Tapeworm Infection

Tapeworm infection
The right clinical information, right where it's needed
Last updated: Sep 07, 2015
Table of Contents
Summary
Basics
Definition
Epidemiology
Aetiology
Pathophysiology
Classification
Prevention
Primary prevention
Diagnosis
8
8
9
Case history
Step-by-step diagnostic approach
Risk factors
11
History & examination factors
12
Diagnostic tests
14
Differential diagnosis
15
Diagnostic criteria
15
Treatment
17
Step-by-step treatment approach
17
Treatment details overview
18
Treatment options
20
Follow up
28
Recommendations
28
Complications
28
Prognosis
28
Guidelines
29
Diagnostic guidelines
29
Treatment guidelines
29
Online resources
31
References
32
Images
35
Disclaimer
39
Summary
Tapeworms belong to the Platyhelminthes phylum. Subclasses include the orders Pseudophyllidea and
Cyclophyllidea.
Humans can be definitive or intermediate hosts.
Extra-intestinal manifestations include cystercercosis (can affect any organ), hydatidosis (can affect any organ
but typically the liver and lungs), and neurocysticercosis (affecting the CNS).
Presentation is variable and is dependent on size, location, and condition of the cyst.
Diagnosis is made by stool examination and serology. Radiology may be necessary for extra-intestinal
manifestations.
Intestinal infection is treated with antihelminthics only.
Extra-intestinal infection may require surgical intervention.
Tapeworm infection
Basics
BASICS
Definition
Tapeworms refer to parasites of the taxonomic class Cestoda, and include the orders Pseudophyllidea and Cyclophyllidea.
They divide their life cycles between two animal hosts. The worms can vary in length from a few millimetres to 25 m, and
can contain thousands of proglottids (tapeworm segments).[1] [2] [Fig-1] Adult tapeworms usually possess an anterior
scolex (head; plural 'scolices') that may be modified with structures or organelles that attach to the host. Therapy is aimed
at the destruction of the scolices, and failure to achieve this will result in regrowth of the tapeworm. When mature, these
parasites reside in the intestinal tract of definitive carnivorous hosts, and larval cysts are formed in the intermediate hosts.
Human tapeworms cause intestinal infection when the immature cysticercoid larvae attach to the intestinal mucosa
using the scolices, and grow by production of proglottid segments.
Certain cestodes can cause extraintestinal infections. Ingested eggs hatch in the intestines and larva migrate to
extraintestinal tissues, where they encyst. Cysts due to Taenia solium within the central nervous system are referred to
as neurocysticercosis, and cysts in other locations are termed cysticercosis. Cysts due to Echinococcus granulosus are
referred to as cystic echinococcosis or hydatid cysts, and cysts due to E multilocularis are referred to as alveolar
echinococcosis.
Epidemiology
Taenia saginata and T solium are prevalent throughout the world. T saginata is commonly found in Europe, the US, South
America, and Africa, and infection usually occurs among those whose diets consist of raw or undercooked beef. [Fig-1]
T solium is endemic in areas of the world where pigs have access to human faecal material (e.g., Latin America, Eastern
Europe, sub-Saharan Africa, India, and elsewhere in Asia).[3] [4] [5] [6] In the US between 2003 and 2012, neurocysticercosis
from T solium led to an estimated 18,584 hospitalisations and cost in excess of US $908 million.[7] Risk of hospitalisation
was reported to be highest in those of Hispanic ethnicity, male sex, and age 20 to 44 years.[7]
Diphyllobothrium latum infection is prevalent in areas of the north temperate and subarctic zones, where freshwater fish
are commonly consumed. The approximate worldwide prevalence is 9 to 10 million people. Infected fish have been
reported worldwide. In North America, highly endemic areas have been found in Alaska and Canada among Native
American populations. In the US, infected fish have been found in regions of the Great Lakes (especially Minnesota and
Michigan) and in Florida and California. Transmission has been brought under control in Western Europe, although cases
have been reported in Finland. Humans are the primary definitive host and the most important reservoir of infection.
The dwarf tapeworm Hymenolepis nana is found in most warm regions of the world. It is the most common tapeworm
infection in the southeastern US and in Latin America, and it is common throughout southern Europe, the Indian
subcontinent, Russia, and the former Soviet republics.[8] [9] [10] [11] Patients infected with H nana are often children,
who present with loose bowel movements.
The greatest prevalence of cystic echinococcosis in humans is found in countries of temperate zones, including southern
South America, the entire Mediterranean littoral, the southern and central areas of the former Soviet Union, central Asia,
China, Australia, and areas of Africa.[1] It is commonly found among populations involved with sheep raising. In the US,
most infections are diagnosed in immigrants from countries in which hydatid disease is highly endemic.
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Tapeworm infection
Basics
Aetiology
Human infection with the dog tapeworm, Echinococccus granulosus, occurs through contact with infected dog (or other
canid) faeces. Infection develops in dogs when they ingest organs of other animals harbouring tapeworm larvae, leading
to infection with the adult tapeworm. Eggs are passed into the faeces of the dog and, if ingested by humans, can result
in the development of complex cysts in tissue (metacestode larval form) and is termed echinococcosis.
Human infection with E multilocularis from foxes, canids, and occasionally cats also occurs through faecal-oral contact.
Eggs are released in faeces and accidentally ingested by humans.
Human infection with Diphyllobothrium latum occurs when undercooked freshwater fish infected with the plerocercoid
larvae of D latum is consumed. Humans are the main definitive host for D latum and the most important reservoir of
infection. These tapeworms can be very large, measuring up to 12 m and containing 3000 to 4000 proglottids. When
eggs are discharged into freshwater, they hatch and release motile embryos, which are ingested by minute waterfleas
(first intermediate hosts). Following ingestion of the waterfleas by larger crustaceans and fish (second intermediate hosts),
these motile embryos develop into larvae (known as sparganum or plerocercoid larvae), which are infectious to humans.
When raw or undercooked infected fish and crustaceans are eaten by humans, these larvae are ingested and develop
into an adult tapeworm in the intestine.[2]
Human infection with Hymenolepis nana, occurs when embryonated eggs from contaminated food, water, or hands or
ingestion of infected insects results in infection. No intermediate host is required and person-to-person transmission
can occur. The disease is most frequently encountered in small children. These eggs are immediately infectious, and
both auto-infection and person-to-person transmission commonly occurs. Outbreaks in families are well described.[2]
Pathophysiology
The presence of the adult tapeworm in the intestine can lead to malabsorption and malnutrition in the host. The presence
of the larval form of the tapeworm in extra-intestinal tissues can lead to various symptoms and signs, including seizures
(from cysts in the brain), hepatomegaly (from cysts in the liver), and cough and/or haemoptysis (from cysts in the lung).
Intestinal infection (e.g., with Diphyllobothrium latum, Hymenolepis nana, Taenia saginata)
Larvae are ingested, oncospheres (embryos) hatch, and adult tapeworms develop inside the human intestinal tract.
Both adult and larval forms may be present in the human intestinal tract (e.g., with H nana).
Adult parasites live in the human intestinal tract, and eggs and proglottids are passed in the faeces.
H nana oncospheres penetrate the bowel mucosa and develop into cysticercoid larvae. Larvae emerge in the bowel
lumen after a period of 5 to 6 days, and develop into adult tapeworms in the ileum. About 20 to 30 days after initial
infection, the adult begins to produce new eggs, which can be found in the faeces and spread the infestation.[2]
BASICS
Human infection with Taenia species occurs whenever undercooked beef (infected with T saginata cysticerci) or pork
(infected with T solium cysticerci) is consumed. Cysticercosis occurs after humans accidentally ingest embryonated T
solium eggs or gravid proglottids from T solium carriers. T solium carriers may contaminate water supplies or contaminate
food directly, as sticky eggs under their fingernails can be transferred during food preparation, causing cysticercosis
and/or neurocysticercosis in consumers.
Tapeworm infection
Basics
Cysticercosis and neurocysticercosis
BASICS
Humans develop cysticercosis by ingesting embryonated Taenia solium eggs or gravid proglottids. Following
ingestion, oncospheres hatch and infect the small intestine or invade through the intestines and migrate to
extraintestinal tissues.
A minimal inflammatory reaction may occur with T saginata, suggesting that these tapeworms have an 'irritative'
effect, perhaps causing clinical symptoms.
Embryos invade the bowel wall and the scolex (tapeworm head with suckers, hooks, and a rudimentary body from
which proglottids are produced by budding) of the larva evaginates, attaches to the upper jejunum, and develops
into an adult worm.
Cysticerci (liquid-filled vesicles consisting of a membranous wall and a nodule containing the evaginated scolex)
develop over a period of 3 weeks to 2 months.
Larvae may form within any extraintestinal tissue. Neurocysticercosis is invasion of the CNS.
Humans with cysticercosis are intermediate or dead-end hosts (i.e., do not transmit infection).
Once present in the parenchyma of host organs, cysts undergo dynamic changes. Initially cysts are vesicular and
filled with clear fluid, and they may elicit a host inflammatory reaction (referred to as the cystic stage). The cysts
start to degenerate and become turbid with an intense inflammatory reaction in surrounding tissue (referred to as
the colloidal stage).[12] The granular stage is next, and is characterised by further degeneration when the cyst
ultimately calcifies.
Neurocysticercosis can be parenchymal or extraparenchymal. Parenchymal disease used to be referred to as active
(when the larvae is viable) and inactive (when the larvae is calcified), but that classification is no longer applicable.
MRI studies have documented that patients with neurocysticercosis seizures, and calcified lesions often have
associated contrast enhancement and oedema. There has been increasing evidence that perilesional oedema,
which occurs episodically, is associated with seizures. There is no evidence to suggest these lesions are associated
with viable parasites. Instead, they may be caused by the release of antigens from the calcified granuloma in
restimulation of host inflammation.
Extraparenchymal neurocysticercosis includes involvement of the subarachnoid space, the ventricles, the spinal
cord, and/or the eye.
Another form of neurocystercosis is referred to as racemose disease. It generally occurs when subarachnoid or
intraventricular cysts proliferate in spite of scolex degeneration, provoking an intense inflammatory response from
hosts.
Mixed neurocysticercosis involves both parenchymal and extraparenchymal disease.[13] [Fig-1] [Fig-2] [Fig-3]
[Fig-4] [Fig-5]
Echinococcosis (hydatiditis)
The life cycle of Echinococcus species involves definitive and intermediate hosts. Humans are accidental hosts.
Once ingested, oncospheres hatch from eggs in the small intestine.
Tapeworm infection
Basics
Hydatid cysts develop and enlarge into space-occupying lesions (metacestode stage) over months to years. Cystic
echinococcosis (due to Echinococcus granulosus infection) or polycystic echinococcosis (due to E vogeli and E
oligarthus infections) occurs when protoscolices form on the inside of the cystic wall. In alveolar echinococcosis
(due to E multilocularis), discrete cysts are absent, and larvae expand by budding and invasive external growth out
from the primary larval lesion.[1] [2] [13] [14]
Classification
Taxonomy[1] [2]
Phylum Platyhelminthes: class Cestoda, order Pseudophyllidea:
Diphyllobothrium latum
D pacificum
D spirometra
Phylum Platyhelminthes: class Cestoda, order Cyclophyllidea:
Species:
Taenia
Hymenolepis
Bertiella
Dipylidium
Mesocestoides
Raillietina
Inermicapsifer
Echinococccus
BASICS
Larva penetrate the intestinal mucosa then enter the blood and/or lymphatic system and migrate to visceral organs,
where the metacestode (hydatid cyst) forms. Hydatid cysts are characterised by outer host reactions with acellular
laminar and inner germinal membranes, forming the endocyst. Brood capsules with multiple protoscolices bud
out from the germinal membrane.[1]
Tapeworm infection
Prevention
Primary prevention
Preventing human tapeworm infections can serve to decrease the number of carriers of tapeworm eggs. Education
regarding routes of transmission, good personal hygiene, careful washing of fruit/vegetables, and hand washing prior to
food preparation could help prevent egg transmission to humans.
Risk of infection can also be reduced with adequate cooking of beef, pork, and fish; inspection of pork for cysticerci;
and/or freezing of meat.
Prevention of cystic echinococcosis can often be achieved merely by avoiding close contact with dogs.
PREVENTION
Preventing infection in pigs can be accomplished by changing pig-raising practices in endemic areas. Prohibition of
home-slaughter of sheep will prevent dogs from consuming infected viscera, thus disrupting the life cycle of the parasite.
Tapeworm infection
Diagnosis
Case history
Case history #1
A 30-year-old Albanian man, who recently migrated to the UK, presents to an outpatient clinic complaining of something
resembling large grapefruit seeds in his stool. He has no past medical history of note and no abdominal pain, bloating,
diarrhoea, or constipation.
Case history #2
A 35-year-old Hispanic man is brought in to the emergency department after having a witnessed tonic-clonic seizure.
Family members say that he was healthy, other than sporadic episodes of headaches. He used to work as a farmer in
his home country in Central America.
Other presentations
Patients with intestinal disease may also present with vague symptoms, including nausea, abdominal distension, oral
symptoms, allergy symptoms (anaphylaxis or urticaria), appetite changes, altered bowel habit, anaemia, pruritus ani,
sleep/behavioural disturbances, and/or descriptions of 'feeling something moving inside'.
Patients with extraintestinal disease may present to primary care providers or emergency departments with symptoms,
including headaches, seizures, abdominal pain, cough, and haemoptysis.
Step-by-step diagnostic approach

