Tapeworm Infection

Tapeworm infection

The r ight c l in ica l informat ion, r ight where it ' s needed

Last updated: Sep 07, 2015

Table of ContentsSummary 3

Basics 4

Definition 4

Epidemiology 4

Aetiology 5

Pathophysiology 5

Classification 7

Prevention 8

Primary prevention 8

Diagnosis 9

Case history 9

Step-by-step diagnostic approach 9

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

Tapeworms belong to the Platyhelminthes phylum. Subclasses include the orders Pseudophyllidea andCyclophyllidea.

◊

Humans can be definitive or intermediate hosts.◊

Extra-intestinal manifestations include cystercercosis (can affect any organ), hydatidosis (can affect any organbut 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-intestinalmanifestations.

◊

Intestinal infection is treated with antihelminthics only.◊

Extra-intestinal infection may require surgical intervention.◊

Summary

Definition

Tapeworms refer toparasitesof the taxonomic classCestoda, and include theordersPseudophyllidea andCyclophyllidea.

They divide their life cycles between two animal hosts. The worms can vary in length from a fewmillimetres to 25m, and

can contain thousands of proglottids (tapeworm segments).[1] [2] [Fig-1] Adult tapeworms usually possess an anterior

scolex (head; plural 'scolices') thatmay bemodifiedwith structures or organelles that attach to thehost. Therapy is aimed

at the destruction of the scolices, and failure to achieve this will result in regrowth of the tapeworm. Whenmature, these

parasites reside in the intestinal tract of definitive carnivoroushosts, and larval cysts are formed in the intermediatehosts.

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 Emultilocularis are referred to as alveolar

echinococcosis.

Epidemiology

Taenia saginata and T solium are prevalent throughout theworld. 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-SaharanAfrica, India, andelsewhere inAsia).[3] [4] [5] [6] In theUSbetween2003and2012,neurocysticercosis

from T solium led to an estimated 18,584 hospitalisations and cost in excess of US $908million.[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 10million 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.

Thegreatest prevalenceof cystic echinococcosis inhumans is found incountriesof 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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BasicsTapeworm infectionBASICS

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Aetiology

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

soliumeggsor gravid proglottids fromT solium carriers.T solium carriersmaycontaminatewater supplies or contaminate

food directly, as sticky eggs under their fingernails can be transferred during food preparation, causing cysticercosis

and/or neurocysticercosis in consumers.

Human infectionwith the dog tapeworm, Echinococccus granulosus, occurs through contactwith 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 Emultilocularis from foxes, canids, and occasionally cats also occurs through faecal-oral contact.

Eggs are released in faeces and accidentally ingested by humans.

Human infection withDiphyllobothrium 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 12m 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 intermediatehosts). Following ingestionof thewaterfleas by larger crustaceans and fish (second intermediatehosts),

thesemotile embryos develop into larvae (known as sparganumor 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

Thepresenceof theadult tapeworm in the intestinecan lead tomalabsorptionandmalnutrition in thehost. Thepresence

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, andadult tapewormsdevelop inside thehuman intestinal tract.

• Both adult and larval formsmay 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.

• Hnanaoncospheres penetrate thebowelmucosa anddevelop into cysticercoid larvae. Larvaeemerge in thebowel

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]

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BASIC

SBasicsTapeworm infection


Cysticercosis and neurocysticercosis

• 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 andmigrate 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 canbeparenchymal or extraparenchymal. Parenchymal diseaseused tobe 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 associatedwith 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.



BasicsTapeworm infectionBASICS


• Larvapenetrate the intestinalmucosa thenenter thebloodand/or lymphatic systemandmigrate to visceral organs,

where themetacestode (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]

• Hydatid cysts develop and enlarge into space-occupying lesions (metacestode stage) overmonths 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 Emultilocularis), 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



BASIC

SBasicsTapeworm infection


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.

Preventing infection in pigs can be accomplished by changing pig-raising practices in endemic areas. Prohibition of

home-slaughter of sheepwill prevent dogs fromconsuming infected viscera, thus disrupting the life cycle of theparasite.



PreventionTapeworm infectionPREVENTION


Case history

Case history #1

A30-year-oldAlbanianman,who recentlymigrated to theUK,presents toanoutpatientcliniccomplainingof something

resembling large grapefruit seeds in his stool. He has no pastmedical history of note andno abdominal pain, bloating,

diarrhoea, or constipation.

