# 138 - 242 Cestode Infections

### 242 Cestode Infections

in the pleural spaces or lungs within another 4–16 weeks and release 
unembryonated eggs into bronchioles. The eggs are then coughed up in 
bloody (“rusty”) sputum and either discharged in sputum or swallowed 
and later excreted in feces. Unembryonated eggs are passed from the 
mammalian host into freshwater ecosystems, where they infect inter­
mediate host snails.

The symptoms and signs of paragonimiasis are fever, cough, hemop­
tysis, and peripheral eosinophilia. Some patients with paragonimiasis 
and low parasite burdens may remain relatively asymptomatic for 
prolonged periods or may have recurrent attacks of cough, sputum 
production, fever, and night sweats that mimic tuberculosis. Infective 
metacercariae may migrate to extrapulmonary sites such as the brain 
(cerebral paragonimiasis).
Pulmonary paragonimiasis is diagnosed by detection of parasite ova 
in sputum and/or feces. Serology can be helpful in egg-negative cases 
and in cerebral paragonimiasis. Anamnestic information about the 
consumption of raw or undercooked freshwater crabs by immigrants, 
expatriates, and returning travelers—and, in the United States, the con­
sumption of raw or undercooked crayfish from freshwater river systems 
where P. kellicotti is endemic—is important in patients presenting with 
fever, cough, hemoptysis, pleural effusions, and peripheral eosinophilia.
TREATMENT
Food-Borne Trematode Infections
Praziquantel and triclabendazole are the two drugs of choice; 
Table 241-2 summarizes the dosages recommended for the various 
trematode infections. All confirmed cases of human paragonimiasis 
should be treated with praziquantel (Table 241-2) to avoid the com­
plications of extrapulmonary disease. Surgical management may be 
needed for pulmonary or cerebral lesions.
PART 5
Infectious Diseases
■
■CONTROL AND PREVENTION
Drugs are currently the main method of controlling the morbidity 
associated with food-borne trematode infections, but integrated pro­
grams (including improved sanitation; food inspections; and informa­
tion, education, and communication campaigns) are important for 
sustainable disease control. Collaboration with other sectors (e.g., 
agricultural, environmental, and educational) is necessary to tackle 
highly complex situations in which human behavior, biological factors, 
and agricultural practices all play a role.
■
■FURTHER READING
Andrade G et al: Decline in infection-related morbidities following 
drug-mediated reductions in the intensity of Schistosoma infec­
tion: A systematic review and meta-analysis. PLoS Negl Trop Dis 
11:e0005372, 2017.
Cucchetto G et al: High-dose or multi-day praziquantel for imported 
schistosomiasis? A systematic review. J Travel Med 26:taz050, 2019.
De Leo GA et al: Schistosomiasis and climate change. BMJ 371:m4324, 
2020.
Fried B, Abruzzi A: Food-borne trematode infections of humans in 
the United States of America. Parasitol Res 106:1263, 2010.
Fürst T et al: Global burden of human food-borne trematodiasis: A 
systematic review and meta-analysis. Lancet Infect Dis 12:210, 2012.
Jordan P et al (eds): Human Schistosomiasis. CAB International, Wall­
ingford, 1993.
Keiser J, Utzinger J: Food-borne trematodiases. Clin Microbiol Rev 
22:466, 2009.
Mcmanus DP et al: Schistosomiasis. Nat Rev Dis Primers 4:13, 2018.
Ross AG et al: Katayama syndrome. Lancet Infect Dis 7:218, 2007.
Sripa B et al: Update on pathogenesis of opisthorchiasis and cholangio­
carcinoma. Adv Parasitol 102:97, 2018.
World Health Organization: Female Genital Schistosomiasis: A 
Pocket Atlas for Clinical Health-Care Professionals. Geneva, World 
Health Organization, 2015. Available at http://brightresearch.org/
wp-content/uploads/2016/05/FGS-pocket-atlas_eng.pdf. WHO/HTM/
NTD/2015.4, 2015. Accessed March 16, 2020.

A. Clinton White, Jr., Miguel M. Cabada

Cestode Infections
Cestodes, or tapeworms, are members of the flatworm phylum 
(Platyhelminthes) and comprise the subphylum (Cestoda). The adult 
worms are segmented worms found in the gastrointestinal tract of the 
definitive host. The larval forms are typically cystic and found in the 
tissues of the intermediate host. Human cestode infections include 
both tapeworm and larval-form infections. For tapeworm infections, 
humans are the definitive hosts, with adult tapeworms living in the 
gastrointestinal tract (Taenia saginata, Dibothriocephalus latus, and 
Dipylidium caninum). Humans are an intermediate or dead-end host 
with larval-stage parasites living in the tissues for Echinococcus spp., 
Spirometra spp., and Taenia multiceps. Humans may be either the 
intermediate hosts or the definitive hosts for Taenia solium and are the 
hosts of both stages of Rodentolepis nana (formerly Hymenolepis nana).
The tapeworm forms are typically elongated and ribbon-shaped 
and attach to the intestinal mucosa by means of sucking cups or hooks 
located on the scolex. A short, narrow neck is found at the base of the 
scolex from which proglottids (segments) form. As proglottids mature, 
they are displaced from the neck by the formation of new, less mature 
segments. The elongating chain of attached proglottids, called the stro­
bila, constitutes the bulk of the tapeworm. The length of the strobila 
varies between species. Some tapeworms consist of more than 1000 
proglottids and may be several meters long. Mature proglottids are 
hermaphroditic and produce eggs, which are intermittently released.
Most human tapeworms require at least one intermediate host to 
complete the life cycle. After ingestion of the eggs or proglottids by an 
intermediate host, the eggs are activated to release the invasive larvae 
(oncospheres). The oncosphere penetrates the intestinal mucosa and 
migrates to tissues and develops into an encysted form known as a 
cysticercus (single scolex), a coenurus (multiple scolices), or a hydatid 
(cyst with daughter cysts, each containing multiple protoscolices). 
After ingestion of the cystic forms by the definitive host, the scolex 
evaginates and develops into a tapeworm.
■
■TAENIASIS SAGINATA AND TAENIASIS ASIATICA
The beef tapeworm T. saginata is found in all countries where raw or 
undercooked beef is eaten. It is most prevalent in sub­Saharan African 
and Middle Eastern countries. Taenia asiatica is closely related to 
T. saginata and is found in Asia, with pigs as intermediate hosts. Since 
the clinical manifestations and morphology of the two species are very 
similar, they are discussed together.
Etiology and Pathogenesis 
Humans serve as the definitive host 
for the adult stage of T. saginata and T. asiatica. The scolex attaches to 
the small intestines and the strobila with 1000–2000 proglottids can 
reach 8 m in length. The scolex of T. asiatica has an unarmed (with no 
hooks) rostellum and four suckers, whereas T. saginata has no rostel­
lum but attaches via four prominent suckers. Each gravid segment 
has 15–30 uterine branches (in contrast to 8–12 for T. solium). The 
eggs of the three human-infecting Taenia species are indistinguishable 
morphologically and are 30–40 μm in diameter, contain the oncosphere 
with six hooklets, and have a thick brown striated shell. Eggs can live for 
months to years on vegetation until they are ingested by cattle or other 
herbivores (T. saginata) or pigs (T. asiatica). After ingestion, the onco­
sphere egresses the egg, invades into the intestinal wall, and is distributed 
throughout the body via the bloodstream. The invasive larva transforms 
into the cysticercus (cystic forms) in muscle or viscera of the intermediate 
host. When raw or undercooked meat containing the larvae is ingested, 
the cysticercus evaginates and forms a tapeworm in the human intestines. 
The adult worm matures over several months to produce eggs. The pro­
glottids or eggs are then shed intermittently with stool.
Clinical Manifestations 
Patients may be asymptomatic or may 
note passing proglottids in their feces. Patients may note the sensation