Historical factors
Patients who are definitive hosts for Taenia solium may also be asymptomatic or may present with vague intestinal
symptoms as above, or with anxiety, headaches, dizziness, urticaria, and a variety of other pleomorphic symptoms.
Patients with H nana may present with an itchy rash.[15]
The majority of patients with cystic echinococcosis (hydatiditis) are asymptomatic, and hydatid cysts are often observed
as incidental findings at autopsy or detected by abdominal ultrasound performed for other reasons. The severity and
nature of the signs and symptoms that may be produced by these tapeworms are extremely varied and never
pathognomonic. Due to the distensible nature of the liver, cysts may grow for years before becoming symptomatic.
Symptoms include right upper quadrant or epigastric pain, nausea, or vomiting. Communication and rupture of hepatic
cysts into the biliary tree is well described and can result in cholangitis and cholestasis. In these instances, patients
present with epigastric pain and RUQ pain, which can be intermittent and mimic gallstone disease. If left untreated,
cholangitis can occur with resultant bacterial superinfection of the cyst cavity and abscess formation. Thoracic
complications of hepatic hydatid cysts are seen in approximately 2% to 11% of cases. Less commonly, portal
hypertension can occur, either by extrinsic compression of the liver, or by obstruction of the inferior vena cava and
hepatic outflow tract. Cysts may rupture into the peritoneal cavity, usually secondary to trauma, with resultant
DIAGNOSIS
Patients with intestinal infection (e.g., with Hymenolepis nana, Diphyllobothrium latum, Taenia saginata) can be
asymptomatic.[8] However, they may present with vague intestinal symptoms including abdominal pain, hunger pain,
sore tongue, sore gums, loss of appetite, increased appetite, weight loss, bloating, constipation, diarrhoea, a feeling
of 'something moving inside', and/or nausea.[2]
Tapeworm infection
Diagnosis
anaphylaxis or secondary cystic echinococcosis. Mild to severe anaphylactoid reactions (and occasionally death) may
follow the sudden massive release of cyst fluid. Intact hydatid cysts in the lungs may cause no symptoms, while chest
pain, cough, or haemoptysis can occur when there is leakage or rupture of the cyst. Rupture or leakage of echinococcal
cysts into the peritoneum usually results in acute or intermittent allergic manifestations (anaphylaxis or urticaria).
When patients are harbouring the adult tapeworm, they may present after noticing large tapeworm segments
(proglottids) in the toilet bowl or after feeling the spontaneous movement of proglottids through the anus. Some
patients with D latum only become aware of the infection when spontaneously passing proglottids. In T saginata
infection, proglottids usually spontaneously emerge out of the anus and in T solium infection, proglottids are usually
passed with stools.
Seizures and headaches are the most common presenting symptoms in patients with neurocysticercosis (NCC). The
disease is pleomorphic and may present with a variety of symptoms depending on the location, the number of
cysticerci, and the associated host response.[16] Increased intracranial pressure can occur in the setting of
intraventricular and subarachnoid disease, and can be life threatening. Sudden death can occur. Subarachnoid disease
can result in stroke or hydrocephalus due to the exuberant host inflammation in response to this form of disease.
Travel, diet, and exposure history, along with compatible clinical syndromes, can help in diagnosing tapeworm
infections.
Physical examination
Physical examination is generally unremarkable in hosts harbouring adult intestinal tapeworm. However, patients
with H nana may have macular-papular skin eruptions,[15] and patients with Echinococcus species infection may
demonstrate signs of echinococcal liver cysts, including hepatomegaly and evidence of sepsis, if biliary tree
communication, with subsequent superinfection, occurs.
DIAGNOSIS
Examination of patients with neurocysticercosis may reveal neurological defects corresponding to central nervous
system cysts. Extraparenchymal neurocysticercosis may present with increased intracranial pressure and hydrocephalus
and tends to be more severe in its presentation.[16]
Stool examination
Stool examination of definitive hosts can help confirm the diagnosis in patients who harbour the adult tapeworm.
The eggs of T saginata and T solium cannot be distinguished; therefore, it is necessary to obtain proglottids, which
can differentiate the two tapeworms.
Infection with D latum is often first recognised in asymptomatic patients when stool examination is performed for
other reasons.
Baseline stool examination for ova and parasites is important prior to starting any treatment.
Serum serology
Serodiagnosis is helpful in many parasitic diseases, but has shown to be problematic in the diagnosis of cysticercosis
due to cross-reactions to other parasites and non-specific binding. In general, assays employing unfractionated
antigen have poor sensitivity and specificity.[1] The enzyme-linked immunotransfer blot (EITB) is an immunoblot
assay employing semi-purified membrane antigens. Binding to any one of seven bands is considered positive. Studies
have confirmed nearly 100% specificity, but rare false positives have been noted with a single gp50 band.[17] The
sensitivity is limited in subjects with either a single lesion or with only calcified lesions.The predictive value of the EITB
assay for neurocysticercosis is better with serum than with CSF.
10
Tapeworm infection
Diagnosis
Complete blood count