Case history #2

A35-year-oldHispanicman is brought in to the emergency department after having awitnessed 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 diseasemay 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'.

Patientswithextraintestinal diseasemaypresent toprimarycareprovidersor emergencydepartmentswith symptoms,

including headaches, seizures, abdominal pain, cough, and haemoptysis.

Step-by-step diagnostic approach

Historical factorsPatients with intestinal infection (e.g., with Hymenolepis nana, Diphyllobothrium latum, Taenia saginata) can be

asymptomatic.[8]However, theymaypresentwithvague intestinal symptoms includingabdominal pain, hungerpain,

sore tongue, sore gums, loss of appetite, increased appetite, weight loss, bloating, constipation, diarrhoea, a feeling

of 'something moving inside', and/or nausea.[2]

Patients who are definitive hosts for Taenia soliummay 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 nanamay present with an itchy rash.[15]

Themajorityofpatientswithcysticechinococcosis (hydatiditis) areasymptomatic, andhydatidcysts areoftenobserved

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 rightupperquadrantor epigastric pain, nausea, or vomiting. Communicationand ruptureofhepatic

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 andmimic 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

DiagnosisTapeworm infection


anaphylaxis or secondary cystic echinococcosis. Mild to severe anaphylactoid reactions (and occasionally death)may

follow the suddenmassive release of cyst fluid. Intact hydatid cysts in the lungsmay cause no symptoms, while chest

pain, cough, or haemoptysis canoccurwhen there is leakageor ruptureof thecyst. Ruptureor leakageof 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 themost common presenting symptoms in patients with neurocysticercosis (NCC). The

disease is pleomorphic andmay 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 subarachnoiddisease, andcanbe life threatening. Suddendeath canoccur. Subarachnoiddisease

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 examinationPhysical examination is generally unremarkable in hosts harbouring adult intestinal tapeworm. However, patients

with H nanamay 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.

Examination of patients with neurocysticercosis may reveal neurological defects corresponding to central nervous

systemcysts. Extraparenchymalneurocysticercosismaypresentwith increased intracranial pressureandhydrocephalus

and tends to be more severe in its presentation.[16]

Stool examinationStool 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 serologySerodiagnosis is helpful inmany 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-purifiedmembrane antigens. Binding to anyoneof sevenbands is consideredpositive. 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.



DiagnosisTapeworm infectionDIAGNOSIS


Complete blood countEosinophilia is not always encountered in tapeworm infections. Helminthic parasitic infections cause eosinophilia

duringmigration 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.

ImagingTheWHOclassifies the stagesofEchinococcusgranulosus into active versus inactive, andclassificationguides therapy.

CE1 is a unilocular anechoic cystic lesion with a double sign. CE2 is a multiseptated, 'rosette-like honeycomb' cyst

(this is amother cyst filledwithdaughter cysts). BothCE1andCE2are consideredactive, usually fertile cysts containing

viable protoscolices. CE3a is a cyst with detachedmembranes (water-lily-sign), while CE3b has daughter cysts in a

solidmatrix. These are considered cysts in the transitional stagewhere the integrity of the cyst has beencompromised

eitherby thehostorbychemotherapy. Acystwithheterogenoushypoechoic/hyperechoic contents andnodaughter

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 20mm 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

Strong

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 undercookedmeat

• 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 latummay occur whenever undercooked fish or crustaceans are ingested.



DIAGNOSIS



ingestion of contaminated water

• Infection with Diphyllobothrium latummay 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 granulosusmay occur from contact with contaminated dog faeces.

children

• Infectedchildren, especially thosewithpruritus ani andpoorhandhygiene, 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 Emultilocularis 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 Echinococccusmultilocularis or

Emultilocularis infections.

• Accidental ingestion of infected insects can result in Hymenolepis nana infection.

History & examination factors

Key diagnostic factors

presence of risk factors (common)

• Key risk factors include living on farms, contact with dogs and/or pigs, ingestion of contaminated water and/or

undercookedmeats 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.

• Spontaneousegressof proglottids per rectum ismost frequently reported inTaenia saginataorT solium infestation.

increased intracranial pressure (common)

• Patients with CNSmanifestations who present with intraventricular or subarachnoid disease (e.g., hydrocephalus)

may have increased intracranial pressures.

seizures (common)

• Patients with CNSmanifestations may present with seizures.