of something moving while the motile proglottids of T. saginata are 
passed. Patients occasionally note abdominal pain or discomfort, nau­
sea, change in appetite, or weakness. Weight loss is unusual.
Diagnosis 
Diagnosis depends on detection of eggs or proglottids 
in the stool. Eggs may not be found by stool examination but are 
sometimes only present in the perianal area; thus, when suspected, 
the perianal region should be examined with use of a cellophanetape swab (as in pinworm infection; Chap. 239). Antigen-detection 
assays are more sensitive than microscopic examination but are not 
commercially available. Distinguishing T. saginata or T. asiatica from 

T. solium requires examination of mature proglottids or the scolex or 
via molecular tests. Eosinophilia and elevated levels of serum IgE are 
usually absent.
TREATMENT
Taeniasis saginata and Taeniasis asiatica
A single dose of praziquantel (10 mg/kg) is highly effective. 
Niclosamide (adult dose, 2 g; 1 g for children weighing 11−34 kg) 
is also effective but is less available. Nitazoxanide can also be used.
Prevention 
Adequate cooking of beef and pork viscera or exposure 
to temperatures as low as 56°C for 5 min will destroy cysticerci. Refrig­
eration, salting for long periods, or freezing at –10°C for 9 days also 
kills the parasites in beef. General preventive measures include inspec­
tion of beef and pork viscera and proper disposal of human feces.
■
■TAENIASIS SOLIUM AND CYSTICERCOSIS
T. solium, also known as the pork tapeworm, causes two forms of infec­
tion in humans: adult tapeworms in the intestine (taeniasis) or larval 
forms in the tissues (cysticercosis). Humans are the only hosts for the 

T. solium tapeworm; pigs are the usual intermediate hosts, although 
other animals may rarely harbor the cysticercus forms.
T. solium has a wide global distribution including all areas where 
pigs are raised with access to human feces. Cysticercosis is highly 
prevalent in Latin America, sub­Saharan Africa, China, India, and 
Southeast Asia. Cysticercosis also occurs in nonendemic nations due to 
the immigration of tapeworm carriers or cysticercosis-infected persons 
from endemic areas.
Etiology and Pathogenesis 
The tapeworms of T. solium reside 
primarily in the small intestines. The scolex attaches to the mucosa 
via sucking disks and the armed rostellum with two rows of hooklets. 
The mature tapeworm can reach a length of 3 m and have up to 1000 
proglottids. The adult tapeworms are thought to live for just few years. 
Each mature proglottid may produce approximately 50,000 eggs. Pro­
glottids are released from the terminal end of the tapeworm intermit­
tently and excreted into the feces. The eggs are immediately infective 
for both humans and pigs. After ingestion of eggs by the intermediate 
host, the oncospheres are released, penetrate the intestinal wall, and 
are carried via the bloodstream to tissues. In the pig, larvae usually 
mature in striated muscle of the neck, tongue, and trunk. By 60–90 days, the 
invasive larvae transform into the encysted larval stage. In the pigs, cys­
ticerci typically survive for months to years, until the pig is slaughtered. 
Humans develop intestinal tapeworm infections after ingestion of 
contaminated pork. Human cysticercosis follows ingestion of T. solium 
eggs. Transmission is associated with close contact with a tapeworm 
carrier. The eggs are sticky and may be found under the fingernails of 
tapeworm carriers. The tapeworm carrier can also infect themselves by 
ingestion of ova, likely via the fecal-oral route.
Clinical Manifestations 
Intestinal infections (taeniasis) with 

T. solium are often asymptomatic. Some patients note passage of pro­
glottids in stool. The proglottids are typically off-white in color and 
1–3 cm in length, 0.5–1 cm wide, and about 1 mm thick. The clinical 
manifestations of cysticercosis are variable. Cysticerci can be found 
anywhere in the body but are commonly detected in the central ner­
vous system (CNS), skeletal muscle, subcutaneous tissue, or the eye. 

Involvement of the brain, spine, or cerebrospinal fluid (CSF) is termed 
neurocysticercosis. The clinical manifestations of human cysticercosis 
vary with the location of the cysticerci as well as with the extent of asso­
ciated inflammatory responses or scarring. The most common clinical 
manifestations are neurologic symptoms. Headache is common with all 
CNS forms of disease. Seizures are the most frequent clinical manifes­
tation and are associated with inflammation of the brain parenchyma 
surrounding the cysticercus. Seizures may be focal, focal with second­
ary generalization, or generalized. Another common clinical manifes­
tation is with symptoms of hydrocephalus, which may result from CSF 
flow obstruction by cysticerci and/or accompanying inflammation 
or communicating hydrocephalus from arachnoiditis. The symptoms 
of increased intracranial pressure may include headache, nausea and 
vomiting, dizziness, and ataxia. Patients with hydrocephalus may pres­
ent with altered mental status or papilledema with altered visual acuity. 
Some patients present with intermittent acute hydrocephalus (termed 
Bruns’ syndrome) associated with change in position due to the cysti­
cercus working as a ball valve. Cysticerci at the base of the brain or in 
the subarachnoid space may cause chronic meningitis or arachnoiditis, 
communicating hydrocephalus, mass lesions, hemorrhages, or strokes.