Eosinophilia is not always encountered in tapeworm infections. Helminthic parasitic infections cause eosinophilia
during migration through host tissue. Tapeworms causing intestinal infections can remain wholly in the lumen of the
gut, while extra-intestinal infections can be walled off. When cystic structures are disrupted, eosinophilia is more
likely.[18]
D latum infections may present with megaloblastic pernicious anaemia due to absorption of vitamin B12 by the
tapeworm. About 40% of people harbouring the worm have reduced serum vitamin B12, but fewer than 2% develop
anaemia.
Imaging
The WHO classifies the stages of Echinococcus granulosus into active versus inactive, and classification guides therapy.
CE1 is a unilocular anechoic cystic lesion with a double sign. CE2 is a multiseptated, 'rosette-like honeycomb' cyst
(this is a mother cyst filled with daughter cysts). Both CE1 and CE2 are considered active, usually fertile cysts containing
viable protoscolices. CE3a is a cyst with detached membranes (water-lily-sign), while CE3b has daughter cysts in a
solid matrix. These are considered cysts in the transitional stage where the integrity of the cyst has been compromised
either by the host or by chemotherapy. A cyst with heterogenous hypoechoic/hyperechoic contents and no daughter
cysts is the CE4 stage while calcified cysts are considered CE5. CE types 4 and 5, which are inactive, have normally
lost their fertility and are degenerative.[Fig-6]
Neuroimaging is the mainstay of diagnosis for NCC, and studies highly suggestive of NCC are considered a major
diagnostic criterion. The combination of a single, round, enhancing lesion, less than 20 mm in diameter, with no
midline shift, in patients without increased intracranial pressure, focal neurological deficits, or evidence of systemic
disease, is highly suggestive of NCC. Resolution of the lesion spontaneously or after anti-cysticercal therapy or
precipitation of symptoms by antiparasitic drugs is also supportive of the diagnosis. All of these are major diagnostic
criteria. MRI is more effective for imaging extraparenchymal cysticerci.[Fig-2] [Fig-3] [Fig-4] [Fig-5] [Fig-7]
Risk factors
living on farms
Farmers and those living in endemic regions where pigs are raised and, in the case of Echinococcus species, living
in regions where dogs herd sheep, are at increased risk of tapeworm infection.
poor hygiene
Tapeworm eggs can be sticky, and are often found under the fingernails of carriers.
Food prepared by carriers can lead to infection in consumers if poor hygiene techniques are employed.
eating or handling undercooked meat

Infection with Taenia species may occur whenever undercooked beef (infected with T saginata cysticerci) or pork
(infected with T solium cysticerci) is ingested.
eating or handling undercooked fish or crustaceans

Infection with Diphyllobothrium latum may occur whenever undercooked fish or crustaceans are ingested.
11
DIAGNOSIS
Strong
Tapeworm infection
Diagnosis
ingestion of contaminated water

Infection with Diphyllobothrium latum may occur when water contaminated by infected fish/crustacean faeces
(or fruit/vegetables washed in water contaminated by infected fish/crustacean faeces) is ingested.
dog owners
Infection with Echinococccus granulosus may occur from contact with contaminated dog faeces.
children
Infected children, especially those with pruritus ani and poor hand hygiene, commonly spread tapeworm infections.
Children are more likely to (accidentally) ingest contaminated fox, canid, and/or cat faeces and therefore more
likely to develop Echinococccus multilocularis or E multilocularis infections.
Ingestion of infected insects (also more common among children) can result in Hymenolepis nana infection.
Weak
outdoor pursuits
Poor hand hygiene commonly adopted when camping and pursuing other outdoor activities increases the risk of
accidentally ingesting contaminated fox, canid, and/or cat faeces and developing Echinococccus multilocularis or
E multilocularis infections.
Accidental ingestion of infected insects can result in Hymenolepis nana infection.
History & examination factors

Key diagnostic factors
presence of risk factors (common)
DIAGNOSIS
Key risk factors include living on farms, contact with dogs and/or pigs, ingestion of contaminated water and/or
undercooked meats and fish, and poor hand hygiene.
worm segments in stool (common)

Patients may present after noticing proglottids in the toilet bowl or after feeling the spontaneous movement of
proglottids through the anus.
Spontaneous egress of proglottids per rectum is most frequently reported in Taenia saginata or T solium infestation.
increased intracranial pressure (common)

Patients with CNS manifestations who present with intraventricular or subarachnoid disease (e.g., hydrocephalus)
may have increased intracranial pressures.
seizures (common)
Patients with CNS manifestations may present with seizures.
All patients from endemic areas who present with new-onset seizures require evaluation for neurocysticercosis.[20]
hepatomegaly (common)
Signs of cysts in the liver may include hepatomegaly.
cough (common)
12
Tapeworm infection
Diagnosis
May indicate cysts in the lungs.
haemoptysis (common)
May indicate cysts in the lungs.
allergy manifestations (uncommon)