• All patients fromendemic areaswhopresentwithnew-onset seizures require evaluation for neurocysticercosis.[20]

hepatomegaly (common)

• Signs of cysts in the liver may include hepatomegaly.

cough (common)





• May indicate cysts in the lungs.

haemoptysis (common)

• May indicate cysts in the lungs.

allergymanifestations (uncommon)

• Rupture or leakage of tapeworm cysts into the peritoneum usually results in acute or intermittent allergy

manifestations (urticaria or anaphylaxis).

• Minimal inflammatory reactionmayoccurwithTaenia saginata, suggesting that these tapewormshave 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.

• About40%ofpeopleharbouring thewormhave reducedserumvitaminB12,but fewer than2%developanaemia.[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 infectedwithHymenolepisnana infectionareoftenchildrenwith loosebowelmovements.Hnana infection

can also present with diffuse persistent abdominal pain.

sleep disturbance (common)

• ManychildrenwithHymenolepisnanahavesleepandbehavioural disturbances thatclearafter tapewormeradication.

headaches (common)

• CNSmanifestations 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)

• ManypatientswithHymenolepisnanahave itchy skineruptions.[15]Patientswitha rupturedor leakingechinococcal

cyst may have urticarial eruptions.

pyrexia (uncommon)

• Signsof cysts in the livermay includeevidenceof sepsis if biliary treecommunications arepresentwith subsequent

superinfection.



DIAGNOSIS



Diagnostic tests

1st test to order

ResultTest

eggs and (gravid/non-gravid)proglottids in stool

stool examination

• Egg release in the stoolmay be variable because of irregular rates of proglottiddetachment and degeneration.

• Examination of the stool samples over several days increases the yield.• Species identification is important, and is usually based onmorphology 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 nanamay be diagnosed by finding

characteristic ova in the faeces.

moderate eosinophilia,megaloblastic perniciousanaemia

FBC

• Many patients with Hymenolepis nana have moderate eosinophilia of 5% to10%.

• Diphyllobothrium latum infectionsmaypresentwithmegaloblastic perniciousanaemia 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.

Taenia soliumwith purifiedglycoproteinantigens (westernblot)

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]

Echinococcus species withpurified glycoprotein antigens(western blot)

Echinococcus ELISA and western blot serology

• Western blot is the confirmatory test for Echinococcus. Serology is 80% to100% sensitive and 88% to 96% specific for liver cyst infections.

• It is less sensitive for lung involvement (50%-56%) and 25% to 26% for otherorgan involvement.[1]

• In the US, ELISA is available through the Centers for Disease Control andPrevention (CDC).

hydatid cystsultrasound

• Abdominal ultrasoundmay detect hydatid cysts (e.g., echinococcosis of theliver). [Fig-6]

brain calcificationCT head

• Neuroimaging is the mainstay of diagnosis for neurocysticercosis (NCC), andstudies highly suggestive of NCC are considered a major diagnostic criteria.The combination of a single, round, enhancing lesion, less than 20mm indiameter, with nomidline shift, in patients without increased intracranialpressure, focal neurological deficits, or evidence of systemic disease is highlysuggestive of NCC. Resolution of the lesion spontaneously or afteranti-cysticercal therapy or precipitation of symptoms by antiparasitic drugs isalso supportive of the diagnosis. All of these are major diagnostic criteria. MRIis more effective for imaging extraparenchymal cysticerci. Calcifications arecommon.[Fig-3] [Fig-7]

extraparenchymal cysticercitapeworm scolex

MRI

• MRI is more effective for imaging extraparenchymal cysticerci.• MRImay also reveal the scolex, which is usually not visible on CT scans. [Fig-2]

[Fig-4] [Fig-5]





Differential diagnosis

Differentiating testsDifferentiating signs /symptoms

Condition

• Western blot negative.• CT head and MRI brain may show

ring-enhancing lesions.

• Patients are normally febrile.• There may also be signs of

tuberculosis elsewhere (e.g.,chronic cough, haemoptysis,bone pain).

Central nervous systemtuberculoma

• Western blot negative. Amoebicserology might be positive.

• Patients are usually febrile withelevated erythrocytesedimentation rates.

