Prevention
Prevention is attained primarily by controlling the mice and rat populations along with good hygiene and sanitation.
Figure 51 D. caninum scolex demonstrating the armed rostellum.
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Taenia solium
General characteristics
T. solium, the pork tapeworm, is the intestinal cestode capable of causing serious pathologic damage to the human host.
Humans serve as the definitive host, whereas pigs serve as the intermediate host. Humans can alsoserve as the intermediate
host. T. solium may result in an intestinal infection in which the larvae mature and reside in the small intestine for up to 25
years. The organisms can grow to be 1.5 to 8 m long and produce more than 1000 proglottids, each containing about
50,000 eggs. Cysticercosis is the extraintestinal form of the disease and can be much more severe. The disease is life
threatening if the organism invades the central nervous system.
Pathogenesis and spectrum of disease
T. solium infection can result in the presence of both adult and larval stages in the human host Infection begins
when the intermediate host ingests embryonated eggs in feces. Once the egg is ingested, the hexacanth embryo
is released into the intestine where the embryo penetrates the mucosa. The embryo then matures into a cyst
(cysticercus) in the tissue. Humans may become infected when they eat raw or undercooked pork containing
embedded cysts. Pork tapeworm infection is usually caused through the ingestion of multiple worms. During
ingestion and subsequent digestion of the infected meat, the cysticercus is released and attaches to the mucosa
within the small intestine of the human host. The cysticercus matures into an adult worm within approximately
5 to 12 weeks. The eggs are then released in the host’s feces. Accidental ingestion of the eggs by the human
host may also result in migration of the embryo through the intestine to other areas of the body.including the
eyes, brain, muscle, or bone. In addition, the proglottids are motile and may migrate out of the anus. Infection
of the adult tapeworm causes few clinical symptoms, although abdominal pain, diarrhea, indigestion, and loss
of appetite may be present as a result of irritation to the mucosa of the intestinal wall. The major complication
with T. solium is cysticercosis (larval forms throughout the body), in which the human host becomes the
intermediate host and harbors the larvae in tissues as previously described.
Laboratory diagnosis
Serologic diagnosis is unreliable for infections with T. solium. Diagnosis of Taenia tapeworm infection is
through the examination of stool samples. Individuals suspected of infection with T. solium should be asked if
they have passed any notable tapeworm segments in their stool.
Additional laboratory findings may include a low-grade eosinophilia, increased serum IgE level, and the
presence of atypical lymphocytes in the cerebrospinal fluid.
Figure 52 T. saginata scolex with suckers.
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Therapy
Adult worms can be eradicated with praziquantel or niclosamide. Expulsion of the scolex must be assured to
assume satisfactory treatment.
Prevention
Good hygiene and immediate treatment are essential for the prevention of autoinfection.
Taenia saginata
General characteristics:
T. saginata or beef tapeworm has a worldwide distribution and is more common than T. solium. The worm can
grow 4 to 12 m and contain 1000 to 2000 segments. T. saginata may produce 100,000 eggs and live up to 25
years in the human intestine.
Epidemiology
T. saginata has a similar life cycle to that of T. solium. Cattle are the intermediate hosts and humans are
infected through the ingestion of cysticerci (larval form) in raw or undercooked beef.
Pathogenesis and spectrum of disease
The life cycle of T. saginata begins with human ingestion of undercooked or raw meet infected with larvae.
The larvae are ingested in the meat and, following digestion, released into the small intestine where the worm
attaches to the mucosa and matures. In about 3 months, the worm may grow up to 4 to 5 m in length and gravid
segments begin to break off and pass in stool. Following deposition of gravid segments in the soil, an
intermediate bovine host may ingest the segments. The segments are digested and the eggs hatch, releasing an
oncosphere that penetrates the muscle tissue. Following penetration of the mucosa the organisms are carried via
the lymphatic vessels and bloodstream throughout the intermediate host. Humans then ingest the infected meat
of the intermediate host, as previously indicated. Humans typically are asymptomatic, or have very mild
indigestion, loss of appetite, vomiting, and abdominal discomfort. A rare case of severe infection may result in
intestinal obstruction and appendicitis. Patients are often unaware of their infection until gravid motile
segments are passed in the feces and cause psychological distress.