Rupture or leakage of tapeworm cysts into the peritoneum usually results in acute or intermittent allergy
manifestations (urticaria or anaphylaxis).
Minimal inflammatory reaction may occur with Taenia saginata, suggesting that these tapeworms have an 'irritative'
effect, which may cause clinical symptoms.
anaemia (uncommon)
Diphyllobothrium latum infections may cause anaemia due to absorption of vitamin B12 by the tapeworm.
About 40% of people harbouring the worm have reduced serum vitamin B12, but fewer than 2% develop anaemia.[19]
Other diagnostic factors

asymptomatic (common)
Many infections are asymptomatic.
Hydatid cysts are frequently only discovered as incidental findings at autopsy.
vague intestinal symptoms (common)

Patients with intestinal disease may present with vague symptoms including abdominal pain, hunger pain, sore
tongue, sore gums, loss of appetite, increased appetite, weight loss, bloating, constipation, diarrhoea, sensation of
'something moving inside', and/or nausea.[2]
Patients infected with Hymenolepis nana infection are often children with loose bowel movements. H nana infection
can also present with diffuse persistent abdominal pain.
sleep disturbance (common)
headaches (common)
CNS manifestations can cause headaches.
Patients from endemic areas who have migraine symptoms or chronic headaches of unclear aetiology should be
considered for evaluation for neurocysticercosis.
rash (common)
Many patients with Hymenolepis nana have itchy skin eruptions.[15] Patients with a ruptured or leaking echinococcal
cyst may have urticarial eruptions.
pyrexia (uncommon)
Signs of cysts in the liver may include evidence of sepsis if biliary tree communications are present with subsequent
superinfection.
13
DIAGNOSIS
Many children with Hymenolepis nana have sleep and behavioural disturbances that clear after tapeworm eradication.
Diagnosis
Tapeworm infection
Diagnostic tests
1st test to order
Test
Result
stool examination
eggs and (gravid/non-gravid)

Egg release in the stool may be variable because of irregular rates of proglottid proglottids in stool
detachment and degeneration.
Examination of the stool samples over several days increases the yield.
Species identification is important, and is usually based on morphology of the
proglottids.
Identification of Taenia solium is significant, and should prompt consideration
of possible cysticercosis in index patients or among household contacts.
Diphyllobothrium latum and Hymenolepis nana may be diagnosed by finding
characteristic ova in the faeces.
FBC
Many patients with Hymenolepis nana have moderate eosinophilia of 5% to
10%.
Diphyllobothrium latum infections may present with megaloblastic pernicious
anaemia due to absorption of vitamin B12 by the tapeworm.
About 40% of people harbouring the worm have reduced serum vitamin B12,
but fewer than 2% develop anaemia.
enzyme-linked immunoelectrotransfer blot (EITB)
EITB is an immunoblot using 7 purified glycoprotein antigens. It has 98%
sensitivity and 100% specificity in patients with more than 1 lesion.
Sensitivity in single-cyst cases may drop to 70%.[17]
DIAGNOSIS
Echinococcus ELISA and western blot serology

Western blot is the confirmatory test for Echinococcus. Serology is 80% to
100% sensitive and 88% to 96% specific for liver cyst infections.
It is less sensitive for lung involvement (50%-56%) and 25% to 26% for other
organ involvement.[1]
In the US, ELISA is available through the Centers for Disease Control and
Prevention (CDC).
ultrasound
moderate eosinophilia,
megaloblastic pernicious
anaemia
Taenia solium with purified

glycoprotein antigens (western
blot)
Echinococcus species with

purified glycoprotein antigens
(western blot)
hydatid cysts
Abdominal ultrasound may detect hydatid cysts (e.g., echinococcosis of the

liver). [Fig-6]
CT head
brain calcification
Neuroimaging is the mainstay of diagnosis for neurocysticercosis (NCC), and

studies highly suggestive of NCC are considered a major diagnostic criteria.
The combination of a single, round, enhancing lesion, less than 20 mm in
diameter, with no midline shift, in patients without increased intracranial
pressure, focal neurological deficits, or evidence of systemic disease is highly
suggestive of NCC. Resolution of the lesion spontaneously or after
anti-cysticercal therapy or precipitation of symptoms by antiparasitic drugs is
also supportive of the diagnosis. All of these are major diagnostic criteria. MRI
is more effective for imaging extraparenchymal cysticerci. Calcifications are
common.[Fig-3] [Fig-7]
MRI
MRI is more effective for imaging extraparenchymal cysticerci.
MRI may also reveal the scolex, which is usually not visible on CT scans. [Fig-2]
[Fig-4] [Fig-5]
14
extraparenchymal cysticerci
tapeworm scolex
Diagnosis
Tapeworm infection
Differential diagnosis
Condition
Differentiating signs /
symptoms
Differentiating tests
Patients are normally febrile.

There may also be signs of
tuberculosis elsewhere (e.g.,
chronic cough, haemoptysis,
bone pain).
Western blot negative.

CT head and MRI brain may show
ring-enhancing lesions.
Amoebic abscess
Patients are usually febrile with

elevated erythrocyte
sedimentation rates.
Western blot negative. Amoebic

serology might be positive.
Migraine
Patients usually have unilateral

motor or sensory signs and
headache.
Stool examination and western

blot negative.
Epilepsy
Patients usually experience

premonitory sensations (fear,
epigastric sensation, dj vu,
jamais vu).
Gastroenteritis
Patients may be febrile with

associated vomiting.
Brain tumour
Patients have focal neurological

deficits according to location.
Liver metastases
Patients may be jaundiced with

ascites. History of cancer.
Western blot negative. Imaging

usually not cystic in appearance
with daughter cysts.
Cholecystitis
Patients may have positive

Murphy's signs with right shoulder
pain.
Western blot negative. Usually has

elevated WBC and fever, and
ultrasound reveals stones and
pericholic fluid.
Sarcoidosis
Patients may have erythema

nodosum, chronic fatigue, and/or
arthralgia.
Alcohol abuse
Patients usually demonstrate

evidence of alcohol withdrawal
including hallucinations and
tremor.
Diagnostic criteria
Diagnostic criteria for neurocysticercosis[21] [22]
Absolute criteria for neurocysticercosis:
Histological demonstration of the parasite from biopsy of a brain or spinal cord lesion
15
DIAGNOSIS
Central nervous system

tuberculoma
Tapeworm infection
Diagnosis
Cystic lesions showing the scolex on CT or MRI

Direct visualisation of subretinal parasites by fundoscopic examination.
Major criteria for neurocysticercosis:
Lesions highly suggestive of neurocysticercosis on neuroimaging studies
Positive serum immunoblot for the detection of anticysticercal antibodies
Resolution of intracranial cyst after therapy with albendazole or praziquantel
Spontaneous resolution of small single lesions.
Minor criteria for neurocysticercosis:
Lesions compatible with neurocysticercosis on neuro-imaging studies; clinical manifestation suggestive of
neurocysticercosis
Positive CSF ELISA for detection of anticysticercal antibodies or cysticercal antigens
Cysticercosis outside the central nervous system.
Epidemiological criteria:
Evidence of a household contact with Taenia solium infection
History of frequent travel to disease-endemic areas
DIAGNOSIS
Individuals coming from or living in an area where cysticercosis is endemic.

