The pork tapeworm Taenia
solium and the beef tapeworm T saginata are
the most common tapeworms of humans. The diseases associated with
infection by these organisms have been known since ancient times,
being found wherever insufficiently cooked pork or beef is eaten.
Human infection with the pork tapeworm is uncommon in the United
States and Canada, although larval infection (ie, cysticercosis)
of swine may still occur. In many areas of the world, especially
Mexico and parts of South and Central America, Africa, southeastern
Europe, India, and China, infection with T solium is
relatively common. Human infection with the larval stage of T
solium (Cysticercus cellulosae), or cysticercosis,
is found wherever adult T solium infection is common.1T
saginata infection occurs among those who eat raw or insufficiently
cooked beef. Human infection with larval T saginata (Cysticercus
bovis) almost never occurs.
Humans are the mandatory definitive hosts who disseminate infection
to porcine or bovine intermediate hosts. Transmission to swine usually
occurs through contaminated soil, where gravid proglottids are deposited
with human feces. Eggs can survive for weeks in moist soil. In cattle,
grazing lands, water, or cattle feed that is contaminated with infected
human feces are sources of infection. Intrauterine infection of calves
has been reported.
Adult worms live in the upper small intestine, with T
solium measuring 2 to 8 m and T saginata measuring
3 to 10 m. The scolex of the pork tapeworm is distinguished by a
crown or rostellum with a double row of hooklets. The scolex of T
saginata is without hooks. The gravid uterus holds thousands
of eggs, each with a mature 6-hooked (ie, hexacanth) embryo. Eggs
are 30 to 40 μm in diameter and similar in both human Taenia species.
If the eggs are ingested by a suitable intermediate host such as
swine (T solium) or cattle (T saginata),
the embryo is liberated, penetrating the intestinal wall and disseminating
via the bloodstream. The embryo of T solium may
invade all tissues of the body and develops into a cysticercus or bladder
worm. Cysticerci are ellipsoidal, white, translucent cysts into
which the scolex is inverted.
When infected meat is eaten, the cysticercus is activated by
gastric juices and bile, which stimulate evagination of the scolex.
The scolex attaches to the jejunal wall, and the embryo becomes
a mature tapeworm in 10 to 12 weeks for T saginata and
5 to 12 weeks for T solium. In humans, the eggs
of T solium are ingested, and the larval stage may
develop in every tissue of the body, a condition known as cysticercosis
cellulosae. In tissue, the larvae cause an inflammatory
infiltrate of eosinophils, plasma cells, neutrophils, and lymphocytes,
with eventual necrosis and fibrosis and subsequent calcification
of the parasite.
Infection with the adult T solium or T
saginata is either asymptomatic or associated with only
mild or moderate complaints including spontaneous discharge of proglottids
from the rectum (98%), abdominal pain (36%) or
nausea (34%), weakness (25%), loss of appetite
(21%) or increased appetite (17%), headache (15%),
constipation (9%), dizziness (8%), diarrhea (6%),
or pruritus ani (4%). Rarely, infection can cause serious,
life-threatening disease by intestinal or appendiceal obstruction,
or by regurgitation and aspiration of a proglottid. Abdominal pain
and nausea are most common in the morning and characteristically
relieved by food. Children are more frequently symptomatic than adults.
Eosinophilia occurs in 5 to 15% of cases.
The larvae of T solium, which are termed oncospheres, escape
from the egg and penetrate the duodenum, enter the lymphatic and
vascular systems, and are widely disseminated throughout the body causing
human cysticercosis which is a serious and sometimes fatal
disease. The disseminated larvae can be found throughout the body.
Cysticerci have been found in almost every tissue and organ of
the body. Small numbers of cysts in muscle or subcutaneous tissue
may be of little consequence, but invasion of the eye, brain, or
heart may be serious. Cysts are most common (in order of frequency)
in subcutaneous tissues, eyes, and brain. Except in the eye, cysts
usually provoke development of a fibrous capsule. Neurocysticercosis
is highly endemic throughout the Western Hemisphere from Mexico
to Chile. In Mexico City, it accounts for as much as 10% of
neurologic admissions and more than 25% of craniotomies: the
prevalence in Mexico in the general population is approximately
4%. Cysticercosis is often observed in the United States,
particularly in urban centers with large Latin American immigrant
Neurocysticercosis is highly endemic throughout the Western Hemisphere
from Mexico to Chile. In Mexico the prevalence in the general population
is approximately 4%; and in Mexico City it accounts for
up to 10% of neurologic admissions and more than 25% of
craniotomies. Autochthonous cases of neurocysticercosis have been
reported in the United States. In U.S. children neurocysticercosis
has been characterized by symptoms of seizure (87%), headache
(32%), nausea and vomiting (32%), and altered
mental status (13%). Fewer than 10% of children
may present with cranial nerve palsies, gait abnormalities, papilledema,
or decreased visual acuity. Sensory changes or fever are never present.2
Neurocysticercosis may present as a leptomeningitis, resembling
tuberculous meningitis, and may cause communicating hydrocephalus. Cysticerci
may be present in the ventricles (most commonly the fourth ventricle)
causing obstructive hydrocephalus. Cysts that are localized at various
sites in brain parenchyma can remain silent for years, only to become
evident when the cysts die, provoking an inflammatory response and
edema. Cysts often calcify and may be found serendipitously. Spinal
cord cysts present as transverse myelitis or arachnoiditis.