Amoebic abscess

• Stool examination and westernblot negative.

• Patients usually have unilateralmotor or sensory signs andheadache.

Migraine

• Western blot negative.• Patients usually experiencepremonitory sensations (fear,epigastric sensation, déjà vu,jamais vu).

Epilepsy

• Western blot negative.• Patients may be febrile withassociated vomiting.

Gastroenteritis

• Western blot negative.• Patients have focal neurologicaldeficits according to location.

Brain tumour

• Western blot negative. Imagingusually not cystic in appearancewith daughter cysts.

• Patients may be jaundiced withascites. History of cancer.

Liver metastases

• Westernblotnegative.Usuallyhaselevated WBC and fever, andultrasound reveals stones andpericholic fluid.

• Patients may have positiveMurphy's signswith right shoulderpain.

Cholecystitis

• Western blot negative.• Patients may have erythemanodosum, chronic fatigue, and/orarthralgia.

Sarcoidosis

• Western blot negative.• Patients usually demonstrateevidence of alcohol withdrawalincluding hallucinations andtremor.

Alcohol abuse

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



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

• 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.





Step-by-step treatment approach

Treatment varies depending upon whether infection is intestinal or extraintestinal.

Intestinal infectionWhen stool examination reveals evidence of tapeworm infection (e.g., Hymenolepis nana, Diphyllobothrium latum,

Taenia saginata, andTsolium), the treatmentof choice is thebroad-spectrumantihelminthicpraziquantel. Praziquantel

has excellent activity against all tapeworms. It is given as a single dose for both children and adults. Infections withH

nana require higher doses.

Other antihelminthic preparations, such as niclosamide, also exist.

CNSmanifestationsCNSmanifestations 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]

Theoptimal dose, duration, and formulationof adjunctive corticosteroid to administerwith antiparasitic therapyhave

not been established. An open-label randomised trial compared conventional dexamethasone dosingwith enhanced

dexamethasone dosing in patients with viable parenchymal neurocysticercosis with recent (within 6months) seizure

activity.[26]Although the studydidnotmeet its primary endpoint of reducing seizuredaysor individualswith 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.Adverseeffectswerenotdifferentbetween the twogroups. Thesedata suggest thatpatientswith 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 burdenmay benefit from combination antiparasitic therapy. One double-blind,

placebo-controlled trial has shown that patients with viable intraparenchymal neurocysticercosis have increased

parasiticidal effect,without increasedsideeffects,withcombination therapyof albendazolepluspraziquantel compared

with albendazole alone. Thebenefitwas largely drivenby the sub-groupof patientswith threeormore viable cysts.[27]

Patients with active ventricular diseasemay 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.

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-sparingpurposes.[28] [29]Therehavebeennocontrolled trialsof subarachnoiddiseasemanagement;



TREATM

ENT

TreatmentTapeworm 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 manifestationsHepatic or thoracic manifestations include echinococcosis (disease with Echinococccus species) and cysticercosis

(infectionwithT solium). Surgical removal is themainstay of treatment of hepatic echinococcal disease.Wide surgical

resection for operable cases (e.g., hepatic lobectomy or liver transplantation) ensures total removal of cysts.

Antihelminthicsareadministeredconcurrently at least2weeksprior to thesurgeryandat least1monthpostoperatively.

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 successwith thePAIR (puncture, aspiration, injection, and reaspiration)procedure

in appropriatepatients. PAIR is performedwithconcurrent albendazole therapy to reduce the riskof 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, druginteractions, and alternative dosing. ( see Disclaimer )

( summary )Acute

TreatmentTx linePatient group

antihelminthic1stintestinal disease

CNS disease

corticosteroid1stinactive parenchymal disease

antihelminthic1stactive parenchymal disease

corticosteroidplus

anti-epilepticadjunct

ventriculoperitoneal shunt + endoscopic removal1stventricular disease with raisedintracranial pressure

antihelminthicplus

corticosteroidplus




TreatmentTapeworm infectionTR

EAT

MENT


( summary )Acute

endoscopic removal of cysticerci1stventricular disease with normalintracranial pressure

antihelminthicplus

corticosteroidplus


ventriculoperitoneal shunt1stsubarachnoid disease

antihelminthicplus

corticosteroidplus


surgery1stspinal cordand/oroptical disease

antihelminthicplus

corticosteroidplus


surgery1sthepatic or thoracic disease

antihelminthicplus

corticosteroidplus

( summary )Ongoing


antihelminthic1stchronic subarachnoid disease

corticosteroidplus

methotrexateadjunct



TREATM

ENT



Treatment options

Acute


antihelminthic1stintestinal disease

» Praziquantel is taken as a single dose. Safety ofpraziquantel in children under 4 years is unknown andis therefore not recommended.[33] Infection withHymenolepis nana requires higher doses ofpraziquantel.