Definitive diagnosis requires 1 absolute criterion or 2 major criteria based on neuro-imaging studies, serological tests,
clinical history, and exposure. Probable diagnosis requires 1 major criterion plus 2 other criteria or 3 major criteria plus
exposure to known infective material.
16
Tapeworm infection
Treatment
Step-by-step treatment approach

Treatment varies depending upon whether infection is intestinal or extraintestinal.
Intestinal infection
When stool examination reveals evidence of tapeworm infection (e.g., Hymenolepis nana, Diphyllobothrium latum,
Taenia saginata, and T solium), the treatment of choice is the broad-spectrum antihelminthic praziquantel. Praziquantel
has excellent activity against all tapeworms. It is given as a single dose for both children and adults. Infections with H
nana require higher doses.
Other antihelminthic preparations, such as niclosamide, also exist.
CNS manifestations
CNS manifestations include disease with T solium (neurocysticercosis) or Echinococccus species.
Active parenchymal disease with cystic lesions and/or enhancing lesions is initially treated with antihelminthics.[23]
[24] The addition of corticosteroids is an effective way to reduce generalised seizures in patients with active
parenchymal cysts.[23] [24] Inactive parenchymal disease (with calcified lesions) does not require treatment with
antihelminthics. However, calcified lesions can be associated with symptomatic perilesional oedema, and some
experts recommend corticosteroids.[25]
The optimal dose, duration, and formulation of adjunctive corticosteroid to administer with antiparasitic therapy have
not been established. An open-label randomised trial compared conventional dexamethasone dosing with enhanced
dexamethasone dosing in patients with viable parenchymal neurocysticercosis with recent (within 6 months) seizure
activity.[26] Although the study did not meet its primary end point of reducing seizure days or individuals with seizures,
the study had two important findings. First, this study found that seizure activity was heightened during days 1 to 21
and decreased after day 21; second, that enhanced dexamethasone dosing reduced seizure activity from days 1 to
21. Adverse effects were not different between the two groups. These data suggest that patients with intraparenchymal
viable neurocysticercosis at risk for seizure during the first 21 days of treatment may benefit from an enhanced
corticosteroid regimen.
Patients with greater disease burden may benefit from combination antiparasitic therapy. One double-blind,
placebo-controlled trial has shown that patients with viable intraparenchymal neurocysticercosis have increased
parasiticidal effect, without increased side effects, with combination therapy of albendazole plus praziquantel compared
with albendazole alone. The benefit was largely driven by the sub-group of patients with three or more viable cysts.[27]
Patients with active ventricular disease may present with obstructive hydrocephalus. Management of these patients
is focused on relieving the intracranial hypertension with ventriculoperitoneal shunting. Once intracranial pressure
is stabilised, endoscopic removal of cysticerci in the lateral, third, and fourth ventricles is performed. Patients with
MRI findings of significant ependymal enhancement (secondary to adherence of lesions to the ependyma) may not
be suitable for this surgery.[16] Concurrent treatment with albendazole is recommended during shunting and/or
cyst removal.
17
TREATMENT
Evidence regarding treatment of subarachnoid disease is limited as the condition is relatively rare and prognosis is
very poor. It is recommended that raised intracranial pressure is initially treated with shunting, and prolonged
antihelminthic treatment is given with slow tapering of corticosteroids.[28] Methotrexate may also be used for
corticosteroid-sparing purposes.[28] [29] There have been no controlled trials of subarachnoid disease management;
Treatment
Tapeworm infection
however, case series in which patients were treated with antiparasitic drugs, corticosteroids, and shunting for
hydrocephalus demonstrated improved prognosis.[28]
Case-specific surgery is the mainstay of treatment for spinal cord disease. Antihelminthics with corticosteroids are
also recommended.
Seizures may be controlled with the use of anti-epileptic treatment.
Hepatic or thoracic manifestations

Hepatic or thoracic manifestations include echinococcosis (disease with Echinococccus species) and cysticercosis
(infection with T solium). Surgical removal is the mainstay of treatment of hepatic echinococcal disease. Wide surgical
resection for operable cases (e.g., hepatic lobectomy or liver transplantation) ensures total removal of cysts.
Antihelminthics are administered concurrently at least 2 weeks prior to the surgery and at least 1 month postoperatively.
In pulmonary hydatid disease, prolonging combination therapy of albendazole and praziquantel from 2 weeks to 4
or 8 weeks prior to surgery led to an increased scolicidal response. Prolonging pre-treatment antihelminthics may
be considered if the patient is at high risk for intraoperative rupture.[30]
Medical therapy alone may result in cure for a small subset of patients, but disease often recurs without surgical
intervention. Recent literature reports success with the PAIR (puncture, aspiration, injection, and reaspiration) procedure
in appropriate patients. PAIR is performed with concurrent albendazole therapy to reduce the risk of cyst dissemination.
The hydatid cyst is aspirated under CT guidance, and a scolicidal agent is instilled into the cyst cavity. Fluid is then
re-aspirated.[31] [32]
Treatment details overview

Consult your local pharmaceutical database for comprehensive drug information including contraindications, drug
interactions, and alternative dosing. ( see Disclaimer )
Acute
( summary )
Patient group
intestinal disease
Tx line
Treatment
1st
antihelminthic
inactive parenchymal disease
1st
corticosteroid
active parenchymal disease
1st
antihelminthic
plus
corticosteroid
adjunct
anti-epileptic
CNS disease
TREATMENT
ventricular disease with raised

intracranial pressure
18
1st
ventriculoperitoneal shunt + endoscopic removal
plus
antihelminthic
plus
corticosteroid
adjunct
anti-epileptic
Treatment
Tapeworm infection
Acute
( summary )
ventricular disease with normal
subarachnoid disease
spinal cord and/or optical disease
hepatic or thoracic disease
1st
endoscopic removal of cysticerci
plus
antihelminthic
plus
corticosteroid
adjunct
anti-epileptic
1st
ventriculoperitoneal shunt
plus
antihelminthic
plus
corticosteroid
adjunct
anti-epileptic
1st
surgery
plus
antihelminthic
plus
corticosteroid
adjunct
anti-epileptic
1st
surgery
plus
antihelminthic
plus
corticosteroid
Ongoing
Patient group
chronic subarachnoid disease
( summary )
Tx line
Treatment
1st
antihelminthic
plus
corticosteroid
adjunct
methotrexate
TREATMENT
19
Treatment
Tapeworm infection
Treatment options
Acute
Patient group
intestinal disease
Tx line
Treatment
1st
antihelminthic
Praziquantel is taken as a single dose. Safety of
praziquantel in children under 4 years is unknown and
is therefore not recommended.[33] Infection with
Hymenolepis nana requires higher doses of
praziquantel.
Niclosamide may also be used in adults and children
of all ages.
Primary options
praziquantel: children 4 years of age and adults:
5-10 mg/kg orally as a single dose; higher doses of
25 mg/kg as a single dose required in Hymenolepis
nana infection
OR
niclosamide: dose depends on type of tapeworm
infection; consult specialist for guidance on dose
CNS disease
inactive parenchymal disease
1st
corticosteroid
Inactive parenchymal disease is when the tapeworm
is calcified (visible as calcifications on imaging).
Corticosteroid therapy can help to control oedema
if patients are symptomatic.
Patients with calcified granulomas on CT scan should
not be treated with antihelminthics. If perilesional
oedema is present, they should not receive
antihelminthics.
Primary options
prednisolone: 40-60 mg orally once daily
OR
TREATMENT
dexamethasone: 6 mg orally once daily

active parenchymal disease
1st
antihelminthic
One double-blind, placebo-controlled trial has shown
that patients with viable intraparenchymal
neurocysticercosis have increased parasiticidal effect,
without increased side effects, with combination
therapy of albendazole plus praziquantel compared
20
Treatment
Tapeworm infection
Acute
Patient group
Tx line
Treatment
with albendazole alone. The benefit was largely driven
by the sub-group of patients with three or more viable
cysts.[27]
Patients with viable cysts in the parenchyma should
be treated for at least 10 days with concomitant
corticosteroids.[23] [24]
Primary options
albendazole: children: 15 mg/kg orally once daily
given in 2 divided doses; adults: 400 mg orally twice
daily
-and praziquantel: children 4 years of age and adults:
50 mg/kg/day given in 3 divided doses
plus
corticosteroid
Active parenchymal disease is when the tapeworm
is alive (scolex may be visible on MRI).
Concurrent corticosteroid therapy can help to control
oedema.
Patients with recent (within 6 months) seizure activity
may benefit from an enhanced dexamethasone dosing
regimen compared to the standard dose regimen.[26]
Primary options
OR
dexamethasone: standard dose: 6 mg/day orally
for 10 days; enhanced dose: 8 mg/day orally (3 mg
orally in the morning and afternoon and 2 mg in
the evening) on days 1-28, followed by a 2-week
taper (decrease dose every 2 days to 6 mg/day, 4
mg/day, 3 mg/day, 2 mg/day, and 1 mg/day, then
0.5 mg/day for 4 days, then stop)
adjunct
anti-epileptic
Adjunctive anti-epileptic therapy may help to control
seizures. Medication and dose are case specific.
1st
ventriculoperitoneal shunt + endoscopic removal