Diagnosis 
The diagnosis of tapeworm infection with T. solium is 
made by the demonstration of eggs or proglottids, as described for 

T. saginata. However, eggs and proglottids are only shed intermittently, 
limiting the sensitivity of direct testing. Antigen-capture enzymelinked immunosorbent assay (ELISA), polymerase chain reaction 
(PCR), and serology for tapeworm stage-specific antigens are more 
sensitive but are only available as research techniques. The diagnosis 
of neurocysticercosis can be difficult since the symptoms are nonspe­
cific and there is no readily available material for demonstration of the 
parasite. A group of international experts proposed revised diagnostic 
criteria (Table 242-1). The diagnosis is only certain with definite dem­
onstration of the parasite (absolute criteria). Definitive diagnosis is 
possible with histologic observation of the parasite in excised tissue, by 
funduscopic visualization of the parasite in the subretinal or vitreous 
spaces of the eye, or by neuroimaging demonstrating a cystic lesion 
containing a characteristic scolex (Fig. 242-1). With high-resolution 
neuroimaging, the scolex can often be identified. In other cases, a 
clinical diagnosis is based on a combination of clinical presentation, 
radiographic studies, exposure or evidence demonstrating presence 
of the parasites by antigen-detection, quantitative PCR, or even nextgeneration sequencing in spinal fluid.
CHAPTER 242
Cestode Infections
Neuroimaging is the primary major diagnostic method (Fig. 242-1). 
Demonstration of a cystic lesion with a mural nodule consistent with 
a scolex (“dot-in-hole”) is diagnostic. Major findings include cystic 
lesions with or without enhancement (e.g., ring enhancement), one or 
more nodular calcifications (which may also have associated edema 
or enhancement), focal enhancing lesions, or cystic lesions in the 
subarachnoid space. Cysticerci in the brain parenchyma are usually 
5–20 mm in diameter and round. Cystic lesions in the subarachnoid 
space or fissures may enlarge up to 6 cm in diameter and may be 
lobulated. The cyst wall for cysticerci in the subarachnoid space or 
ventricles is usually very thin, and the cyst fluid is often isodense with 
CSF. Thus, obstructive hydrocephalus or enhancement of the basilar 
meninges may be the only finding on computed tomography (CT) in 
extraparenchymal neurocysticercosis. However, since these findings 
are less specific, they are considered only minor criteria. Cysticerci 
in the ventricles or subarachnoid space are more readily identified by 
magnetic resonance imaging (MRI), especially fast imaging employing 
steady-state acquisition (FIESTA) or three-dimensional constructive 
interference in steady state (3D CISS). CT is more sensitive than MRI 
in identifying calcified lesions, whereas MRI is more sensitive than CT 
for identifying small cystic lesions, scolexes, and enhancement. Sponta­
neous resolution, resolution after albendazole therapy, or mobile cystic 
lesions within the ventricles are findings that can support the diagnosis 
of neurocysticercosis.
Exposure history significantly modifies the interpretation of neu­
roimaging studies. Detection of specific antibodies to or antigens of 

T. solium are major exposure criteria. Antibody tests using unfractionated

TABLE 242-1  Revised Diagnostic Criteria for Neurocysticercosisa
	1.	 Absolute criteria
	
a.	 Histologic demonstration of the parasite from biopsy of a brain or spinal 
cord lesion
	
b.	 Visualization of subretinal cysticercus
	
c.	 Conclusive demonstration of a scolex with a cystic lesion on neuroimaging 
studies
	2.	 Neuroimaging criteria
	
a.	 Major neuroimaging criteria
Cystic lesions without a discernible scolex, typical small enhancing 
lesions, multilobulated cystic lesions in the subarachnoid space, typical 
parenchymal brain calcifications
	
b.	 Confirmative neuroimaging criteria
Resolution of cystic lesions spontaneously or after cysticidal drug therapy
Migration of ventricular cysts documented on sequential neuroimaging 
studies
	
c.	 Minor neuroimaging criteria
Obstructive hydrocephalus or abnormal enhancement of basal 
leptomeninges
	3.	 Clinical/exposure criteria
	
a.	 Major clinical/exposure criteria
Detection of specific anticysticercal antibodies (e.g., by enzyme-linked 
immunoelectrotransfer blot [EITB]) or cysticercal antigens by wellstandardized immunodiagnostic tests
Cysticercosis outside the central nervous system
Evidence of a household contact with T. solium infection
	
b.	 Minor clinical/exposure criteria
Clinical manifestations suggestive of neurocysticercosis
Individuals coming from or living in an area where cysticercosis is endemic
PART 5
Infectious Diseases
aDiagnosis is confirmed by one absolute criterion, by two major criteria or one 
major and one confirmatory neuroimaging criteria plus any clinical/exposure 
criterion, or by one major neuroimaging criterion plus two clinical/exposure 
criteria (including at least one major clinical/exposure criterion), together with the 
exclusion of other pathologies producing similar neuroimaging findings. A probable 
diagnosis is supported by one major neuroimaging criterion plus any two clinical/
exposure criteria or by one minor neuroimaging criterion plus at least one major 
clinical/exposure criterion.
Source: Reproduced with permission from OH Del Brutto et al: Revised diagnostic 
criteria for neurocysticercosis. J Neurol Sci 372:202, 2017.
antigens (e.g., ELISAs using crude parasite antigen) have high rates 
of false-positive and false-negative results and should be avoided. 
An immunoblot assay (enzyme-linked immunoelectrotransfer blot 
[EITB]) using lentil lectin–purified glycoproteins is >99% specific and 
sensitive in patients with multiple cysts. However, patients with single 
intracranial lesions or with calcifications may be seronegative. Serum 
samples are more sensitive than CSF using EITB. Each of the diagnostic 
antigens has been cloned, and assays using recombinant or synthetic 
antigens are in development. Assays using monoclonal antibodies to 
detect parasite antigen in the blood, CSF, or urine may also facilitate 
diagnosis and patient follow-up. Antigen-detection assays are currently 
available commercially in Europe but not in the United States. More 
recently, real-time PCR has been employed for diagnosis and follow-up 
of extraparenchymal disease.
Other major clinical/exposure criteria for neurocysticercosis include 
the presence of cysticerci outside the CNS (e.g., typical cigar-shaped 
calcifications in muscle) or exposure to a tapeworm carrier or a house­
hold member infected with T. solium. Minor clinical/exposure criteria 
include residence in an endemic village or clinical symptoms sugges­
tive of neurocysticercosis (e.g., seizures or obstructive hydrocephalus).
Studies from India validated clinical criteria for diagnosis in selected 
cases. In patients from endemic areas who had single enhancing lesions 
presenting with seizures, a normal physical examination, and no evi­
dence of systemic disease (e.g., no fever, adenopathy, or chest radio­
graphic abnormalities), the presence on CT of round lesions 5–20 mm 