» Niclosamidemay also be used in adults and childrenof all ages.

Primary options

» praziquantel: children ≥4 years of age and adults:5-10mg/kg orally as a single dose; higher doses of25mg/kgasasingledose required inHymenolepisnana infection

OR

» niclosamide: dose depends on type of tapeworminfection; consult specialist for guidance on dose

CNS disease

corticosteroid1stinactive parenchymal disease

» Inactive parenchymal disease is when the tapewormis calcified (visible as calcifications on imaging).

» Corticosteroid therapy can help to control oedemaif patients are symptomatic.

»PatientswithcalcifiedgranulomasonCTscanshouldnot be treated with antihelminthics. If perilesionaloedema is present, they should not receiveantihelminthics.

Primary options

» prednisolone: 40-60 mg orally once daily

OR

» dexamethasone: 6 mg orally once daily

antihelminthic1stactive parenchymal disease

»Onedouble-blind, placebo-controlled trial has shownthat patients with viable intraparenchymalneurocysticercosis have increased parasiticidal effect,without increased side effects, with combinationtherapy of albendazole plus praziquantel compared




EAT

MENT


Acute

TreatmentTx linePatient groupwith albendazole alone. The benefit was largely drivenby the sub-group of patients with three ormore viablecysts.[27]

» Patients with viable cysts in the parenchyma shouldbe treated for at least 10 days with concomitantcorticosteroids.[23] [24]

Primary options

» albendazole: children: 15mg/kg orally once dailygiven in2divideddoses; adults: 400mgorally twicedaily-and-» praziquantel: children ≥4 years of age and adults:50 mg/kg/day given in 3 divided doses

corticosteroidplus

» Active parenchymal disease is when the tapewormis alive (scolex may be visible on MRI).

»Concurrent corticosteroid therapycanhelp tocontroloedema.

»Patientswith recent (within6months) seizure activitymaybenefit fromanenhanceddexamethasonedosingregimen compared to the standard dose regimen.[26]

Primary options


OR

» dexamethasone: standard dose: 6 mg/day orallyfor 10 days; enhanced dose: 8mg/day orally (3mgorally in the morning and afternoon and 2mg inthe evening) on days 1-28, followed by a 2-weektaper (decrease dose every 2 days to 6 mg/day, 4mg/day, 3 mg/day, 2 mg/day, and 1mg/day, then0.5 mg/day for 4 days, then stop)


»Adjunctive anti-epileptic therapymayhelp to controlseizures. Medication and dose are case specific.

ventriculoperitoneal shunt + endoscopic removal1stventricular disease with raisedintracranial pressure » Neurocysticercosis patients often have evidence of

hydrocephalus or raised intracranial pressure andrequire ventriculoperitoneal shunting.

» Endoscopic removal has emerged as the treatmentof choice in intraventricular cysts due toneurocysticercosis.



TREATM

ENT



Acute


antihelminthicplus

» Albendazole treatment is continued for between 8and 30 days and can be repeated as necessary.

» Praziquantel is given as a higher dose on day 1 andlower doses for 29 consequent days.

Primary options

» albendazole: children: 15mg/kg orally once dailygiven in2divideddoses; adults: 400mgorally twicedaily

OR

» praziquantel: children ≥4 years of age andadults:100mg/kg/day orally given in 3 divideddoses for 1 day, followed by 50mg/kg/day givenin 3 divided doses for 29 days

corticosteroidplus


Primary options


OR




endoscopic removal of cysticerci1stventricular disease with normalintracranial pressure » Once intracranial pressure is stabilised, endoscopic

removal of cysticerci in the lateral, third, and fourthventricles is performed. Patients with MRI findings ofsignificant ependymal enhancement (secondary toadherence of lesions to the ependyma) may not besuitable for this surgery.[16]

antihelminthicplus

» Albendazole treatment is continued for between 8and 30 days and can be repeated as necessary.