Laboratory diagnosis
The stool should be examined for proglottids and eggs; eggs may also be present on anal swabs. The eggs of T.
saginata are indistinguishable from those of T. solium. The uterus of T. saginata is longer than wide and
typically contains 15 to 18 lateral branches on each side . The scolex has four suckers and is unarmed or does
not contain any hooklets (Figure 52). Stool specimens should be handled with care since the eggs cannot be
distinguished from those of T. solium. Slight eosinophilia may develop.
Therapy
Recommended treatment includes praziquantel or niclosamide. Treatment of T. saginata can be considered
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successful when no proglottids are passed for 4 consecutive months.
Prevention
Beef should be inspected for cysticerci and thoroughly cooked before ingesting
Tissue Cestodes:
Cestodes (Tapeworms) Tissue (Larval Forms):
Taenia solium
Echinococcus granulosus
Echinococcus multilocularis
Taenia multiceps
Spirometra mansonoides
Tissue cestodes do not reach the adult stage in the human host. The organism infect the human in their
intermediate or cyst stage. The infections are much more serious than those caused by the adult tapeworm. The
parasites can cause serious disease, or even death. Larval cestodes cause infection by accidental ingestion of
eggs excreted from the intermediate hos and they lodge in various organs and tissues in the human body.
Diagnosis of larval infections can be problematic.
TAENIA SOLIUM
General characteristics
Taenia solium, also known as the pork tapeworm, causes an intestinal infection from eating contaminated
pork . The adult worm usually causes no clinical disease. Humans may accidentally become the intermediate
host and ingest eggs from human feces. This typically occurs when an individual is already infected with adult
T. solium. Autoinfection occurs when the individual swallows eggs from improper hand washing. Humans may
develop the larval infection, which could result in cysticercosis. Cysticercosis is usually asymptomatic unless
larvae invade the central nervous system (CNS), the globe of the eye, or other muscle and tissues.
Pathogenesis and spectrum of disease
Clinical signs and symptoms depend on the location, viability, and number of the cysticerci present. Cysticerci
can develop in any organ or tissue of the body. The severity of the symptoms depends on the body site involved
and may not appear for years after the initial infection. The most severe cases are found in the central nervous
system and the eye. Once cysticerci localize in the brain, the organism causes a condition referred to as
neurocysticercosis. Infection can cause epileptic-type seizures, headaches, mental disturbances, meningitis, or
sudden death. Cysticerci can also be found in the eye and must be removed to avoid permanent eye damage,
including blindness. Much of the damage from cysticercosis is caused by the severe inflammatory host
response that occurs after the cysticerci have died. Antibodies are produced and offer the patient secondary
immunity.
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Laboratory diagnosis
Cysticercosis can be difficult to diagnose. T. solium eggs are found in stools in fewer than half the patients with
cysticercosis. Demonstration of eggs or proglottids in the feces is an indication of Taenia infection but does not provide a
diagnosis for cysticercosis . Definitive diagnosis usually requires the identification of cysticercus in the tissue. The
organism is surgically removed and microscopically examined for the presence of suckers and hooks on the scolex. The
cysticercus is round to oval, translucent, and about 5 mm or more in diameter. The organism has a scolex with four suckers
and a rostellum with a circle of hooks. Fine needle aspiration cytology may be helpful in the diagnosis and eliminates the
need for surgical biopsy. Diagnosis may also be made using computed tomography (CT) scans and magnetic resonance
imaging (MRI). Radiographs may also be useful in detecting calcifying cysticerci within tissue. Ocular cysticercosis may be
diagnosed by visual identification of the larval worm. Serologic procedures (such as enzymelinked immunosorbent assay
[ELISA]) may also be used as a useful tool to aid in diagnosis, but may not be sensitive enough in light infections. The
Centers for Disease Nucleic acid-based methods and species-specific polymerase chain reaction (PCR) have been described
to differentiate Taenia species.
Therapy
Cysticercosis should be treated with corticosteroids, anticonvulsants, and surgery if deemed appropriate.
Surgery may be required for ocular, spinal, or brain involvement.
Prevention
Education, meat inspection, and improvement of sanitation measures are the key preventive measures.