Cysts may be found asymptomatically in the vitreous, but if they
occur in the retina, there may be visual impairment, scotoma, or
retinal detachment. Cysticerci in the myocardium may cause arrhythmias
and cardiac failure.
Observation of gravid proglottids is required for a specific
diagnosis; the presence of Taenia eggs in the stool
is insufficient. Before initiating therapy, the species of Taenia must
be identified because disseminated cysticercosis theoretically can
be caused iatrogenically in individuals with T solium infection
if, during therapy, they should regurgitate gravid proglottids into
the upper GI tract where gastric and duodenal fluids activate the
The species of the proglottid can be identified by pressing the
segment between two glass microscope slides and counting the main lateral
branches of the uterus. T solium usually has 7
to 13 branches on each side; T saginata usually
has 15 to 20 lateral branches on each side (Fig.
340-1). Fecal examination, especially with T saginata infection,
often is unrewarding because intact gravid proglottids tend to be
eliminated or crawl out onto the perianal area before they disintegrate
and release their eggs. Thus, the perianal cellophane-tape method,
similar to that used to diagnose pinworms, may be more effective
for recovering Taenia ova.
Approximately 10% of patients with neurocysticercosis
have eosinophilia. The findings on lumbar puncture are rarely helpful,
and findings range from normal to isolated high protein levels with
or without an inflammatory pleocytosis. Eosinophilia may be present occasionally
in the CSF. A lumbar puncture should not be done in the presence
of suspected increased intracranial pressure.
Radiographic findings are often useful. Soft-tissue radiographic
studies may reveal characteristic numerous, tiny, curvilinear calcifications
in the muscle. MRI or CT will demonstrate cysts in all stages in
the meninges and parenchyma (Fig. 340-2).
Contrast-enhancement studies with metrizamide often are necessary
to demonstrate isodense cysts in the ventricles.
Neurocysticercosis. Magnetic resonance image with several
cysts, some showing a punctate, dense image corresponding to the
(Source: Courtesy of David Botero and J.P.S.
Nobrega, University of Sao Paulo, Brazil.)
In the past, ELISA has been the most frequently used diagnostic method
to detect cysticercus antibodies in both serum and cerebrospinal
fluid (CSF). This test can be highly sensitive, but may cross-react
with other helminth antibodies, especially Echinococcus.
The enzyme-linked immunoelectrotransfer blot (EITB) is highly specific
and sensitive, although sensitivity is low when fewer than 2 parenchymal
cysts are present. In a recent series of children presenting with
neurocysticercosis in the United States, fewer than 30% had
positive EITB. Examination of the serum is more sensitive than the CSF.
In patients with clinical and radiologic features of cysticercosis, negative
serology may be an indication for biopsy, especially if the patient
is from an area of low endemicity. Elevated titers in CSF are particularly
useful if they exceed those in the serum. High positive titers are
more often seen in those individuals with hydrocephalus or meningeal
Adult tapeworm infections are treated successfully if the scolex
is eliminated. An effective agent with few untoward effects is niclosamide
(Yomesan) but this agent is only inconsistently available in the
United States. For Taenia infections, the single
dose for adults consists of 4 tablets or 2 g chewed thoroughly after
a light meal. For children weighing 11 to 34 kg, a single dose of
2 tablets (1 g) is recommended, and for those children weighing
more than 34 kg, a single dose of 3 tablets (1.5 g) is recommended.
For patients with T solium infection, therapy probably should
be administered in the physician’s office. An antiemetic
may be administered 30 minutes before the antihelminthic. If the
patient does not have a bowel movement within 2 hours, a mild saline
purge should be provided. Alternatively, praziquantel, an acylated
isoquinole-pyrazine, is highly active against most tapeworm infections. It
can be given in a single dose of 10 to 20
mg/kg in taeniasis.
Until recently, surgical intervention was the only definitive
therapeutic option for the treatment of neurocysticercosis. Medical
therapy remains controversial.1 When viable cysts
are present, albendazole may be indicated. Currently, albendazole
is the drug of choice; the daily dose is 15 mg/kg in 2
divided doses for 8 to 28 days. In recent studies, shorter courses have
been as successful as longer courses of therapy.3 Corticosteroids
may be given before and during therapy to ameliorate or attenuate
symptoms associated with cyst death, ensuing inflammation, and possible
cerebral edema. Currently, therapy is recommended for children with “active” cysts,
indicated on computerized tomography as ring-enhancing lesions.
Some physicians prefer to treat all children rather than waiting
for the natural resolution of the cyst. Others recommend that children
be treated only if they are symptomatic. It is uncertain whether
children with few cysts, with or without seizures as the predominant
symptom, will benefit from treatment. However, recent controlled
studies show approximately 50% reduction of cyst size at
3 months posttreatment and a threefold reduction of seizures in albendazole-treated
versus placebo-treated children. Hydrocephalus, which is a common complication
of neurocysticercosis, can only be alleviated by the placement of
a ventricular-peritoneal shunt. Intraventricular cysts will not
respond to albendazole or praziquantel.
Seizures are not always relieved by treatment of the cysticercosis.
Therefore, if a patient with cysticercosis is receiving anticonvulsive
therapy, it should be continued and may be required indefinitely.4