Primary options




EAT

MENT


Acute

TreatmentTx linePatient group» albendazole: children: 15mg/kg orally once dailygiven in2divideddoses; adults: 400mgorally twicedaily

OR


corticosteroidplus


Primary options


OR




ventriculoperitoneal shunt1stsubarachnoid disease

» Patients with evidence of hydrocephalus or raisedintracranial pressure require ventriculoperitonealshunting.

antihelminthicplus

» Prolonged treatment with albendazole is required inthe racemose form in the subarachnoid space. Theendpoint for treatment is not clear, but it is suggestedthat the MRI be followed, along with the CSF(pleocytosis and glucose), to help establish when todiscontinue treatment. Patients also requireprolongedcorticosteroids toavoidcomplicationsdue to thehost'sinflammatory response such as hydrocephalus andstroke.


Primary options


OR



TREATM

ENT



Acute

TreatmentTx linePatient group» praziquantel: children ≥4 years of age andadults:100mg/kg/day orally given in 3 divideddoses for 1 day, followed by 50mg/kg/day givenin 3 divided doses for 29 days

corticosteroidplus

»Concurrent corticosteroid therapycanhelp tocontrolthe host's inflammatory response.

Primary options


OR




surgery1stspinal cordand/oroptical disease

» Themainstay of treatment is case-specific surgeryfor disease involving the eye. Many spinal cases are inthe subarachnoid spine and can be treated withprolonged albendazole. Surgery is indicated if thereare symptoms that require decompression.

antihelminthicplus

» Albendazole treatment is continued for prolongedperiods of time.


Primary options


OR


corticosteroidplus

» Concurrent corticosteroid therapy can help swellingin the spinal cord and control resulting arachnoiditis.




EAT

MENT


Acute


Primary options


OR




surgery1sthepatic or thoracic disease

» Surgery is usually mainstay of treatment forechinococcosis patients with CE2 (mother cysts filledwith daughter cysts) or CE3b cysts (cysts that havepartial solidification with daughter cysts). CE1 cysts(cystswithnodaughter cysts)maybegoodcandidatesfor PAIR (puncture, aspiration, injection, andre-aspiration) procedure. Inactive cysts (those with nodaughter cysts on ultrasound [CE4] and calcified cysts[CE5]) should be watched and followed by ultrasound.

antihelminthicplus

»Albendazole is administered concurrently for at least2 weeks pre-operatively and 1 to 3monthspostoperatively.

» In pulmonary hydatid disease, prolongingcombination therapy of albendazole and praziquantelfrom2weeks to 4 or 8 weeks prior to surgery led to anincreased scolicidal response. Prolongingpre-treatment antihelminthics may be considered ifthepatient is at high risk for intraoperative rupture.[30]

Primary options


OR

» albendazole: children: 15mg/kg orally once dailygiven in2divideddoses; adults: 400mgorally twicedaily-and-» praziquantel: children ≥4 years of age and adults:50 mg/kg/day given in 3 divided doses

corticosteroidplus



TREATM

ENT



Acute

TreatmentTx linePatient group»Concurrent corticosteroid therapycanhelp tocontroloedema.

Primary options


OR


Ongoing


antihelminthic1stchronic subarachnoid disease

» Prolonged treatment with albendazole is required inthe racemose form in the subarachnoid space. Theendpoint for treatment is not clear, but it is suggestedthat the MRI be followed, along with the CSF(pleocytosis and glucose), to help establish when todiscontinue treatment. Patients also requireprolongedcorticosteroids toavoidcomplicationsdue to thehost'sinflammatory response such as hydrocephalus andstroke.

» Albendazole treatment is continued for prolongedperiods of time.

Primary options


corticosteroidplus

»Concurrent corticosteroid therapycanhelp tocontrolthehost inflammatory response toavoidcomplicationssuch as hydrocephalus and strokes. These should betapered over time.