in diameter with no midline shift was almost always caused by neu­
rocysticercosis. Definite or probable diagnosis can be made using 
the criteria and combinations of criteria listed in the footnote of 

Table 242-1. Patients often have CSF pleocytosis with a predominance 
of lymphocytes, neutrophils, or eosinophils. The protein level in CSF 
may be elevated; the glucose concentration is usually normal but can 
be markedly reduced.
TREATMENT
Taenia solium and Cysticercosis
Tapeworm infection by T. solium infection is treated with a single 
dose of praziquantel (10 mg/kg). However, praziquantel may occa­
sionally trigger an inflammatory response in the CNS if con­
comitant cryptic cysticercosis is present. Niclosamide (2 g) is also 
effective but is not as widely available.
INITIAL MANAGEMENT OF NEUROCYSTICERCOSIS
Initial management of neurocysticercosis should focus on treat­
ment of seizures or hydrocephalus. Seizures can be controlled 
with antiseizure medications. Seizure medications can usually be 
tapered after 6 months in patients with single enhancing lesions in 
whom imaging normalizes and in whom there are no breakthrough 
seizures. Subjects with multiple parenchymal lesions require more 
prolonged therapy. However, antiseizure medications can often be 
tapered off after 2 years if lesions resolve without development of 
calcifications and patients remain free of seizures. Patients with 
calcified lesions are at higher risk of recurrent seizures, especially if 
the lesions are associated with perilesional edema or enhancement.
MANAGING HYDROCEPHALUS
For patients with hydrocephalus, the reduction of intracranial 
pressure should be the priority of the initial therapy. Patients with 
cysticerci in the cerebral ventricles typically present with obstruc­
tive hydrocephalus, and the preferred approach is removal of the 
cysticercus via neurosurgery. Cysticerci in the lateral or third ven­
tricles should be removed via neuroendoscopy. Antiparasitic drugs 
make the cysticerci more friable and should be avoided prior to 
surgery. The cysticerci in the fourth ventricle can be approached 
by microdissection using a posterior approach or, in some cases, 
via neuroendoscopy. When complete removal of the cysticercus is 
not possible, a diverting procedure, such as ventriculoperitoneal 
shunting, can be used to manage hydrocephalus. Historically, shunt 
failure was a major problem. The risk of shunt failure may be lim­
ited by administration of antiparasitic drugs and glucocorticoids.
ANTIPARASITIC DRUGS AND ANTI-INFLAMMATORY THERAPY
Antiparasitic drug treatment is never an emergency in neuro­
cysticercosis and should wait until patients are stabilized with 
antiseizure and anti-inflammatory medications and exclusion of 
intraocular disease. Antiparasitic drugs should never be started 
in patients with elevated intracranial pressure. Antiparasitics do 
hasten resolution of neuroradiologic abnormalities in parenchymal 
neurocysticercosis. Clinical benefits consist mainly of decreasing 
the number of recurrent generalized seizures. In viable parenchy­
mal cysticercosis, most authorities recommend antiparasitic drugs, 
especially albendazole (15 mg/kg per day for 8–28 days). A combi­
nation of albendazole and praziquantel (50 mg/kg per day) is more 
effective in patients with more than two cystic lesions. A longer 
course or combination therapy is needed in patients with multiple 
subarachnoid cysticerci. Both antiparasitic agents may exacerbate 
the inflammatory response around the dying parasite, thereby exac­
erbating seizures or hydrocephalus. Patients receiving these drugs 
should be carefully monitored. High-dose glucocorticoids should 
always be used during treatment (e.g., dexamethasone 0.1–0.4 mg/kg 
per day or prednisone 60 mg/d).
For patients with subarachnoid cysts or giant cysticerci, antiinflammatory medications such as glucocorticoids are needed to 
reduce arachnoiditis and accompanying vasculitis. Most authorities 
recommend prolonged courses of antiparasitic drugs as well as 
shunting when hydrocephalus is present. Patients typically require 
prolonged anti-inflammatory treatment along with antiparasitics.

FIGURE 242-1  Neurocysticercosis is caused by Taenia solium. Neurologic infection can be classified based on the location and viability of the parasites. Upper left: 
Parenchymal viable cysts (FLAIR MRI sequence). Upper center: Parenchymal viable cysts (postcontrast T1 MRI sequence). Upper right: Single enhancing lesion 
(postcontrast T1 MRI sequence). Bottom left: Extensive basal subarachnoid neurocysticercosis in the anterior fossa (FLAIR MRI sequence). Bottom center: Viable cyst 
in the fourth ventricle (FLAIR MRI sequence). Bottom right: Intraparenchymal brain calcifications (noncontrasted CT scan). Lesions are marked with arrowheads. FLAIR, 
fluid-attenuated inversion recovery. (Modified with permission from White AC Jr, Garcia HH. Updates on the management of neurocysticercosis. Curr Opin Infect Dis. 
2018;31(5):377-382. Lippincott Williams & Wilkins.)
Methotrexate and, in some cases, tumor necrosis factor inhibitors 
have been used as steroid-sparing agents in patients requiring pro­
longed therapy. In patients with diffuse cerebral edema and elevated 
intracranial pressure due to multiple inflamed parenchymal lesions, 
glucocorticoids are the mainstay of therapy, and antiparasitic drugs 
should be avoided. For ocular and spinal lesions, drug-induced 
inflammation may cause irreversible damage. Intraocular disease 
should be managed surgically. Recent data suggest that spinal dis­
ease is best managed using both medical and surgical therapy.
Prevention 
Prevention of T. solium tapeworm infection consists of 
precautions in handling pork, as described for T. asiatica, and thoroughly 
cooking or freezing pork to destroy the cysticerci. Pork inspections and 
condemnation of infected meat prevent transmission. The prevention 
of cysticercosis involves good personal hygiene including handwash­
ing, effective disposal of feces, and treatment and prevention of human 
intestinal infections. Optimal eradication programs to eradicate T. solium 
in endemic areas include mass chemotherapy administered to human 
and porcine populations and vaccinations of pigs. A vaccine for porcine 
infection is licensed in India and a few other countries.
■
■ECHINOCOCCOSIS
Echinococcosis (also known as hydatid disease) refers to infection 
by the larval stage of Echinococcus species (E. granulosus sensu lato, 

