CESTODE (Tape-worm)

Causal Agents:
The cestode Diphyllobothrium latum (the fish or broad tapeworm), the largest human tapeworm.
Several other Diphyllobothrium species have been reported to infect humans, but less frequently;
they include D. pacificum, D. cordatum, D. ursi, D. dendriticum, D. lanceolatum, D. dalliae, and D.
yonagoensis.

Life Cycle:

Geographic Distribution:
Diphyllobothriasis occurs in areas where lakes and rivers coexist with human consumption of raw
or undercooked freshwater fish. Such areas are found in the Northern Hemisphere (Europe,
newly independent states of the former Soviet Union (NIS), North America, Asia), and in Uganda
and Chile.

Clinical Features:
Diphyllobothriasis can be a long-lasting infection (decades). Most infections are asymptomatic.
Manifestations may include abdominal discomfort, diarrhea, vomiting, and weight loss. Vitamin
B12 deficiency with pernicious anemia may occur. Massive infections may result in intestinal
obstruction. Migration of proglottids can cause cholecystitis or cholangitis.
Laboratory Diagnosis:
Microscopic identification of eggs in the stool is the basis of specific diagnosis. Eggs are usually
numerous and can be demonstrated without concentration techniques. Examination of
proglottids passed in the stool is also of diagnostic value.

Treatment:
Praziquantel* is the drug of choice. Alternatively, Niclosamide can also be used to treat
diphyllobothriasis.

Causal Agents:
The cestodes (tapeworms) Taenia saginata (beef tapeworm) and T. solium (pork tapeworm).
Taenia solium can also cause cysticercosis.

Life Cycle:

Life cycle of Taenia saginata and Taenia solium. Humans are the only definitive hosts for
Taenia saginata and Taenia solium.

Geographic Distribution:
Both species are worldwide in distribution. Taenia solium is more prevalent in poorer
communities where humans live in close contact with pigs and eat undercooked pork and in very
rare in Muslim countries.
Clinical Features:
Taenia saginata taeniasis produces only mild abdominal symptoms. The most striking feature
consists of the passage (active and passive) of proglottids. Occasionally, appendicitis or
cholangitis can result from migrating proglottids. Taenia solium taeniasis is less frequently
symptomatic than Taenia saginata taeniasis. The main symptom is often the passage (passive)
of proglottids. The most important feature of Taenia solium taeniasis is the risk of development of
cysticercosis.

Laboratory Diagnosis:
Microscopic identification of eggs and proglottids in feces is diagnostic for taeniasis, but is not
possible during the first 3 months following infection, prior to development of adult tapeworms.
Repeated examination and concentration techniques will increase the likelihood of detecting light
infections. Nevertheless, speciation of Taenia is impossible if solely based on microscopic
examination of eggs, because all Taenia species produce eggs that are morphologically identical.
Eggs of Taenia sp. are also indistinguishable from those produced by cestodes of the genus
Echinococcus (tapeworms of dogs and other canid hosts). Microscopic identification of gravid
proglottids (or, more rarely, examination of the scolex) allows species determination.

Treatment:
Treatment is simple and very effective. Praziquantel* is the drug of choice.

Causal Agents:
Hymenolepiasis is caused by two cestodes (tapeworm) species, Hymenolepis nana (the dwarf
tapeworm, adults measuring 15 to 40 mm in length) and Hymenolepis diminuta (rat tapeworm,
adults measuring 20 to 60 cm in length). Hymenolepis diminuta is a cestode of rodents
infrequently seen in humans and frequently found in rodents.

Life Cycle: Hymenolepis nana

Hymenolepis diminuta

Geographic Distribution:
Hymenolepis nana is the most common cause of all cestode infections, and is encountered
worldwide. In temperate areas its incidence is higher in children and institutionalized groups.
Hymenolepis diminuta, while less frequent, has been reported from various areas of the world.

Clinical Features:
Hymenolepis nana and H. diminuta infections are most often asymptomatic. Heavy infections
with H. nana can cause weakness, headaches, anorexia, abdominal pain, and diarrhea.