Neurocysticercosis patients often have evidence of
hydrocephalus or raised intracranial pressure and
require ventriculoperitoneal shunting.
Endoscopic removal has emerged as the treatment
of choice in intraventricular cysts due to
neurocysticercosis.
21
TREATMENT
ventricular disease with raised

Treatment
Tapeworm infection
Acute
Patient group
Tx line
plus
Treatment
antihelminthic
Albendazole treatment is continued for between 8
and 30 days and can be repeated as necessary.
Praziquantel is given as a higher dose on day 1 and
lower doses for 29 consequent days.
Primary options
daily
OR
praziquantel: children 4 years of age and
adults:100 mg/kg/day orally given in 3 divided
doses for 1 day, followed by 50 mg/kg/day given
in 3 divided doses for 29 days
plus
corticosteroid
oedema.
Primary options
OR
adjunct
anti-epileptic
ventricular disease with normal

1st
endoscopic removal of cysticerci

Once intracranial pressure is stabilised, endoscopic
removal of cysticerci in the lateral, third, and fourth
ventricles is performed. Patients with MRI findings of
significant ependymal enhancement (secondary to
adherence of lesions to the ependyma) may not be
suitable for this surgery.[16]
plus
antihelminthic
TREATMENT
Albendazole treatment is continued for between 8

and 30 days and can be repeated as necessary.
Primary options
22
Treatment
Tapeworm infection
Acute
Patient group
Tx line
Treatment
daily
OR
plus
corticosteroid
oedema.
Primary options
OR
adjunct
anti-epileptic
subarachnoid disease
1st
ventriculoperitoneal shunt
Patients with evidence of hydrocephalus or raised
intracranial pressure require ventriculoperitoneal
shunting.
plus
antihelminthic
Prolonged treatment with albendazole is required in
the racemose form in the subarachnoid space. The
endpoint for treatment is not clear, but it is suggested
that the MRI be followed, along with the CSF
(pleocytosis and glucose), to help establish when to
discontinue treatment. Patients also require prolonged
corticosteroids to avoid complications due to the host's
inflammatory response such as hydrocephalus and
stroke.

daily
OR
23
TREATMENT
Primary options
Treatment
Tapeworm infection
Acute
Patient group
Tx line
Treatment
plus
corticosteroid
the host's inflammatory response.
Primary options
OR
adjunct
anti-epileptic
spinal cord and/or optical disease
1st
surgery
The mainstay of treatment is case-specific surgery
for disease involving the eye. Many spinal cases are in
the subarachnoid spine and can be treated with
prolonged albendazole. Surgery is indicated if there
are symptoms that require decompression.
plus
antihelminthic
Albendazole treatment is continued for prolonged
periods of time.
Primary options
daily
OR
TREATMENT

plus
corticosteroid
Concurrent corticosteroid therapy can help swelling
in the spinal cord and control resulting arachnoiditis.
24
Treatment
Tapeworm infection
Acute
Patient group
Tx line
Treatment
Primary options
OR
adjunct
anti-epileptic
hepatic or thoracic disease
1st
surgery
Surgery is usually mainstay of treatment for
echinococcosis patients with CE2 (mother cysts filled
with daughter cysts) or CE3b cysts (cysts that have
partial solidification with daughter cysts). CE1 cysts
(cysts with no daughter cysts) may be good candidates
for PAIR (puncture, aspiration, injection, and
re-aspiration) procedure. Inactive cysts (those with no
daughter cysts on ultrasound [CE4] and calcified cysts
[CE5]) should be watched and followed by ultrasound.
plus
antihelminthic
Albendazole is administered concurrently for at least
2 weeks pre-operatively and 1 to 3 months
postoperatively.
In pulmonary hydatid disease, prolonging
combination therapy of albendazole and praziquantel
from 2 weeks to 4 or 8 weeks prior to surgery led to an
increased scolicidal response. Prolonging
pre-treatment antihelminthics may be considered if
the patient is at high risk for intraoperative rupture.[30]
Primary options
daily
OR
plus
corticosteroid
25
TREATMENT