ECHINOCOCCUS GRANULOSUS
General characteristics
Echinococcus is the smallest of all tapeworms (3 to 9 mm long) with three to five proglottids. It contains a
scolex with four suckers and a rostellum with hooks to attach to the intestinal wall. E. granulosus is a tapeworm
found in the small intestine of the definitive host, the canine. Eggs are ingested by the intermediate hosts and
include a variety of mammals including sheep, cattle, moose, and humans. There are several strains of
Echinocococcus granulosus that have been identified, with the dog-sheep strain being the most common.
Humans are typically accidental hosts and are considered a dead-end since the life cycle of the organism is
unable to continue in a human host. Oncospheres hatch in the intestine of the intermediate host and invade the
circulatory system, where they develop into hydatid cysts. Disease symptoms vary with the site and size of the
cyst. Echinococcosis (hydatid disease) results from the presence of one or more cysts (hydatids), which can
develop in any tissue.
Pathogenesis and spectrum of disease
Hydatid disease in humans is potentially dangerous depending on the size and location of the cyst. Some cysts
may remain undetected for many years until they grow large enough to affect other organs. Many humans live
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day-to-day without ever knowing they are infected. The cyst is very slow growing in humans. It is usually
fluid-filled and has a germinal layer from which many thousands of scolices are budded. These are known as
daughter cysts (brood capsules), which attach to the germinal layer or free-float in the cyst. The scolices in the
hydatid fluid resemble grains of sand and are called hydatid sand (Figures 53). The result is a unilocular cyst
containing future adult worms. The cyst may resemble a slow-growing tumor. Infections in the liver or lungs
may be asymptomatic for many years, but the pressure eventually causes noticeable symptoms. The majority of
the hydatid cysts occur within the liver. Cysts within the liver cause chronic abdominal pain and allergic
reactions and may result in cholangitis (infection of the common bile duct) and cholestasis (interference with
flow of bile from the liver). Cysts that develop in the lungs may cause infections and abscesses and result in
chronic cough, shortness of breath, and chest pain. During the life cycle of the cyst, there may be occasional
seepage of fluid into the host tissue and circulation causing sensitization or activation of the immune response
from the presence of the parasite. The rupture and release of the fluid of a hydatid cyst may cause anaphylactic
shock as a result of the primary sensitization in a previously asymptomatic individual. If a cyst bursts within the
human body, many new cysts may be released that are typically eliminated via the host’s cellular immune
response. Leaking fluid from a cyst may cause notable eosinophilia.
Laboratory diagnosis
Clinical symptoms of a slow-growing abdominal tumor with or without eosinophilia are suggestive of infection.
Human infection ranges from asymptomatic to severe, including death. Diagnosis is made through the
identification of cysts in the infected organ, accompanied with positive serologic tests. A variety of serologic
tests are available including ELISA, indirect hemagglutination, and latex agglutination. Both false positives and
false negatives may occur; therefore clinical history is extremely important for diagnosis. Ultrasound, magnetic
resonance imaging (MRI), and computed tomography (CT) have
Figure 53:, Echinococcus granules.A B, Ovum. C, Scolex.
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improved the diagnosis and may provide visualization of the fluid-filled cysts. Calcified cysts can be visualized
using conventional x-ray. Microscopic examination of the cyst fluid for the identification of the scolices can be
useful in diagnosis. A 1% eosin stain may be added to the fluid to assist in the visualization and determination
as to whether or not the cyst is viable. Nonviable scolices will stain with the eosin whereas viable scolices will
not.
Therapy
Surgery is the most common form of treatment. The procedure involves surgical removal of cysts or
inactivation of hydatid sand by injecting the cyst with 10% formalin and then removing it. Extreme care must
be taken to avoid spillage. Albendazole is the drug of choice to kill the scolices within the cyst, reduce the size
of the cyst, and prevent recurrence. Mebendazole and praziquantel have also been shown to be effective.
Prevention
Preventive measures include avoiding contact with infected dogs and deworming animals regularly. Effective
control includes educating the population concerning the danger and means of transmission of hydatid disease
as well as maintaining good hygiene and practicing safe disposal of dog feces. Slaughtered animals must be
disposed of properly, to prevent dogs from exposure to contaminated materials and interrupt the Echinococcus
life cycle.