Laboratory Diagnosis:
The diagnosis depends on the demonstration of eggs in stool specimens. Concentration
techniques and repeated examinations will increase the likelihood of detecting light infections.

Treatment:
Praziquantel* is the drug of choice.

Causal Agent:
Dipylidium caninum (the double-pored dog tapeworm) mainly infects dogs and cats, but is
occasionally found in humans.
Life Cycle:

Geographic Distribution:
Worldwide. Human infections have been reported in Europe, the Philippines, China, Japan,
Argentina, and the United States.

Clinical Features:
Most infections with Dipylidium caninum are asymptomatic. Pets may exhibit behavior to relieve
anal pruritis (such as scraping anal region across grass or carpeting). Mild gastrointestinal
disturbances may occur. The most striking feature in animals and children consists of the
passage of proglottids. These can be found in the perianal region, in the feces, on diapers, and
occasionally on floor covering and furniture. The proglottids are motile when freshly passed and
may be mistaken for maggots or fly larvae.

Laboratory Diagnosis:
The diagnosis is made by demonstrating the typical proglottids or egg packets in the stool or the
environment.

Treatment:
Treatment for both animals and humans is simple and very effective. Praziquantel is given either
orally or by injection (pets only). The medication causes the tapeworm to dissolve within the
intestines. Since the worm is usually digested before it passes, it may not be visible in the dog's
stool. These drugs are generally well tolerated.
Causal Agent:
Human echinococcosis (hydatidosis, or hydatid disease) is caused by the larval stages of
cestodes (tapeworms) of the genus Echinococcus. Echinococcus granulosus causes cystic
echinococcosis, the form most frequently encountered; E. multilocularis causes alveolar
echinococcosis; E. vogeli causes polycystic echinococcosis; and E. oligarthrus is an extremely
rare cause of human echinococcosis.

Life Cycle:

Geographic Distribution:
E. granulosus occurs practically worldwide, and more frequently in rural, grazing areas where
dogs ingest organs from infected animals. E. multilocularis occurs in the northern hemisphere,
including central Europe and the northern parts of Europe, Asia, and North America. E. vogeli
and E. oligarthrus occur in Central and South America.

Clinical Features:
Echinococcus granulosus infections remain silent for years before the enlarging cysts cause
symptoms in the affected organs. Hepatic involvement can result in abdominal pain, a mass in
the hepatic area, and biliary duct obstruction. Pulmonary involvement can produce chest pain,
cough, and hemoptysis. Rupture of the cysts can produce fever, urticaria, eosinophilia, and
anaphylactic shock, as well as cyst dissemination. In addition to the liver and lungs, other organs
(brain, bone, heart) can also be involved, with resulting symptoms. Echinococcus multilocularis
affects the liver as a slow growing, destructive tumor, with abdominal pain, biliary obstruction, and
occasionally metastatic lesions into the lungs and brain. Echinococcus vogeli affects mainly the
liver, where it acts as a slow growing tumor; secondary cystic development is common.
Laboratory Diagnosis:
The diagnosis of echinococcosis relies mainly on findings by ultrasonography and/or other
imaging techniques supported by positive serologic tests. In seronegative patients with hepatic
image findings compatible with echinococcosis, ultrasound guided fine needle biopsy may be
useful for confirmation of diagnosis; during such procedures precautions must be taken to control
allergic reactions or prevent secondary recurrence in the event of leakage of hydatid fluid or
protoscolices.

Treatment:
Surgery is the most common form of treatment for echinococcosis, although removal of the
parasite mass is not usually 100% effective. After surgery, medication may be necessary to keep
the cyst from recurring. The drug of choice for treatment echinococcosis is albendazole
(Echinococcus granulosus). Some reports have suggested the use of albendazole or
mebendazole for Echinococcus multilocularis infections.

CESTODES LARVAE
Humans can serve as the intermediate host for several species of cestodes. For example,
infections with cysticerci of Taenia cause cysticercosis, and infections with hydatid of
Echinococcus cause hydatid disease. Humans can also served as the second intermediate host
for some pseudophyllidean cestodes. In such cases the metacestode stage, normally called a
plerocercoid, is called a sparganum, and the resulting infection is called sparganosis.