Primary options


OR


methotrexateadjunct




EAT

MENT


Ongoing

TreatmentTx linePatient group»Methotrexatemaybeusedasacorticosteroid-sparingagent during ongoing treatment withcorticosteroids.[29]

Primary options

» methotrexate: consult specialist for guidance ondose



TREATM

ENT



Recommendations

Monitoring

Stools are to be re-examined at 1 to 3months after antihelminthic treatment. In some cases treatment can be givenagain 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

LikelihoodTimeframeComplications

mediumvariablesepsis

Hepatic lesions can be complicated by biliary tree communications andmay result in sepsis.[1] The cysts cancommunicate with the biliary tree and become superinfected with bacteria. If left untreated the patients can becomeseptic with bowel organisms.

lowvariablepernicious anaemia

Pernicious anaemia can occur in a small number of patientswithDiphyllobothrium latum due to absorption of vitaminB12 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.



Follow upTapeworm infectionFO

LLOWUP

http://patient.info/doctor/cestodes-tapeworms


Diagnostic guidelines

Europe

Guidelines for diagnosis and treatment of liver alveococcosis caused by Echinococcusmultilocularis

Last published: 2007Published by: Poznan University of Medical Sciences (Poland)

Summary: Recommendations fordiagnosisusing imaging, ELISAandWesternblot, andhistopathologyandmoleculartechniques.

International

Proposed diagnostic criteria for neurocysticercosis

Last published: 2001Published by: Neurology

Summary: Diagnostic criteria for neurocysticercosis based on objective clinical, imaging, immunological, andepidemiological data.

North America

New concepts in the diagnosis andmanagement of neurocysticercosis (Taenia solium)

Last published: 2005Published 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 Echinococcusmultilocularis

Last published: 2007Published by: Poznan University of Medical Sciences (Poland)

Summary: Recommendations for optimal management, which includes radical surgery and concomitant long-termtreatment with albendazole.



GUIDELIN

ES

GuidelinesTapeworm infection

http://www.ncbi.nlm.nih.gov/pubmed/18075150


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2912527/

http://www.ajtmh.org/content/72/1/3.full




International

Current consensus guidelines for treatment of neurocysticercosis

Last published: 2002Published by: International panel of experts in taeniasis/cysticercosis

Summary: Therapeuticdecisionsare individualised, includingwhether touseantiparasitic drugs, basedon thenumber,location, and viability of the parasites within the nervous system. Growing cysticerci are actively managed either withantiparasitic drugs or surgical excision. The management of intracranial HTN secondary to neurocysticercosis isprioritised before other forms of therapy are considered. Seizures are managed in the same way as other causes ofsecondary seizures (remote symptomatic seizures). This is because they are due to an organic focus that has beenpresent for a long time.

Guidelines for treatment of cystic and alveolar echinococcosis in humans

Last published: 1996Published by:WHO Informal Working Group on Echinococcosis

Summary: Surgery remains the first choice for cystic echinococcosis, as there is potential to totally remove theparasite and completely cure the patient. However, chemotherapy with benzimidazole compounds (albendazole ormebendazole) and the recentlydevelopedPAIR (puncture, aspiration, injection, reaspiration)procedurewithconcomitantchemotherapy offer further treatment options. Chemotherapy is not yet satisfactory, as cure can be expected in onlyabout 30% of patients and improvement in only 30% to 50% after 12months of follow-up. Alveolar echinococcosis isgenerally severe, with higher than90%mortality in untreated patients. Radical surgery is recommended in all operablecases but must be followed by chemotherapy.

North America

Evidence-based guideline: treatment of parenchymal neurocysticercosis

Last published: 2013Published by: American Academy of Neurology

Summary: A review of the evidence that informs different management strategies in intraparenchymalneurocysticercosis in children and adults.

Oceania

Staying Healthy: Preventing infectious diseases in early childhood education and careservices (5th ed)

Last published: 2013Published by: National Health and Medical Research Council (Australia)

Summary: Updated recommendations for preventing spread of infectious disease in child care.