ECHINOCOCCUS MULTILOCULARIS
General characteristics
Although rarely found in the brain of humans, E. multilocularis causes alveolar hydatid disease, which is a fatal
form of echinococcosis. It is the most lethal of all helmintic diseases. The cyst is extremely dangerous because
it lacks a laminated membrane and develops a series of connected chambers. The chambers contain little or no
fluid and rarely contain a scolex. The morphology of the cyst is very similar to that of E. granulosus, but the
adult organisms are much smaller (1.2 to 3.7 mm).The cysts are very resistant to cold temperatures.
Pathogenesis and spectrum of disease
Figure 54:Echinococcus granulosus, hydatid sand (300×). (Inset)
Two individual hooklets (1000×)
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Alveolar hydatid disease is a highly lethal, destructive disease. The cyst of E. multilocularis grows slowly and
may take years to produce clinical symptoms. Many cysts are asymptomatic during the life of the infected
individual and are sometimes found during autopsy, surgery, or imaging scans related to other clinical
conditions. The severity of symptoms depends on the location of the cyst and the size, as seen with E.
granulosus. Cysts form primarily in the liver and metastasize to the lung or brain. Cysts in the liver are not
restricted with a laminated cyst wall and are capable of expansion into a multicystic structure. This
multilocular (many chambers) hydatid cyst is often mistaken for a hepatic sarcoma, making diagnosis difficult.
This disease is often fatal.
Laboratory diagnosis
Ultrasound, CT scans, and MRI are used to visualize the cyst and can be supported with serologic testing.
Serologic tests, such as ELISA, are sensitive and highly specific.
Therapy
The most common treatment is to remove the parasite Surgically. Treatment with mebendazole and albendazole
has been used successfully
Prevention
Controlling rodents is an important means of prevention along with educating the public at risk to avoid
exposure to infective feces. Practicing good hygiene and periodically deworming household pets are also
helpful.
Taenia multiceps
General characteristics
T. multiceps is a tapeworm that causes coenurosis in humans. The coenurus (larval form) may cause
destructive damage or death, but is an extremely rare disease in
humans. The coenurus is a unilocular cyst similar to cysticercus, although the worm has multiple scolices.
Daughter cysts may also be seen. The body of T. multiceps is 5 to 6 cm long and consists of 200 to 250
segments. The scolex has 4 suckers and a proboscis (tubular appendage) with 22 to 32 hooks arranged in 2
rows.
Pathogenesis and spectrum of disease
The oncosphere hatches and penetrates the intestinal wall of the intermediate host. The embryo is carried via
the bloodstream to various parts of the body including the brain, eyes, and central nervous system, where the
organism lodges and the coenurus develops. The coenurus develops into multiple daughter cysts. Symptoms
include headache, vomiting, paralysis, and blindness. The coenurus causes a serious disease called coenurosis
in sheep and in dogs that have eaten the brains of infected sheep. This clinical condition is known as gid,
sturdy, or staggers.
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Laboratory diagnosis
Diagnosis is similar to that for Echinococcus infection. CT and MRI may be useful for detecting the cysts.
Microscopic identification can be used if the cyst has been removed surgically. Currently, there are no serologic
tests available.
Therapy
Treatment is similar to that for Echinococcus. The most common treatment is surgery if possible, although the
drugs used for cysticercosis may also be effective against coenurus infection.
Prevention
dogs associated with sheep and other livestock should not be fed the brain or spinal cord from infected animals
and should be dewormed regularly. good hygiene should be practiced and care taken not to eat or drink
anything contaminated with dog feces.
Spirometra mansonoides
General characteristics
Sparganosis is an infection caused by the plerocercoid larvae of Spirometra. The larvae (spargana) are white,
wrinkled, and ribbon-shaped. They may be 3 mm wide and up to 30 cm long. The sparganum has bothria
(longitudinal grooves) instead of suckers. No scolex is present, which can help differentiate Spirometra from
Taenia solium.
Pathogenesis and spectrum of disease
Spargana migrate and lodge anywhere in the human body. Clinical symptoms depend on which organs or
tissues are involved. Spargana can live for several years before symptoms develop. Sparganosis is usually
asymptomatic until the larvae grow and cause an inflammatory reaction. Painful nodules can develop in the
tissues. A variety of symptoms may occur, including seizure, weakness, headache, and eye pain that can lead to
blindness if left untreated.