Sparganosis; It is almost impossible to identify spargana to species, so it is unclear how

many or which species of pseudophyllidean cestodes will infect humans. Humans can be
infected by ingesting infected first intermediate hosts (e.g., infected copepods in drinking water)
or infected second intermediate hosts (e.g., raw or undercooked amphibians, reptiles or
mammals). Sparganosis has been reported from many countries of the world, but is most
common in eastern Asia.
Once in the human host the spargana can migrate to virtually any part of the body and grow to be
quite large (up to 14 inches or 5.5 cm). The pathology associated with sparganosis depends on
the number and size of spargana and the organs involved. Infections consisting of one or two
spargana in the deep muscles might cause no overt symptoms and go undiagnosed. Infections
in the eye can result in blindness, while infections of subdermal tissues can result in painful
"lumps" that might be misdiagnosed as cancer.

Cysticercosis; Pigs normally serve as the intermediate host for the pork tapeworm
(Taenia solium), and humans are infected with the adult stage of the tapeworm when they ingest
an immature tapeworm (a cysticercus cellulose) in raw or undercooked pork. However, if humans
ingest eggs of T. solium, they can be infected with cysticerci, resulting in a condition known as
cysticercosis. What might be the source of these eggs? Humans harbor the adult stage of this
tapeworm, and it is the adult stage that produces eggs. Thus, many cases of cysticercosis
probably result from a person ingesting eggs that are produced by a tapeworm living in his or her
own intestinal tract. Poor personal hygiene is one obvious way in which this could occur. It is
also possible for the proglottids of T. solium to migrate anteriorly from the small intestine into the
stomach and then back into the small intestine. Should this occur the eggs in the proglottids
would hatch resulting in the potential for a massive infection of cysticerci. People can also be
infected via food contaminated with eggs, or via eggs present in a household or work
environment. Since the tapeworm's proglottids can crawl out of the anus and contaminate
clothing, furniture, etc., or drop to the ground, such contamination could occur in the absence of
any visible source of "fecal" contamination.

Once the eggs hatch in the human's small intestine, the larvae penetrate the lining of the small
intestine and enter the blood stream. From here the larvae can be distributed to any organ in the
body. The larvae then grow into the metacestode stage, a cysticercus. Mature cysticerci can
range in size from 5 mm in diameter up to 20 cm (almost 8 inches!) in diameter.

The pathology associated with cysticercosis depends on which organs are infected and the
number of cysticerci. A infection consisting of a few small cysticerci in the liver or muscles would
likely result in no overt pathology and go unnoticed. In fact, many cases of human cysticercosis
are discovered only during routine autopsies. On the other hand, even a few cysticerci (perhaps
only one), if located in a particularly "sensitive" area of the body, might result in irreparable
damage. For example, a cysticercus in the eye might lead to blindness, a cysticercus in the
spinal cord could lead to paralysis, or a cysticercus in the brain (neurocysticercosis) could lead to
traumatic neurological damage. Thus, even though infections with adult T. solium are rarely
a problem, treatment of such infections is absolutely essential.

Historically, diagnosis of cysticercosis has been difficult. However, there are now several
immunological tests available that will detect the presence of cysticerci, and improved imaging
techniques such as CAT and MRI can be very useful in detecting cysticerci in various organs.

Hydatidosis (hydatid disease); The life cycle of Echinococcus granulosus includes

dogs (and other canines) as the definitive host, and a variety of species of warm blooded
vertebrates (sheep, cattle, goats, and humans) as the intermediate host. The adult worms are
very small, usually consisting of only three proglottids (total length = 3-6 mm), and they live in the
dog's small intestine. Eggs are liberated in the host's feces, and when these eggs are ingested
by the intermediate host they hatch in the host's small intestine. The larvae in the eggs penetrate
the gut wall and enter the circulatory system. The larvae can be distributed throughout the
intermediate host's body (although most end up in the liver) and grow into a stage called a
hydatid cyst.

