CESTODES (TAPEWORMS)

I. GENERAL
1. The tapeworms are hermaphroditic worms, which as adults parasitize the
gastrointestinal tract of vertebrates.
2. They are segmented /flat shape
A. TAPEWORM ANATOMY:
1. HEAD or SCOLEX, with adhesive organs, at anterior end of worm.
Attachment to the intestinal mucosa is accomplished by the scolex.

2. PROGLOTTIDS, the multiple, hermaphroditic, egg-producing units.

These are the flattened segments of the worm body.
Medically important species of cestode.
a. Diphyllobothrium latum has a SCOLEX with elongated, slit-like
attachment organs
Fish tape worm
b. Taenia saginata has four muscular SUCKERS
Beef tape worm.
c. Taenia solium has similar muscular SUCKERS
Pork tape worm.
d. Hymenolepis nana
Dwarf tape worm.
e. Echinococcus granulosis
Dog tape worm.

B. TAPEWORM LIFECYCLE:
The DEFINITIVE HOST ingests the larval form. Worms mature from larval
forms in the intestine of definitive host. The definitive host harbors ADULT
WORMS in the intestine. EGGS are passed in the stool.
Eggs are ingested by the INTERMEDIATE HOST. LARVAE develop from
eggs in the intermediate host and penetrate the host intestinal mucosa.
Larvae develop into ENCYSTED FORMS in tissues of intermediate host.
The CYSTICERCUS is the encysted form of the Taenia species. The
HYDATID is the encysted form of the Echinococcus.

NOTE: Diphyllobothrium latum has two intermediate hosts.

C. HUMAN DISEASE CAUSED BY TAPEWORMS
1. ADULT (WORM) STAGE:
a. Taenia saginata, Taenia solium, Diphyllobothrium latum.
b. The presence of adult tapeworms in the human GI tract only rarely
causes symptomatic disease. People usually only become aware
of the infection when proglottids are passed in the feces.
NOTE:
T. solium causes human disease in both adult and larval
stages.
2. LARVAL (CYST) STAGE (i.e., Cysticercosis):
a. Echinococcus granulosus, Echinococcus multilocularis, Taenia
solium
b. The presence of the cyst stage of the tapeworm in extraintestinal
tissues causes signs and symptoms relative to the site of the
expanding cyst.

D. LABORATORY IDENTIFICATION OF TAPEWORMS:

Morphology of the proglottid (degree of branching, configuration, size) is
important in distinguishing T. solium, T. saginata, and sometimes D.
latum.
Eggs of T. solium and T. saginata are morphologically indistinguishable,
but the eggs of D. latum are operculated.
II. Taenia saginata:
A. Epidemiology: Humans are the only definitive host. Cows and
certain other herbivores are intermediate hosts. Disease is very rare in
the U.S., because of industrialization of beef production and meat
inspection.
Ingestion of poorly cooked beef containing
B. Mode of transmission:
larvae. Larvae mature in human jejunum to mature worms; worms
release eggs that pass in the stool. Cattle ingest fodder contaminated
with eggs. Embryos mature into larvae within bovine muscle.
Macroscopically visible larval cysts in meat give it a "measled"
appearance.
C. Clinical manifestations: Usually minimal symptomatology.
D. Pathology: Minimal. Extremely rare: gastrointestinal obstructions.
E. Laboratory diagnosis: Examination of STOOL for proglottids or eggs.
Eggs of Taenia species are indistinguishable, so definitive diagnosis
requires examination of proglottids. The treatment for intestinal Taenia
saginata and T. solium are the same, so definitive diagnosis is not
necessary for treatment.
F. Treatment: Niclosamide. Praziquantel is used in the treatment of
cysticercosis. Surgical excision of cysts may be necessary.
III. Taenia solium: TAENIASIS
A. Epidemiology: Disease is very rare in the U. S., although it is
prevalent through much of the third world, including Mexico.
B. Mode of transmission: Infection by ingestion of poorly cooked pork
containing encysted larvae.
C. Clinical manifestations: Usually minimal symptoms.
D. Pathology: Adult worm inhabits the human jejunum and sheds eggs
which pass in the stool. Pigs ingest the eggs which release embryos in
the GI tract. The embryos travel to systemic tissue where they
transform into encysted larvae (i.e., cysticerci). Humans are infected
by eating undercooked meat containing the cysticerci.
E. Laboratory diagnosis: Examine STOOL for proglottids or eggs; T.
solium can be
distinguished from T. saginata by the proglottid branching. T. solium
have proglottids with 5-10 primary uterine branches, but T. saginata
proglottids have 15-20.

F. Treatment: Niclosamide or praziquantel.

IV. Taenia solium: CYSTICERCOSIS
A. Epidemiology: A period of months to years may elapse between
exposure to the parasite and development of symptoms. Therefore,
cysticercosis must be considered in the United States in a patient
suspicious symptomatology and a history including prior residence in
endemic regions.
B. Mode of transmission: Humans accidentally become the intermediate
host by ingestion of fecally contaminated food or water (most common)
or autoinfection (eggs from anus to hand to mouth) or reverse
peristalsis (rare).
C. Clinical manifestations: Clinical manifestations reflect the organ
system affected by the cyst(s). The most common clinical
manifestation results from CNS involvement. Symptoms include
headache, seizures, paresis. (Cysticercosis is a common cause of
childhood seizures in Mexico.)
D. Pathology: Embryos emerge from the ingested egg and travel
through the human body where cysticerci develop. Common sites of
encystment include the CNS, eye, heart, muscle, and skin. Symptoms
result from mass effects of the expanding cyst(s) or from the host
inflammatory response to degenerating cysts.
E. Laboratory diagnosis: Radiological tests (especially CT or NMR of the
head with CNS symptoms shows ring-enhancing lesions), serologic
tests, sometimes examination of cyst at surgery.
F. Treatment: Treatment is based on the site of cysts and the resulting
symptomatology. Therapy can include surgical excision and treatment
with praziquantel.
V.