daily
-and praziquantel: children 4 years of age and adults:
50 mg/kg/day given in 3 divided doses
Treatment
Tapeworm infection
Acute
Patient group
Tx line
Treatment
oedema.
Primary options
OR
Ongoing
Patient group
chronic subarachnoid disease
Tx line
Treatment
1st
antihelminthic
Prolonged treatment with albendazole is required in
the racemose form in the subarachnoid space. The
endpoint for treatment is not clear, but it is suggested
that the MRI be followed, along with the CSF
(pleocytosis and glucose), to help establish when to
discontinue treatment. Patients also require prolonged
corticosteroids to avoid complications due to the host's
inflammatory response such as hydrocephalus and
stroke.
Albendazole treatment is continued for prolonged
periods of time.
Primary options
daily
plus
corticosteroid
the host inflammatory response to avoid complications
such as hydrocephalus and strokes. These should be
tapered over time.
Primary options
TREATMENT
OR
adjunct
26
methotrexate
Treatment
Tapeworm infection
Ongoing
Patient group
Tx line
Treatment
Methotrexate may be used as a corticosteroid-sparing
agent during ongoing treatment with
corticosteroids.[29]
Primary options
methotrexate: consult specialist for guidance on
dose
TREATMENT
27
Follow up
Tapeworm infection
FOLLOW UP
Recommendations
Monitoring
Stools are to be re-examined at 1 to 3 months after antihelminthic treatment. In some cases treatment can be given
again if there is evidence of persistent or recurrent infection.[33]
Patient instructions
Patients should be advised on the importance of good hand hygiene, careful washing of fresh fruit and vegetables,
and thorough cooking of pork, beef, and fish.
Further patient information is available online. [Patient UK: Cestodes (tapeworms)]
Complications
Complications
sepsis
Timeframe
variable
Likelihood
medium
Hepatic lesions can be complicated by biliary tree communications and may result in sepsis.[1] The cysts can
communicate with the biliary tree and become superinfected with bacteria. If left untreated the patients can become
septic with bowel organisms.
pernicious anaemia
variable
low
Pernicious anaemia can occur in a small number of patients with Diphyllobothrium latum due to absorption of vitamin
B12 by tapeworms.
Prognosis
Intestinal tapeworms have an excellent prognosis. Treatment response in patients with parenchymal cystic
neurocysticercosis or uncomplicated hepatic or thoracic echinococcal cysts is generally favourable, and prognosis is
good. Prognosis for extraparenchymal neurocysticercosis, especially subarachnoid disease, is poor.
28
Tapeworm infection
Guidelines
Diagnostic guidelines
Europe
Guidelines for diagnosis and treatment of liver alveococcosis caused by Echinococcus
multilocularis
Published by: Poznan University of Medical Sciences (Poland)
Last published: 2007
Summary: Recommendations for diagnosis using imaging, ELISA and Western blot, and histopathology and molecular
techniques.
International
Proposed diagnostic criteria for neurocysticercosis
GUIDELINES
Published by: Neurology
Summary: Diagnostic criteria for neurocysticercosis based on objective clinical, imaging, immunological, and
epidemiological data.
North America
New concepts in the diagnosis and management of neurocysticercosis (Taenia solium)
Published by: The American Society of Tropical Medicine & Hygiene
Summary: Diagnosis involves recognising oedema surrounding old, calcified cysts during symptomatic episodes;
identification and sequencing of specific antigens; and development of new assays.
Treatment guidelines
Europe
Guidelines for diagnosis and treatment of liver alveococcosis caused by Echinococcus
multilocularis
Published by: Poznan University of Medical Sciences (Poland)
Summary: Recommendations for optimal management, which includes radical surgery and concomitant long-term
treatment with albendazole.
29
Guidelines
Tapeworm infection
International
Current consensus guidelines for treatment of neurocysticercosis
Published by: International panel of experts in taeniasis/cysticercosis
Summary: Therapeutic decisions are individualised, including whether to use antiparasitic drugs, based on the number,
location, and viability of the parasites within the nervous system. Growing cysticerci are actively managed either with
antiparasitic drugs or surgical excision. The management of intracranial HTN secondary to neurocysticercosis is
prioritised before other forms of therapy are considered. Seizures are managed in the same way as other causes of
secondary seizures (remote symptomatic seizures). This is because they are due to an organic focus that has been
present for a long time.
Guidelines for treatment of cystic and alveolar echinococcosis in humans
GUIDELINES
Published by: WHO Informal Working Group on Echinococcosis
Summary: Surgery remains the first choice for cystic echinococcosis, as there is potential to totally remove the
parasite and completely cure the patient. However, chemotherapy with benzimidazole compounds (albendazole or
mebendazole) and the recently developed PAIR (puncture, aspiration, injection, reaspiration) procedure with concomitant
chemotherapy offer further treatment options. Chemotherapy is not yet satisfactory, as cure can be expected in only
about 30% of patients and improvement in only 30% to 50% after 12 months of follow-up. Alveolar echinococcosis is
generally severe, with higher than 90% mortality in untreated patients. Radical surgery is recommended in all operable
cases but must be followed by chemotherapy.
North America
Evidence-based guideline: treatment of parenchymal neurocysticercosis
Published by: American Academy of Neurology
Summary: A review of the evidence that informs different management strategies in intraparenchymal
neurocysticercosis in children and adults.
Oceania
Staying Healthy: Preventing infectious diseases in early childhood education and care
services (5th ed)
Published by: National Health and Medical Research Council (Australia)
Summary: Updated recommendations for preventing spread of infectious disease in child care.
30
Tapeworm infection
Online resources
Online resources
1.
Patient UK: Cestodes (tapeworms) (external link)
ONLINE RESOURCES
31
Tapeworm infection
References
REFERENCES
Key articles
Garcia HH, Gilman R, Martinez M, et al. Cysticercosis as a major cause of epilepsy in Peru. Lancet. 1993;341:197-200.
Abstract
Del Brutto OH, Rajshekhar V, White AC Jr, et al. Proposed diagnostic criteria for neurocysticercosis. Neurology.
2001;57:177-183. Full text Abstract
Garca HH, Evans CA, Nash TE, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol
Rev. 2002;15:747-756. Full text Abstract
Garcia HH, Gonzales I, Lescano AG, et al. Efficacy of combined antiparasitic therapy with praziquantel and albendazole
for neurocysticercosis: a double-blind, randomised controlled trial. Lancet Infect Dis. 2014;14:687-695. Abstract
Khuroo MS, Wani NA, Javid G, et al. Percutaneous drainage compared with surgery for hepatic hydatid cysts. N Engl
J Med. 1997;337:881-887. Full text Abstract
Smego RA Jr, Bhatti S, Khaliq AA, et al. Percutaneous aspiration-injection-reaspiration drainage plus albendazole or
mebendazole for hepatic cystic echinococcosis: a meta-analysis. Clin Infect Dis. 2003;37:1073-1083. Abstract
References
1.
Schantz PM, Kern P, Brunetti R. Echinococcus. In: Guerrant RL, Walker DH, Weller PF, eds. Tropical infectious diseases:
principles, pathogens and practice. 1st ed. Oxford, UK: Churchill Livingstone; 2005:1304-1326.
2.
Wittner M, Tanowitz HB, White AC. Taenia and other tapeworms. In: Guerrant RL, Walker DH, Weller PF, eds. Tropical
infectious diseases: principles, pathogens & practice. 1st ed. Oxford, UK: Churchill Livingstone; 2005:1327-1340.
3.
Garcia HH, del Brutto OH. Taenia solium cysticercosis. Inf Dis Clin North Am. 2000;14:97-119. Abstract
4.
Verastegui M, Gilman RH, Garcia HH, et al. Prevalence of antibodies to unique Taenia solium onchosphere antigens
in Taeniasis and human and porcine cysticercosis. Am J Trop Med Hyg. 2003;69:438-444. Full text Abstract
5.
Gonzalez AE, Garcia HH, Gilman RH, et al. Control of Taenia solium. Acta Trop. 2003;87:35-42. Abstract
6.
Zoli A, Shey-Njila O, Assana E, et al. Regional status, epidemiology and impact of Taenia solium cysticercosis in
Western and Central Africa. Acta Trop. 2003;8:35-42. Abstract
7.
O'Neal SE, Flecker RH. Hospitalization frequency and charges for neurocysticercosis, United States, 2003-2012.
Emerg Infect Dis. 2015;21:969-976. Full text Abstract
8.
Khalil HM, el Shimi S, Sarwat MA, et al. Recent study of Hymenolepis nana infection in Egyptian children. J Egypt
Soc Parasitol. 1991;21:293-300. Abstract
9.
Aria HP. Biology of the tapeworm Hymenolepis diminuta. New York, NY: Academic Press; 1980.
32
Tapeworm infection
References
Biswash H, Arora RR, Sehgal S. Epidemiology of Hymenolepis nana infections in a selected rural community. J
Commun Dis. 1978;10:170-174.
11.
Mason PR, Patterson BA. Epidemiology of Hymenolepis nana infections in primary school children in urban and
rural communities in Zimbabwe. J Parasitol. 1994;80:245-250. Abstract
12.
Del Brutto OH, Sotelo J, Roman GC. Neurocysticercosis: a clinical handbook. Lisse, The Netherlands: Swets and
Zeitlinger; 1998.
13.
Bandres JC, White AC Jr, Samo T, et al. Extraparenchymal neurocysticercosis: report of five cases and review of
management. Clin Infect Dis. 1992;15:799-811. Abstract
14.
Garcia HH, Wittner M, Coyle CM, et al. Cysticercosis. In: Guerrant RL, Walker DH, Weller PF, eds. Tropical infectious
diseases: principles, pathogens and practice. 1st ed. Oxford, UK: Churchill Livingstone; 2005:1289-1303.
15.
Di Lernia V, Ricci C, Albertini G. Skin eruption associated with Hymenolepis nana infection. Int J Dermatol.
2004;43:357-359. Abstract
16.
Cuetter AC, Garcia-Bobadilla J, Guerra LG, et al. Neurocysticercosis: focus on intraventricular disease. Clin Infect Dis.
1997;24:157-164. Abstract
17.
Proao-Navarez JV, Meza-Lucas A, Mata-Ruiz O, et al. Laboratory diagnosis of human neurocysticercosis: double-blind
comparison of enzyme-linked immunosorbent assay and electroimmunotransfer blot assay. J Clin Microbiol Rev.
18.
Mejia R, Nutman TB. Evaluation and differential diagnosis of marked, persistent eosinophilia. Semin Hematol.
19.
Groove D. A history of human helminthology. Wallingford, UK: CAB International; 1990.
20.
Garcia HH, Gilman R, Martinez M, et al. Cysticercosis as a major cause of epilepsy in Peru. Lancet. 1993;341:197-200.
Abstract
21.
Del Brutto OH, Rajshekhar V, White AC Jr, et al. Proposed diagnostic criteria for neurocysticercosis. Neurology.
22.
Garcia HH, Del Brutto OH, Nash TE, et al. New concepts in the diagnosis and management of neurocysticercosis
(Taenia solium). Am J Trop Med Hyg. 2005;72:3-9. Full text Abstract
23.
Baird RA, Wiebe S, Zunt JR, et al. Evidence-based guideline: treatment of parenchymal neurocysticercosis: report
of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology.
24.
Otte WM, Singla M, Sander JW, et al. Drug therapy for solitary cysticercus granuloma: a systematic review and
meta-analysis. Neurology. 2013;80:152-162. Full text Abstract
25.
Garca HH, Evans CA, Nash TE, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol
Rev. 2002;15:747-756. Full text Abstract
33
REFERENCES
10.
REFERENCES
Tapeworm infection
References
26.
Garcia HH, Gonzales I, Lescano AG, et al. Enhanced steroid dosing reduces seizures during antiparasitic treatment
for cysticercosis and early after. Epilepsia. 2014;55:1452-1459. Full text Abstract
27.
Garcia HH, Gonzales I, Lescano AG, et al. Efficacy of combined antiparasitic therapy with praziquantel and albendazole
for neurocysticercosis: a double-blind, randomised controlled trial. Lancet Infect Dis. 2014;14:687-695. Abstract
28.
Proao JV, Madrazo I, Avelar F, et al. Medical treatment for neurocysticercosis characterized by giant subarachnoid
cysts. N Engl J Med. 2001;345:879-885. Full text Abstract
29.
Mitre E, Talaat KR, Sperling MR, et al. Methotrexate as a corticosteroid-sparing agent in complicated
neurocysticercosis. Clin Infect Dis. 2007;44:549-553. Abstract
30.
Koul PA, Singh AA, Ahanger AG, et al. Optimal duration of preoperative anti-helminthic therapy for pulmonary
hydatid surgery. ANZ J Surg. 2010;80:354-357. Abstract
31.
Khuroo MS, Wani NA, Javid G, et al. Percutaneous drainage compared with surgery for hepatic hydatid cysts. N Engl
J Med. 1997;337:881-887. Full text Abstract
32.
Smego RA Jr, Bhatti S, Khaliq AA, et al. Percutaneous aspiration-injection-reaspiration drainage plus albendazole or
mebendazole for hepatic cystic echinococcosis: a meta-analysis. Clin Infect Dis. 2003;37:1073-1083. Abstract
33.
The Medical Letter. Drugs for parasitic infections. New Rochelle, NY: The Medical Letter; 2007.
34
Tapeworm infection
Images
Images
IMAGES
Figure 1: Adult tapeworm identified as Taenia saginata