Hydatid cysts have the ability to grow quite large; cysts the size of golf balls are not uncommon,
and cysts the size of basketballs are reported on rare occasions. The pathology associated with
hydatid disease in the intermediate host depends on the size of the cyst and its location. One or
two small cysts in the liver of a host might go unnoticed for years. However, a single large cyst in
the liver could prove fatal. Hydatid disease is far more serious when the cysts are found in other
locations, particularly the brain.

The infection is transmitted to the definitive host when the hydatid cyst is eaten. As one might
suspect, this species of parasite is more common in areas of the world where dogs are used to
herd sheep. Under most circumstances humans are a "dead end" in the life cycle, but hydatid
disease in humans remains a serious problem because the disease can cause such serious
pathology.

The interior of a hydatid cyst is filled with "protoscolices" (singular = protoscolex), each of which
has the ability to grow into an adult worm when ingested by a canine host. A small cyst might
contain hundreds of protoscolices; a large cyst might contain tens of thousands! This
tremendous reproductive potential poses a problem in the intermediate host (particularly in
humans). If a hydatid cyst breaks open, each protoscolex could grow into a new hydatid cyst.
How might this happen? A sharp blow to the abdomen might rupture a cyst in the liver. A number
of cases have been reported in which cysts have been damaged during routine surgery, allowing
the cyst's contents to leak into the patient's abdominal cavity.
 TREMATODE (Flukes)

Causal Agents:
The trematodes Fasciola hepatica (the sheep liver fluke) and Fasciola gigantica, parasites of
herbivores that can infect humans accidentally.

Life Cycle:

Geographic Distribution:
Fascioliasis occurs worldwide. Human infections with F. hepatica are found in areas where sheep
and cattle are raised, and where humans consume raw watercress, including Europe, the Middle
East, and Asia. Infections with F. gigantica have been reported, more rarely, in Asia, Africa, and
Hawaii.

Clinical Features:
During the acute phase (caused by the migration of the immature fluke through the hepatic
parenchyma), manifestations include abdominal pain, hepatomegaly, fever, vomiting, diarrhea,
urticaria and eosinophilia, and can last for months. In the chronic phase (caused by the adult
fluke within the bile ducts), the symptoms are more discrete and reflect intermittent biliary
obstruction and inflammation. Occasionally, ectopic locations of infection (such as intestinal wall,
lungs, subcutaneous tissue, and pharyngeal mucosa) can occur.

Laboratory Diagnosis:
Microscopic identification of eggs is useful in the chronic (adult) stage. Eggs can be recovered in
the stools or in material obtained by duodenal or biliary drainage. They are morphologically
indistinguishable from those of Fasciolopsis buski. False fascioliasis (pseudofascioliasis) refers
to the presence of eggs in the stool resulting not from an actual infection but from recent ingestion
of infected livers containing eggs. This situation (with its potential for misdiagnosis) can be
avoided by having the patient follow a liver-free diet several days before a repeat stool
examination. Antibody detection tests are useful especially in the early invasive stages, when the
eggs are not yet apparent in the stools, or in ectopic fascioliasis.

Antibody Detection
The acute manifestations of human fascioliasis may precede the appearance of eggs in the stool
by several weeks; immunodiagnostic tests may be useful for early indication of Fasciola infection
as well as for confirmation of chronic fascioliasis when egg production is low or sporadic and for
ruling out "pseudofascioliasis" associated with ingestion of parasite eggs in sheep or calves' liver.
The current tests of choice for immunodiagnosis of human Fasciola hepatica infection are
enzyme immunoassays (EIA) with excretory-secretory (ES) antigens combined with confirmation
of positives by immunoblot. Specific antibodies to Fasciola may be detectable within 2 to 4
weeks after infection, which is 5 to 7 weeks before eggs appear in stool. Sensitivity for the FAST-
ELISA format of EIA was reported to be 95%, while sensitivity for the immunoblot using 12-, 17-,
and 63-kDa antigens appeared to be 100%. However, some cross-reactivity occurs in the FAST-
ELISA with serum specimens of patients with schistosomiasis. Antibody levels decrease to
normal 6 to 12 months after chemotherapeutic cure and can be used to predict the success of
therapy.