Laboratory diagnosis
Definitive diagnosis is usually made by removal and identification of the sparganum from infected tissue.
Clinical history, ELISA, MRI, and CT can all be used together to presumptively diagnose sparganosis.
Eosinophilia may also be present.
Therapy
Praziquantel has been used with limited success. Surgical removal of the complete sparganum is the treatment
of choice.
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Prevention
Prevention strategies should include safe drinking water practices, and awareness of the dangers of consuming
raw fish and amphibians. Water in contaminated areas should be boiled before consumption.
Intestinal Trematodes:
Helminths Trematodes (Flukes) Intestinal:
Fasciolopsis buski
Heterophyes heterophyes
Metagonimus yokogawai
The intestinal trematodes (flukes) are members of the phylum Platehelminthe (flatworms), are
dorsoventrically flattened, and require at least one intermediate host (a freshwater snail).
Human infection occurs by ingestion of metacercariae encysted on freshwater vegetation or fish. Most
trematodes are hermaphroditic (both ovaries and testes are contained within each adult worm).
The parasites are typically identified from eggs shed in the feces. The adult worms are located in the small
intestine, where they lay eggs that may be embryonated or remain unembryonated until they are shed from the
body via feces. The egg continues developing after reaching the water, and a ciliated, free-swimming
miracidium larva is released. The miracidium enters a snail host and develops into a redia (cylindrical larvae),
followed by development into tailed cercariae.
The cercariae emerge from the snail and encyst as a metacercariae (encrusted larvae) on water plants or fish.
A human host ingests raw or undercooked plants (Fasciolopsis buski) or fish (Heterophyes heterophyes,
Metagonimus yokogawai) containing the metacercariae, which exycyst in the intestinal tract, attach, and mature
into adults .
Fasciolopsis buski
General characteristics
The adults of F. buski have an elongated shape and range from 20 to 75 mm long to approximately 8 to 20 mm
wide , They have an oral sucker at the anterior end and a ventral sucker located about midway to the posterior
end. The eggs, which are indistinguishable from those of Fasciola hepatica (Figure 55), are oval and elongated,
transparent, and yellow-brown with an operculum (lid) at one end, and they range in size from 130 to 140 μm
long to 80 to 85 μm wide and may be unembryonated.
Pathogenesis and spectrum of disease
the intestinal attachment site of the adult worms often becomes locally inflamed and ulcerated, and may
hemorrhage. moderate to heavy infections may cause abdominal pain, diarrhea, intestinal obstruction, and
edema of the abdomen and lower extremities, and may result in inadequate absorption of vitamin b12.
eosinophilia is commonly observed.
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Prevention
Infection can be prevented by making sure that water plants and fish are properly cooked before eating. In
addition, changes are needed in agricultural practices and health education in the endemic areas.
Heterophyes heterophyes: and metagonimus yokogawai
General characteristics
Adult H. heterophyes worms range in size from 1.0 to 1.7 mm in length by 0.3 to 0.4 mm in width, and have a
broadly rounded posterior. M. yokogawai adults range in size from 1.0 to 2.5 mm long to approximately 0.4 to
0.8 mm wide.
The adult H. heterophyes also has an additional sucker, the genital sucker, which surrounds the genital pore.
The eggs are small, yellow-brown, embryonated, and operculated and may have minimal opercular shoulders.
Eggs range in size from 26 to 30 long μm to 15 to 17 μm wide, and may be indistinguishable between the two
species.
Pathogenicity and spectrum of disease
Infections with a small number of worms may be asymptomatic. Symptoms in heavy infections may include
abdominal pain, diarrhea with a large amount of mucus, and ulceration of the intestinal wall. Eggs may gain
entry into intestinal capillaries and lymphatics, where they can be carried to the heart, brain, spinal cord, or
other tissues, causing emboli or granuloma formation.
Prevention
Avoid ingestion of raw, inadequately cooked, and pickled or salted fish. The risk of infection could be greatly
reduced by improved sanitary conditions and health education programs.
