below:

  • Emphasize good personal hygiene and proper disposal of sewage. Because some rodents can carry the parasite (44% of hamsters in one study), good handwashing after handling pets should be reinforced.

  • Use contact precautions because H nana eggs in stool are infectious.


Prognosis is excellent, with or without treatment.

Patient Education

Emphasize the importance of good hand washing, personal hygiene, and sanitary living conditions.