E. multilocularis, or E. vogeli). E. granulosus sensu lato parasites 

CHAPTER 242
Cestode Infections
produce cystic hydatid disease or cystic echinococcosis, which is preva­
lent worldwide in most areas where livestock is raised in association 
with dogs. E. granulosus sensu lato is a complex of several distinct spe­
cies with important genotypic and phenotypic differences. Human cys­
tic echinococcosis is caused by E. granulosus sensu stricto (genotypes 1–3), 
E. canadensis (genotypes 6–8 and 10), and E. ortleppi (genotype 5). 
Some classify genotypes 6 and 7 as a separate species—E. intermedius. 
E. granulosus sensu lato parasites are found on all continents, with areas 
of high prevalence in western China, central Asia, the Middle East, the 
Mediterranean region, eastern Africa, and parts of South America. 

E. multilocularis causes multilocular or alveolar echinococcosis charac­
terized by locally invasive lesions. Alveolar echinococcosis is prevalent 
in Alpine, sub-Arctic, and Arctic regions of the northern hemisphere, 
including western China, central Asia, central and northern Europe, 
and in isolated areas of North America with an expanding range of 
endemic areas. Neotropical echinococcosis (formerly termed polycys­
tic hydatid disease) is caused by E. vogeli and E. oligarthrus, which are 
only found in limited foci in South America.
Echinococcal species require both intermediate and definitive hosts. 
The definitive hosts are usually canines (dogs, foxes, wolves) that har­
bor the small tapeworms in the intestine and shed eggs in stool. After 
the ingestion of eggs, oncospheres invade through the intestines into 
the circulatory system and form cysts in the intermediate hosts 
including sheep, cattle, goats, camels, pig, and horses for E. granulosus 
sensu lato and mice and other rodents for E. multilocularis. When a dog

(E. granulosus) or fox/wolf (E. multilocularis) ingests viscera containing 
cysts, the protoscolices in the cyst fluid develop into tapeworms in the 
intestine, completing the life cycle. Humans are a dead-end intermedi­
ate host and not part of the parasite’s life cycle.

Etiology 
The adult tapeworms of E. granulosus sensu lato are small 
(5­ mm long) and live for 5–20 months in the small intestine of dogs. 
Each tapeworm has only three proglottids: one immature, one mature, 
and one gravid. The latter are shed and release eggs that are morpho­
logically similar to Taenia eggs. Heavy infections of dogs with many 
tapeworms are common in endemic areas. When humans ingest the 
eggs, the invasive oncospheres are released from eggs, penetrate the 
intestinal mucosa, enter the portal circulation, and are carried mostly 
to the liver and lungs. However, virtually any organ can be infected 
including kidneys, spleen, heart, bone, and brain. Larvae of E. granu­
losus sensu lato develop into fluid-filled unilocular hydatid cysts. The 
wall of the cystic lesion consists of an external membrane and an inner 
germinal layer, which are surrounded by the host’s adventitial layer that 
may contain different patterns of inflammation and fibrosis. Daughter 
cysts and germinating cystic structures called brood capsules develop 
from the inner aspect of the germinal layer. New organisms, called 
protoscolices, develop in large numbers within the brood capsule. A 
protoscolex is an invaginated scolex with the capacity to form an adult 
tapeworm if ingested by a definitive host or form a new cystic lesion if 
released in the intermediate host’s tissues. The cysts expand slowly over 
a period of years and may contain thousands of protoscolices.
E. multilocularis has a life cycle involving wild canines such as foxes 
or wolves, which are the main definitive hosts. Domestic dogs can also 
serve as definitive hosts of these tapeworms. Small rodents are the 
main intermediate hosts. Humans are dead-end intermediate hosts 
that develop alveolar echinococcosis. The larval stage of this parasite 
forms multilocular, small irregular cysts with proliferating and invasive 
capacity. The parasite larvae invade the host tissue by peripheral exten­
sion of processes from the germinal layer. These lesions do not contain 
brood capsules or protoscolices.
PART 5
Infectious Diseases
Clinical Manifestations 
The slowly enlarging echinococcal cysts 
generally remain asymptomatic for years until their expanding size elicits 
organ-specific symptoms. Spontaneous or traumatic rupture may lead to 
type I allergic reactions including anaphylaxis. The liver is involved in 
two-thirds of E. granulosus sensu lato infections and nearly all E. multi­
locularis infections. The lungs are involved in about 20% of E. granulosus 
sensu lato infections. The parasites are often discovered incidentally on a 
routine x-ray or ultrasound study prior to onset of symptoms.
Symptoms of hepatic cystic echinococcosis may include abdomi­
nal fullness or pain or a palpable mass in the right upper quadrant. 
A
B
FIGURE 242-2.  Imaging studies of cystic echinococcosis. A. Chest x-ray film of a patient with bilateral cysts. The hollow arrows show well-defined cyst walls with a 
complicated right chest cyst and an intact left chest cyst. B. Liver ultrasound of a patient with CE1 cysts. The hollow arrow shows a well-defined bilayer cyst wall.