Laboratory diagnosis
Identification of the intestinal trematodes is made by recovery of eggs, or in rare cases adults, from stool
specimens using a sedimentation method such as formalinethyl acetate. The sediment may be examined in a
wet mount with or without iodine. Because the eggs of Fasciolopsis buski are identical to those of Fasciola
Figure 55 Fasciola egg. The eggs of F. buski and F. hepatica are indistinguishable
morphologically.
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hepatica, and those of Heterophyes heterophyes and Metagonimus yokogawai are very similar, diagnosis may
also require assessment of symptoms, obtaining a travel history, and/or recovery of adult worms.
Treatment
The drug of choice for treatment of intestinal trematode infection is praziquantel (Biltricide), an isoquinoline
derivative administered orally in three doses for 1 day.
Liver and Lung Trematodes:
Trematodes (Flukes) Liver/Lung:
Clonorchis (Opisthorchis) sinensis
Opisthorchis viverrini
Fasciola hepatica
Paragonimus westermani
Paragonimus mexicanus
Clonorchis sp., Opisthorchis sp. and Fasciola sp. Live in the biliary ducts of humans. Paragonimus spp. are
found in the lungs and in other body sites.
The liver flukes:
General characteristics
The adults of these trematodes live in the biliary ducts and in heavy infections may be also found in the
gallbladder. Two of these, Clonorchis sinensis (the Chinese liver fluke) and Opisthorchis viverrini (the
Southeast Asian liver fluke), are elongated and narrow and much smaller than Fasciola (the sheep liver fluke).
These flukes also all require a freshwater snail as an intermediate host.
Life cycle
The life cycle of the liver flukes is very similar to that of the intestinal flukes. The adult worms produce eggs
in the biliary ducts that are then excreted from the body in the feces. The free-swimming miracidium is released
from the egg in freshwater and enters the snail host where it develops into a redia and then a cercariae, which
leaves the snail and enters the water (Figure 56).
The cercariae of Clonorchis and Opisthorchis are ingested by a second intermediate host, a freshwater fish.
The cercariae then encyst and develop into the metacercariae within the intermediate host. The metacercaria is
the infective stage for humans. When infected freshwater fish are eaten raw or undercooked, the metacercariae
will excyst in the duodenum and then travel to the bile duct where they mature. The cercariae of Fasciola
encyst on freshwater vegetation, such as watercress and water chestnuts, and develop into metacercariae. When
the infected vegetation is eaten raw, the metacercariae will excyst in the duodenum and then travel to the bile
duct and mature.
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Pathogenesis and spectrum of disease:
Light infections with C. sinensis or O. viverrini are most common, and may be asymptomatic. Heavier
infections with these flukes may present with fever, abdominal pain, and jaundice. Eosinophilia and increased
serum levels of immunoglobulin E (IgE) may be observed. Severe infections may cause obstruction of the
biliary ducts, resulting in enlargement and tenderness of the liver, cirrhosis, cholecystitis (inflammation of the
gallbladder), and cholangiocarcinoma (cancerous growth in bile duct epithelium).
Even light infections with Fasciola may cause fever, abdominal pain, nausea, diarrhea, enlargement and
tenderness of the liver, jaundice, nonproductive cough, eosinophilia, and elevated serum IgE levels. More
severe infections may result in obstruction of the biliary ducts, cirrhosis, cholecystitis, and cholangiocarcinoma.
During migration in the human body, the larvae may penetrate the peritoneal cavity, and adult flukes may then
be found in the intestinal walls, lungs, heart, or brain.
Laboratory diagnosis
Identification of the liver flukes is primarily made by recovery of the eggs in feces using a sedimentation
method and a wet mount with or without iodine staining. There is also serologic testing available in the United
States for diagnosis of Fasciola. Enzyme immunoassay (EIA) and enzyme-linked immunosorbent assay
(ELISA) serum IgG antibody testing is performed at private references laboratories.
Therapy :
The drug of choice for treatment of infections with Clonorchis and Opisthorchis is praziquantel given orally
three times for 1 day. An alternative drug is albendazole, a benzimidazole group drug, given once daily for 7
days. The drug of choice for Fasciola is bithionol (praziquantel is not effective) given orally every other day for
10 to 15 doses.
Prevention :
Human infection can be prevented by ensuring that fish and aquatic vegetation are properly cooked before
consumption, as well as by the improvement of sanitary conditions along with the education of good personal
hygiene.