Diphyllobrothium latum:
A. Epidemiology: Worldwide. Disease occurs wherever undercooked,
salted, or pickled freshwater fish is eaten by humans. Human feces
release eggs into the freshwater thereby infecting the fish.
B. Mode of transmission: Humans are infected by eating fresh-water fish
containing the infectious larval forms.
C. Clinical manifestations: Disease is only rarely symptomatic. Intestinal
obstruction can occur.

D. Pathology: In the human intestine, the larva matures into an adult

worm, which attaches to the small bowel mucosa. Eggs shed into
freshwater release larva which pass through two intermediate hosts.
There is minimal direct pathology due to the adult worm.
NOTE: The adult worm can split the vitamin B12-intrinsic factor complex
and prevent absorption of B 12 by the human host. Symptomatic B 12
deficiency is very rare, but this is always a test question.
E. Laboratory diagnosis: Examine STOOL for characteristic operculated
egg & proglotttids.
F. Treatment:

Niclosamide or praziquantel.

VI. Echinococcus granulosus:

A. Epidemiology:
Humans are aberrant hosts. Disease occurs in
people (e.g., herders or hunters) who have close contact with dogs that
may feed contaminated wild herd animals.
B. Mode of transmission: Disease has a zoonotic pattern of
transmission. Humans ingest eggs shed by dogs that have fed on
infected domestic or wild herbivores. The pastoral form is endemic in
the American southwest, Australia, and New Zealand. The sylvatic
form, maintained by wolves or coyotes feeding on moose, caribou, or
deer, is endemic in Alaska, western Canada, and California.
C. Clinical manifestations: Disease is due to the mass effect of enlarging
cysts, with symptoms that depend on site of encystment. In the
pastoral form of the disease, cysts in the liver present as tender
palpable hepatic masses. Cysts in the lung may present as an
incidental finding on chest x-ray or as cough and hemoptysis.
D. Pathology: Dogs & other canines are definitive hosts. The adult
worm in dogs is very small, with only three (3) proglottids. Eggs are
shed in feces. Sheep and cattle (and wild herbivores in sylvatic form)
are intermediate hosts which ingest the eggs and harbor the cysts. In
humans, the larvae penetrate the intestinal mucosa, invade submucosal
venules, and are distributed to tissue where HYDATID forms. Hydatid
cysts enlarge at 1 cm/yr. Common hydatid sites: liver, lung, bone.
Hydatid cysts contain multiple BROOD CAPSULES containing
SCOLICES. If cysts rupture either spontaneously or during surgical
removal, ANAPHYLAXIS can occur.
E. Laboratory diagnosis: The diagnosis is usually suggested by the
patient history or by radiological findings (e.g., large hepatic cyst).
Patients usually have eosinophilia. Diagnosis usually confirmed
serology and/or examination of material removed at surgery.

F. Treatment:
Surgical excision is the treatment of choice.
Mebendazole may be used when surgery is contraindicated or if cysts
spill at surgery.
VII.

Echinococcus multilocularis: Etiologic agent of only minor importance.

A. Epidemiology: USSR, Canada, and parts of Alaska. Foxes and dogs
are definitive hosts. Rodents are usually the intermediate host.
Humans are aberrant intermediate hosts who acquire disease usually
by eating wild berries contaminated with fox or dog feces.
B. Pathology: Larvae typically localize in the liver. Cysts have no
capsule, so honeycombed masses of vesicles form. Prognosis is
poor.

VIII. Hymenolepis nana: The dwarf tapeworm (2-4 cm in length).

A. Epidemiology: H. nana occurs worldwide in humans and is also a
common murine parasite, occasionally developing its cysticercoid
stage in beetles. It is the MOST COMMON tapeworm infection in
North America.
B. Mode of transmission: Ingestion of contaminated grain and flour with
beetles. Autoinfection very common in children in day-care centers.
Children are especially at risk of infection.
C. Clinical manifestations: In cases with low intestinal parasite burden,
there are no symptoms. In heavy infections, especially if
autoinfection and hyperinfection occur, patients can experience
diarrhea, abdominal pain, headache, anorexia, and other vague
complications.
D. Pathology: Life cycle is simple and does not require an intermediate.
Embryonated eggs are ingested and develop in the intestinal villi into
a larval cysticercoid stage. This larva attaches its four muscular
suckers and crown of hooklets to the small intestine and the adult
worm produces a strobila of egg-laden proglottids. Eggs passed in
the feces are then immediately and directly infective, initiating
another cycle. Infection may also be acquired by ingesting infected
insect intermediate hosts. AUTOINFECTION (reinfection of the small
intestine when eggs are released internally) and HYPERINFECTION
also occur, causing subsequent increases in worm burden. Eggs
hatch in the intestine, develop into a cysticercoid larvae, and then
grow into adult worms without leaving the host.
E. Laboratory diagnosis: The diagnosis is usually suggested by the
presence of characteristic H. nana eggs upon stool examination (8-10
polar filaments lying between the membrane of the 6-hooked embryo
and the shell).
F. Treatment: Praziquantel is the drug of choice-, an alternative is
niclosamide.