Compression of a bile duct or leakage of cyst fluid into the biliary tree 
may present with symptoms mimicking cholelithiasis. Jaundice can 
result from biliary obstruction. Rupture of or leakage from a hydatid 
cyst may present more acutely with symptoms including fever, pruri­
tus, urticaria, eosinophilia, or anaphylaxis. Cystic echinococcosis in 
the lungs may present with chronic cough, shortness of breath, chest 
pain, or hemoptysis. Rupture into the bronchial tree leads to sudden 
expectoration of the cyst fluid and membranes and rupture into the 
pleural cavity may produce pleuritic chest pain and hydatid empyema. 
Rupture of hydatid cysts, which can occur spontaneously, after trauma, 
or during surgery, may lead to release of protoscolices into the patient’s 
tissues, each of which can form new cysts. Hydatid disease may also 
involve bone (invasion of the medullary cavity with bony erosion pro­
ducing pathologic fractures), the CNS (space-occupying lesions), the 
heart (conduction defects, pericarditis), and the pelvis (pelvic mass).
E. multilocularis characteristically presents as a slow-growing 
hepatic mass, which typically presents decades after the initial infec­
tion. The lesions resemble tumors causing progressive destruction of 
the liver and extension into adjoining structures. Frequent symptoms 
include upper-quadrant and epigastric discomfort. Physical examina­
tion may reveal liver enlargement and obstructive jaundice. The lesions 
may infiltrate adjoining organs (e.g., diaphragm, kidneys, or lungs) or 
may metastasize to the spleen, lungs, or brain.
Diagnosis 
Imaging studies are the main diagnostic methods to 
detect and evaluate echinococcal cysts. Chest x-ray or CT can iden­
tify pulmonary cysts due to E. granulosus sensu lato, which appear as 
rounded masses of uniform density (Fig. 242-2).
Ultrasound, CT, or MRI can be used to identify cystic echinococ­
cosis lesions in solid organs of the abdomen, particularly in the liver. 
The ultrasound classification proposed by the World Health Organiza­
tion Informal Working Group on Echinococcosis has diagnostic and 
management applications for liver cystic echinococcosis (Figs. 242-2 
and 242-3). MRI can also be used to classify lesions. MRI and CT may 
be more useful than ultrasound to evaluate the presence of cyst com­
plications, such as communication with the biliary tree, that preclude 
some management options. Imaging of cystic echinococcosis shows 
well-defined cysts walls and, in some cases, internal trabeculation, 
dense cyst material, and/or calcifications (Fig. 242-3). In some cases, 
the protoscolices and brood capsules of E. granulosus complex may be 
visible within the cysts as fine particles termed hydatid sand. Identi­
fication of daughter cysts within the larger cyst is diagnostic of cystic 
echinococcosis disease. Eggshell or mural calcification on CT is also 
diagnostic of E. granulosus infection. In contrast, ultrasound or CT of 
alveolar hydatid cysts often reveals an indistinct solid mass. Some cases 
will display central necrosis or plaque-like calcifications.

Imaging of cystic echinococcosis
Ultrasound
CT scan
MRI
CE 1
CE 2
CE 3a
CE 3b
CE 4
CE 5
FIGURE 242-3  Management of cystic hydatid disease caused by Echinococcus granulosus should be based on viability of the parasite, which can be estimated from 
radiographic appearance. Staging is done by imaging studies including ultrasound, CT, or MRI and includes lesions classified as active, transitional, and inactive. Active 
cysts include types CL (with a cystic lesion and no visible cyst wall), CE1 (with a visible cyst wall and internal echoes [snowflake sign]), and CE2 (with a visible cyst 
wall and internal septation). Transitional cysts may have detached laminar membranes (CE3a) or may be partially collapsed (CE3b). Inactive cysts include types CE4 

(a nonhomogeneous mass) and CE5 (a cyst with a thick calcified wall).
For cystic echinococcosis disease, a definitive diagnosis can also be 
made by the examination of aspirated fluids for protoscolices and/or 
hooklets. However, due to the potential risk of fluid leakage resulting 
in either dissemination of infection or, more rarely, anaphylactic reac­
tions, aspiration should only be performed by experienced interven­
tionists and following the precautions used for percutaneous treatment 
(see below). Serodiagnostic assays can be useful, but current serologic 
tests are insensitive and cannot be used to exclude the diagnosis of 
echinococcosis. ELISA and immunoblot assays for specific antibody 
are positive in ~90% of cases of hydatid liver disease. By contrast, the 
sensitivity is only ~50% for patients with cysts in the lungs.
TREATMENT
Echinococcosis
CYSTIC HYDATID DISEASE
Optimal treatment of cystic echinococcosis varies depending on 
the size, stage, location, and clinical manifestations of cysts. In the 
past, surgery was the main treatment method, but numerous studies 

CHAPTER 242
Cestode Infections
have demonstrated that other treatment modalities may be just as 
effective and lead to less morbidity. Staging is recommended for 
cystic echinococcosis of the liver, which allows assessment of the 
cyst size and viability (Fig. 242-3). CL, CE1, and CE3a lesions <5 cm 
in diameter may respond well to chemotherapy with albendazole 
alone. Other small liver cysts (<5 cm) such as CE2 or CE3b are 
less responsive to medical treatment alone. Larger CE1 lesions and 
uncomplicated CE3a lesions in the liver can often be managed by 
PAIR (percutaneous aspiration, instillation of scolicidal agents, and 
reaspiration). Contraindications to PAIR include cysts communi­
cating with the biliary tree, large cysts (>10 cm), or superficial cysts, 
which are more likely to rupture and spill protoscolices. Albenda­
zole (15 mg/kg daily in two divided doses) should be initiated at 
least 2 days before the procedure and continued for at least 4 weeks 
afterward. Fine-needle ultrasound or CT-guided aspiration should 
enter the cyst through solid tissues to limit spillage of cyst fluid. 
Aspiration can confirm the diagnosis by microscopic demonstra­
tion of protoscolices or hooks. After aspiration, bilirubin should 
be measured in the cyst fluid using a dipstick, or contrast material 
should be injected to detect occult communications with the biliary

tract. If no bile is found and no communication is visualized, instil­
lation of scolicidal agents (usually hypertonic saline) and reaspira­
tion are performed. PAIR, when performed by a skilled practitioner, 
results in cure and relapse rates equivalent to surgery, with less 
perioperative morbidity and shorter hospitalization. In some cen­
ters, CE2 lesions have been treated by modified catheter drainage, 
including puncture of each daughter cyst within the primary cyst.