Treatment:
Unlike infections with other flukes, Fasciola hepatica infections may not respond to praziquantel.
The drug of choice is triclabendazole with bithionol as an alternative.

Causal Agent:
The trematode Fasciolopsis buski, the largest intestinal fluke of humans.

Life Cycle:
Geographic Distribution:
Asia and the Indian subcontinent, especially in areas where humans raise pigs and consume
freshwater plants.

Clinical Features:
Most infections are light and asymptomatic. In heavier infections, symptoms include diarrhea,
abdominal pain, fever, ascites, anasarca and intestinal obstruction.

Laboratory Diagnosis:
Microscopic identification of eggs, or more rarely of the adult flukes, in the stool or vomitus is the
basis of specific diagnosis. The eggs are indistinguishable from those of Fasciola hepatica.

Treatment:
Praziquantel* is the drug of choice.

Causal Agents:
Schistosomiasis is caused by digenetic blood trematodes. The three main species infecting
humans are Schistosoma haematobium, S. japonicum, and S. mansoni. Two other species, more
localized geographically, are S. mekongi and S. intercalatum. In addition, other species of
schistosomes, which parasitize birds and mammals, can cause cercarial dermatitis in humans.

Life Cycle:
Geographic Distribution:
Schistosoma mansoni is found in parts of South America and the Caribbean, Africa, and the
Middle East; S. haematobium in Africa and the Middle East; and S. japonicum in the Far East.
Schistosoma mekongi and S. intercalatum are found focally in Southeast Asia and central West
Africa, respectively.

Clinical Features:
Many infections are asymptomatic. Acute schistosomiasis (Katayama's fever) may occur weeks
after the initial infection, especially by S. mansoni and S. japonicum. Manifestations include
fever, cough, abdominal pain, diarrhea, hepatospenomegaly, and eosinophilia. Occasionally
central nervous system lesions occur: cerebral granulomatous disease may be caused by ectopic
S. japonicum eggs in the brain, and granulomatous lesions around ectopic eggs in the spinal cord
from S. mansoni and S. haematobium infections may result in a transverse myelitis with flaccid
paraplegia. Continuing infection may cause granulomatous reactions and fibrosis in the affected
organs, which may result in manifestations that include: colonic polyposis with bloody diarrhea
(Schistosoma mansoni mostly); portal hypertension with hematemesis and splenomegaly (S.
mansoni, S. japonicum, S. mansoni); cystitis and ureteritis (S. haematobium) with hematuria,
which can progress to bladder cancer; pulmonary hypertension (S. mansoni, S. japonicum, more
rarely S. haematobium); glomerulonephritis; and central nervous system lesions.

Laboratory Diagnosis:
Microscopic identification of eggs in stool or urine is the most practical method for diagnosis.
Stool examination should be performed when infection with S. mansoni or S. japonicum is
suspected, and urine examination should be performed if S. haematobium is suspected.
Eggs can be present in the stool in infections with all Schistosoma species. The examination can
be performed on a simple smear (1 to 2 mg of fecal material). Since eggs may be passed
intermittently or in small amounts, their detection will be enhanced by repeated examinations
and/or concentration procedures (such as the formalin - ethyl acetate technique). In addition, for
field surveys and investigational purposes, the egg output can be quantified by using the Kato-
Katz technique (20 to 50 mg of fecal material) or the Ritchie technique.
Eggs can be found in the urine in infections with S. haematobium (recommended time for
collection: between noon and 3 PM) and with S. japonicum. Detection will be enhanced by
centrifugation and examination of the sediment. Quantification is possible by using filtration
through a Nucleopore® membrane of a standard volume of urine followed by egg counts on the
membrane.
Tissue biopsy (rectal biopsy for all species and biopsy of the bladder for S. haematobium) may
demonstrate eggs when stool or urine examinations are negative.

Treatment:
Safe and effective drugs are available for the treatment of schistosomiasis. The drug of choice is
praziquantel for infections caused by all Schistosoma species. Oxamniquine has been effective
in treating infections caused by S. mansoni in some areas in which praziquantel is less effective.