From the personal collections of Dr Christina Coyle and Dr Maheen Saeed
Figure 2: Cystic stage - neurocysticercosis: MRI scan showing cystic lesion in the frontal lobe; a scolex can be seen within
the cyst
35
IMAGES
Tapeworm infection
Images
Figure 3: Colloidal stage - neurocysticercosis: CT scan showing ring enhancing cystic lesion in the temporal lobe and
perilesional oedema
Figure 4: Granular stage - neurocysticercosis: MRI scan showing enhancing lesion without perilesional oedema
36
Tapeworm infection
Images
Figure 6: Echinococcus of liver with daughter cyst on ultrasound: multivesicular, multiseptated cysts, where daughter
cyst completely fills the unilocular mother cyst; cyst produces a wheel-like structure
37
IMAGES
Figure 5: Calcified stage - neurocysticercosis: MRI scan of multiple calcified lesions in a patient with neurocysticercosis
Images
IMAGES
Tapeworm infection
Figure 7: Echinococcus of liver with daughter cyst on CT scan: CT scan showing multiple daughter cysts, some solidified
and some partially calcified
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Tapeworm infection
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Disclaimer
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Group Ltd ("BMJ Group") tries to ensure that the information provided is accurate and up-to-date, but we do not warrant
that it is nor do our licensors who supply certain content linked to or otherwise accessible from our content. The BMJ
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39
Contributors:
// Authors:
Jose A. Serpa, MD, MS, CTropMed
Assistant Professor of Medicine
Program Director, Infectious Diseases Fellowship, Baylor College of Medicine, Houston, TX
DISCLOSURES: JAS declares that he has no competing interests.
Andrew Chou, MD
Chief Fellow
Infectious Diseases , Baylor College of Medicine , Houston , TX
DISCLOSURES: AC declares that he has no competing interests.
// Acknowledgements:
Dr Jose A. Serpa and Dr Andrew Chou would like to gratefully acknowledge Dr Christina Coyle and Dr Maheen Saeed, previous
contributors to this monograph.
DISCLOSURES: CC is an author of several references cited in this monograph. MS declares that she has no competing interests.
// Peer Reviewers:
William A. Petri, Jr, MD, PhD, FACP
Chief and Professor of Medicine
Division of Infectious Diseases and International Health, University of Virginia Health System, Charlottesville, VA
DISCLOSURES: WAP declares that he has no competing interests.
Linda Kalilani, MBBS, MPhil, PhD
Epidemiologist
College of Medicine, University of Malawi , Zomba, Malawi
DISCLOSURES: LK declares that she has no competing interests.
Paul Roberts, MD
Assistant Professor
Family Medicine, Mayo Clinic, Jacksonville, FL
DISCLOSURES: PR declares that he has no competing interests.

Tapeworm Infection

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Tapeworm infection

The right clinical information, right where it's needed

Last updated: Sep 07, 2015

Step-by-step diagnostic approach

History & examination factors

Step-by-step treatment approach

Treatment details overview

Humans can be definitive or intermediate hosts.

Intestinal infection is treated with antihelminthics only.

Extra-intestinal infection may require surgical intervention.

Cysticercosis and neurocysticercosis

Step-by-step diagnostic approach

Complete blood count

eating or handling undercooked meat

eating or handling undercooked fish or crustaceans

ingestion of contaminated water

History & examination factors

worm segments in stool (common)

increased intracranial pressure (common)

May indicate cysts in the lungs.

allergy manifestations (uncommon)

Other diagnostic factors

vague intestinal symptoms (common)

sleep disturbance (common)

eggs and (gravid/non-gravid)

Echinococcus ELISA and western blot serology

Taenia solium with purified

Echinococcus species with

Abdominal ultrasound may detect hydatid cysts (e.g., echinococcosis of the

Neuroimaging is the mainstay of diagnosis for neurocysticercosis (NCC), and

Patients are normally febrile.

Western blot negative.

Patients are usually febrile with

Western blot negative. Amoebic

Patients usually have unilateral

Stool examination and western

Patients usually experience

Western blot negative.

Patients may be febrile with

Western blot negative.

Patients have focal neurological

Western blot negative.

Patients may be jaundiced with

Western blot negative. Imaging

Patients may have positive

Western blot negative. Usually has

Patients may have erythema

Western blot negative.

Patients usually demonstrate

Western blot negative.

Central nervous system

Cystic lesions showing the scolex on CT or MRI

Individuals coming from or living in an area where cysticercosis is endemic.

Step-by-step treatment approach

Hepatic or thoracic manifestations

Treatment details overview

inactive parenchymal disease

active parenchymal disease

ventricular disease with raised

ventriculoperitoneal shunt + endoscopic removal

spinal cord and/or optical disease

hepatic or thoracic disease

endoscopic removal of cysticerci

dexamethasone: 6 mg orally once daily