Patients with treatment failure can often be treated again suc­
cessfully with PAIR or additional courses of medical therapy. 
Response to treatment is best assessed by serial imaging studies, 
with attention to cyst size and consistency. Cysts may not dem­
onstrate complete radiologic resolution even though no viable 
protoscolices are present. Those cysts classified as CE4 or CE5 are 
considered nonviable and require periodic reevaluations to assess 
for reactivation.
Surgery remains the treatment of choice for complicated cystic 
echinococcosis (e.g., cysts communicating with the biliary tract), 
for most thoracic and intracranial cysts, and when PAIR is not pos­
sible. Liver cysts should be removed via a pericystectomy, in which 
the entire cyst and the surrounding fibrous tissue are removed 
to prevent spillage and recurrence. Recent reports demonstrate 
that, in experienced hands, cysts can often be safely removed by 
laparoscopic or robotic surgery. The risks posed by leakage of fluid 
during surgery or PAIR include anaphylaxis and dissemination of 
protoscolices. Spillage can be minimized by careful dissection and 
using surgical draping soaked in hypertonic saline. Infusion of 
scolicidal agents is no longer recommended because of problems 
with hypernatremia, intoxication, or sclerosing cholangitis. Alben­
dazole should be administered adjunctively, beginning several days 
to weeks before resection of the liver cyst and continuing for several 
weeks afterwards. Albendazole at 10-15 mg/kg divided in two daily 
doses (400 mg BID in adults) is recommended for treatment in 
association with clinical and laboratory monitoring.
ALVEOLAR HYDATID DISEASE
Surgical resection is required to attempt cure of E. multilocularis 
infection. Complete removal of the parasite continues to offer the 
best chance for cure. Patients who have undergone presumed cura­
tive resection should be treated with albendazole for at least 2 years 
after presumptively curative surgery. Positron emission tomography 
can be used to follow disease activity. Unfortunately, most cases are 
only diagnosed at a stage in which complete resection is impos­
sible; in these cases, albendazole treatment should be continued 
indefinitely, with careful monitoring. In some cases of larger lesions, 
complete removal of the liver followed by liver transplantation has 
been used. Unfortunately, the immunosuppression required to pre­
vent rejection of the transplanted liver also promotes proliferation 
of E. multilocularis and reinfection of the transplanted liver. Thus, 
indefinite treatment with albendazole is required.
PART 5
Infectious Diseases
Prevention 
Cystic echinococcosis can be prevented by adminis­
tering praziquantel to infected dogs, by preventing dogs from having 
access to viscera from infected animals, or by vaccinating sheep. Limit­
ing the number of stray dogs that are more likely to evade prevention 
measures may help decrease transmission. In Europe, E. multilocu­
laris infection is associated with human settlement encroaching into 
forested areas, gardening in those areas, and collecting activities in 
forested areas. Thus, gloves and hand hygiene should be used in these 
situations. Praziquantel-impregnated bait can be used to treat tape­
worms in wild canines.
■
■RODENTOLEPIS NANA (PREVIOUSLY HYMENOLEPIS 
NANA)
The dwarf tapeworm, previously known as H. nana, is the most com­
mon human cestode infection. Recent molecular data have led to the 
reclassification of this organism to a different genus and new name 
Rodentolepis nana. R. nana is endemic worldwide, including tem­
perate and tropical regions. Transmission is mostly person-to-person 
by the fecal-oral route.

Etiology and Pathogenesis 
R. nana is the only human cestode 
that does not require an intermediate host. Both the larval and adult 
stages coexist in the intestine of infected persons. The adult tapeworm 
is only ~2 cm long and lives in the human proximal ileum. The tiny 
proglottids are rarely seen in the stool. They release spherical eggs, 
30–44 μm in diameter, containing the invasive larvae termed onco­
sphere, which has six hooklets. The eggs are immediately infective after 
leaving the host and survive for ≤10 days in the environment. After the 
eggs are ingested, the oncosphere is released, penetrates the intestinal 
villi, and develops into the cysticercoid larval form within the epithe­
lium. After a few days, these larvae reenter the intestinal lumen, attach 
to the mucosa, and mature into adult tapeworms over 10–12 days. The 
life span of adult R. nana worms is typically ~4–10 weeks. However, 
infection is perpetuated by cycles of reinfection and autoinfection in 
which some eggs hatch in the intestinal lumen and form the cysticer­
coid larva without leaving the host.
Clinical Manifestations 
R. nana infection is most often asymp­
tomatic. However, infection may be associated with diarrhea, abdomi­
nal pain, and weight loss, particularly in children with the highest 
burden of infection.
Diagnosis 
Infection is diagnosed by finding the characteristic R. nana 
eggs in microscopy of the stool.
TREATMENT
Rodentolepis nana Infection
The treatment of choice for R. nana is praziquantel (25 mg/kg 
once), which is active against both the adult worms and the cysti­
cercoids in the intestinal wall. Nitazoxanide (500 mg twice a day for 
3 days) has been used as an alternative treatment.
Prevention 
Since R. nana is acquired by the fecal-oral route, 
improved sanitation and personal hygiene can be used to eliminate 
disease. Hand washing in the household and school is important. 
Mass chemotherapy and improved hygiene have been used to control 
epidemics.
■
■HYMENOLEPIASIS DIMINUTA
Hymenolepis diminuta is a cestode of rodents that occasionally causes 
infection in small children. Infection is acquired by ingesting uncooked 
cereal and other foods contaminated by fleas and other insects that 
serve as intermediate hosts for H. diminuta. Infection is diagnosed by 
detection of eggs in the stool. The treatment of choice is praziquantel 
(25 mg/kg once).
■
■DIPHYLLOBOTHRIASIS (DIBOTHRIOCEPHALUS/
ADENOCEPHALUS)
The broad fish tapeworms comprised several species that were for­
merly classified under the genus Diphyllobothrium. Molecular and 
phylogenetic studies have now demonstrated several important dif­
ferences between these parasites, which led to modification of the 
taxonomic classification of cestodes of the Diphyllobothriidae family 
infecting humans. Dibothriocephalus latus (formerly Diphyllobothrium 
latum), Adenocephalus pacificus (formerly Diphyllobothrium pacifi­
cum), and Dibothriocephalus nihonkaiensis (formerly Diphyllobothrium 
nihonkaiensis) are the most common species infecting humans. These 
parasites were initially identified in freshwater lakes, rivers, and deltas 
of the Northern Hemisphere and central Africa. However, they are 
also found in marine environments in the northern Pacific Ocean 