GuidelinesTapeworm infectionGUIDELINES

http://cmr.asm.org/content/15/4/747.full

http://www.who.int/zoonoses/resources/echinococcosis/en/

https://www.aan.com/Guidelines/Home/ByTopic?topicId=23

http://www.nhmrc.gov.au/guidelines/publications/subject/Child%20health

http://www.nhmrc.gov.au/guidelines/publications/subject/Child%20health


Online resources

1. Patient UK: Cestodes (tapeworms) (external link)



ONLIN

ERESO

URCES

Online resourcesTapeworm infection

http://patient.info/doctor/cestodes-tapeworms


Key articles

• GarciaHH,GilmanR,MartinezM, et al. Cysticercosis as amajor causeof epilepsy inPeru. 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

• GarcíaHH, EvansCA,NashTE, et al. Current consensusguidelines for treatmentof neurocysticercosis. ClinMicrobiol

Rev. 2002;15:747-756. Full text Abstract

• GarciaHH,Gonzales I, LescanoAG, et al. Efficacyof combinedantiparasitic therapywithpraziquantel andalbendazole

for neurocysticercosis: a double-blind, randomised controlled trial. Lancet Infect Dis. 2014;14:687-695. Abstract

• KhurooMS, 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. SchantzPM,KernP, Brunetti R. Echinococcus. In: Guerrant RL,WalkerDH,Weller PF, eds. Tropical infectiousdiseases:

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.



ReferencesTapeworm infectionREFE

RENCES

http://www.ncbi.nlm.nih.gov/pubmed/8093496?tool=bestpractice.bmj.com




http://cmr.asm.org/content/15/4/747.long



http://www.nejm.org/doi/full/10.1056/NEJM199709253371303#t=article








http://wwwnc.cdc.gov/eid/article/21/6/14-1324_article




10. 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. Proaño-Navarez JV,Meza-LucasA,Mata-RuizO, et al. Laboratorydiagnosisofhumanneurocysticercosis: 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. GarciaHH,GilmanR,MartinezM, et al. Cysticercosis as amajor causeof epilepsy inPeru. 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. GarcíaHH, EvansCA,NashTE, et al. Current consensusguidelines for treatmentof neurocysticercosis. ClinMicrobiol

Rev. 2002;15:747-756. Full text Abstract



REFE

RENCES

ReferencesTapeworm infection





http://jcm.asm.org/content/40/6/2115.long










http://www.neurology.org/content/80/15/1424.long




http://cmr.asm.org/content/15/4/747.long



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. GarciaHH,Gonzales I, LescanoAG, et al. Efficacyof combinedantiparasitic therapywithpraziquantel andalbendazole

for neurocysticercosis: a double-blind, randomised controlled trial. Lancet Infect Dis. 2014;14:687-695. Abstract

28. Proaňo 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. KhurooMS, 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.



ReferencesTapeworm infectionREFE

RENCES




http://www.nejm.org/doi/full/10.1056/NEJMoa010212#t=article




http://www.nejm.org/doi/full/10.1056/NEJM199709253371303#t=article




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 withinthe cyst




IMAGES

ImagesTapeworm infection


Figure 3: Colloidal stage - neurocysticercosis: CT scan showing ring enhancing cystic lesion in the temporal lobe andperilesional oedema


Figure 4: Granular stage - neurocysticercosis: MRI scan showing enhancing lesion without perilesional oedema




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Figure 5: Calcified stage - neurocysticercosis: MRI scan of multiple calcified lesions in a patient with neurocysticercosis


Figure 6: Echinococcus of liver with daughter cyst on ultrasound: multivesicular, multiseptated cysts, where daughtercyst completely fills the unilocular mother cyst; cyst produces a wheel-like structure




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Figure 7: Echinococcus of liver with daughter cyst on CT scan: CT scan showingmultiple daughter cysts, some solidifiedand some partially calcified




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Contributors:

// Authors:

Jose A. Serpa, MD, MS, CTropMed

Assistant Professor of MedicineProgram Director, Infectious Diseases Fellowship, Baylor College of Medicine, Houston, TXDISCLOSURES: JAS declares that he has no competing interests.

Andrew Chou, MD

Chief FellowInfectious Diseases , Baylor College of Medicine , Houston , TXDISCLOSURES: 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, previouscontributors 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 MedicineDivision of Infectious Diseases and International Health, University of Virginia Health System, Charlottesville, VADISCLOSURES: WAP declares that he has no competing interests.

Linda Kalilani, MBBS, MPhil, PhD

EpidemiologistCollege of Medicine, University of Malawi , Zomba, MalawiDISCLOSURES: LK declares that she has no competing interests.

Paul Roberts, MD

Assistant ProfessorFamily Medicine, Mayo Clinic, Jacksonville, FLDISCLOSURES: PR declares that he has no competing interests.

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Tapeworm Infection