(D. nihonkaisensis) and the Pacific coast of South America (A. pacificus).
Etiology and Pathogenesis 
The adult tapeworm can reach a 
length of up to 25 m, making them the longest tapeworms of humans. 
The scolex attaches to the small intestinal mucosa by a modified sucker 
called bothria, which is located on the elongated scolex. The mature 
tapeworms have 3000–4000 proglottids, producing ~1 million eggs per 
day. D. latus eggs hatch in fresh water and release the free-swimming 
coracidium. The coracidia are ingested by small freshwater crustaceans

(Cyclops or Diaptomus species). Within the infected crustaceans, the 
procercoid larvae develop. When the infected crustaceans are ingested 
by fish, the procercoid larva migrate to the fish’s flesh and transform 
into a sparganum or plerocercoid larva. Humans acquire the infection 
by ingesting infected raw or smoked fish. Within 3–5 weeks, the tape­
worm matures into an adult in the human intestine. For A. pacificus, 
the definite hosts include seals, dogs, and humans, and the second 
intermediate hosts are marine fish.
Clinical Manifestations 
Most infections by these tapeworms are 
asymptomatic. Some patients note abdominal discomfort, diarrhea, 
vomiting, weakness, or weight loss. The proglottids may be passed in 
stool or found incidentally during endoscopy. Diphyllobothriidae can 
cause acute abdominal pain or intestinal obstruction in rare cases. 

D. latus tapeworms have avid receptors for vitamin B12 that can inter­
fere with absorption and, in patients with other risk factors, produce 
vitamin B12 deficiency. In patients with B12 deficiency, pernicious anemia 
and neurologic sequelae may develop.
Diagnosis 
The diagnosis is made by the detection of the character­
istic eggs in the stool. The eggs possess a single shell with an opercu­
lum at one end and a knob at the other, which may be confused with 
trematode eggs by the inexperienced technician. Mild to moderate 
eosinophilia may be detected. Examination of the tapeworms passed 
also provides a diagnosis, as proglottids have a characteristic uterus 
with a rosette-like shape.
TREATMENT
Diphyllobothriasis
Praziquantel (5–10 mg/kg once) is highly effective against all 
Diphyllobothriid species. Parenteral vitamin B12 may be given for 
B12 deficiency.
Prevention 
Heating fish to 54°C for 5 min or freezing at –18°C for 
24 h kills the larval forms. Placing fish in brine with a high salt concen­
tration for long periods can also kill the plerocercoid larvae.
■
■DIPYLIDIASIS
Dipylidium caninum is a common tapeworm of dogs and cats. Dogs, 
cats, and occasionally humans become infected by swallowing fleas 
harboring the intermediate forms (cysticercoid larvae). Children are 
more often infected than adults. Infections are usually asymptomatic 
except for the passage of motile proglottids in stool and, less often, 
vague abdominal symptoms. The diagnosis is made by the detection 
of proglottids or the characteristic egg packets in the stool. Eggs within 
the packet resemble other Taenia eggs. The motile proglottids resemble 
flattened grains of rice and, in small children, may migrate out of the 
anus. Praziquantel is the treatment of choice. Prevention should mainly 
focus on antiparasitic and flea treatment of dogs and cats.

■
■SPARGANOSIS
The plerocercoid larvae of Diphyllobothriid tapeworms of the genus 
Spirometra cause human sparganosis. Dogs, cats, and pigs are hosts of 
the adult tapeworm; crustaceans of the Cyclops species in fresh water 
are the first intermediate host; and snakes, frogs, or birds are the sec­
ond intermediate hosts. Human infection commonly follows topical 
application of poultices with infected flesh from snakes, frogs, or birds 
used in traditional medicine. Infection can also be acquired by the 
ingestion of water containing infected Cyclops and raw or undercooked 
meat from infected snakes, birds, or some mammals. Infection com­
monly presents as a subcutaneous swelling that contains the parasite. 
Periorbital infections can present with swelling and intraocular infec­
tions may lead to blindness. Infections of the brain can present as a 
mass or slowly migrating lesions. Proliferative lesions may cause tissue 
infiltration and are poorly responsive to medical treatment. Surgical 
excision is used to treat localized sparganosis.

■
■COENUROSIS
Coenurosis is a rare infection of humans by the larval stage (coenurus) 
of the dog tapeworms Taenia multiceps or Taenia serialis. The main 
clinical manifestations are space-occupying cystic lesions in various 
tissues. The commonly involved tissues include the CNS or subcuta­
neous tissue. Surgical excision is usually required for both definitive 
diagnosis and treatment. There are limited data on response to anti­
parasitic treatment.
Acknowledgment
The authors acknowledge and thank Peter F. Weller, MD, author of prior 
editions of this chapter.
CHAPTER 242
■
■FURTHER READING
Brunetti E et al: Expert consensus for the diagnosis and treatment of 
cystic and alveolar echinococcosis in humans. Acta Trop 114:1, 2010. 
Del Brutto OH et al: Revised diagnostic criteria for neurocysticercosis. 
Cestode Infections
J Neurol Sci 372:202, 2017. 
Kern P et al: The echinococcoses: Diagnosis, clinical management and 
burden of disease. Adv Parasitol 96:259, 2017.
Nash TE et al: Natural history of treated subarachnoid neurocysticer­
cosis. Am J Trop Med Hyg 102:78, 2020. 
Nguyen DC et al: The brief case: The boy who cried worm. J Clin 
Microbiol 61:e00553, 2013.
Wen H et al: Echinococcosis: Advances in the 21st century. Clin 
Microbiol Rev 32:e00075, 2019. 
White AC Jr et al: Diagnosis and treatment of neurocysticercosis: 
2017 clinical practice guidelines by the Infectious Diseases Society of 
America (IDSA) and the American Society of Tropical Medicine and 
Hygiene (ASTMH). Clin Infect Dis 66:1159, 2018.

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