Figure 56 Cercaria of a liver fluke. Figure 57Clonorchis sinensis egg.
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THE LUNG FLUKES:
General characteristics
The genus Paragonimus contains several species known to infect humans. Paragonimus westermani is the
most common and widely distributed lung fluke. The adult worms live in the lungs and produce eggs that may
be present in sputum, or if expectorated and swallowed, may be present in feces. Like other trematodes, a
freshwater snail is required as an intermediate host.
Life cycle:
Reservoir hosts for P. westermani include dogs and cats, and those for P. mexicanus include domestic and
wild pigs, and dogs. Species of Paragonimus may also be found in other freshwater crab- or crayfish-eating
mammals. The adult worms, encapsulated in the lungs, produce eggs that leave the lung via the bronchioles,
stimulating a cough response. The eggs are then swallowed and eventually excreted in the feces. The freeswimmingmiracidium is released from the egg in freshwater and enters the snail host where it develops into a
redia and then a cercariae, which leaves the snail and enters the water. The cercariae then enter a second
intermediate host, a crab or crayfish, where they encyst and develop into metacercariae. The metacercaria is the
infective stage for humans. When infected freshwater crabs and crayfish are eaten raw or undercooked, the
metacercariae will excyst in the duodenum and then migrate through the intestinal wall, and eventually through
the diaphragm and into the lungs where they encapsulate (usually in pairs) and mature .
Pathogenesis and spectrum of disease
Light infections may be asymptomatic. The migration of the metacercariae through muscle and tissue may
cause local pain and immune response to tissue damage.
In the lungs, the immune response causes infiltration of eosinophils and neutrophils. Serum IgE levels are
usually elevated. Eventually the adult worms are encapsulated in a granuloma. Presence of the worms in the
lungs usually results in a chronic cough, with possible production of blood-tinged sputum. The cough provides
a mechanism to transport eggs up into the throat where they are swallowed and then may be excreted in the
feces. The larvae of P. mexicanus may migrate to other areas of the body, frequently causing the formation of
subcutaneous or lower abdominal nodules. The larvae of Paragonimus may even enter the brain (rarely), where
they can cause severe damage.
Laboratory diagnosis
The eggs may be recovered from sputum, and occasionally in feces using a sedimentation concentration
method. The eggs may be observed in a wet mount (with/without iodine stain) (Figure 58).
Charcot-Leyden crystals may also be observed in sputum or lung tissue specimens. Charcot-Leyden crystals are
slender and pointed at both ends. The crystals normally appear colorless and stain purplish to red with
trichrome. Elevated levels of eosinophils in whole blood and elevated IgE levels in serum may be present.
Lesions in the lungs may be observed in x-ray. Serum IgG EIA and immunoblot testing, and EIA serum and
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cerebrospinal fluid (CSF) IgG antibody testing is performed at private reference laboratories; cross reactivity
with other species and trematodes may occur.
Therapy
The drug of choice for treatment of Paragonimus infections is praziquantel given three times a day for 2 days.
Prevention
Human infection can be prevented by not eating pickled, raw, or undercooked crabs and crayfish. Care
should also be taken to properly clean utensils used in the preparation of these foods. Improvement of sanitary
conditions and practices may also help to reduce the prevalence of these infections.
BloodTrematodes:
Schistosoma mansoni
Schistosoma haematobium
Schistosoma japonicum
Schistosoma intercalatum
Schistosoma Mekongi
There are four species of blood flukes that are primarily associated with disease in humans (known as
schistosomiasis, bilharziasis, or snail fever), all belonging to the genu Schistosoma. These four species are
Schistosoma haematobium, S. japonicum (Oriental blood fluke), S. mekongi, and S. mansoni. A fifth species, S.
intercalatum, is a pathogen primarily in animals but has been associated with human disease. The blood flukes
differ
in morphology and life cycle characteristics from the other trematodes, but because they all belong to the same
genus, they are very similar, and may be difficult to distinguish from each other. They do, however, require a
freshwater snail as the only intermediate host.
Figure 58: Paragonimus westermani egg.
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General characteristics
Unlike the other trematodes, adult schistosomes are not flattened, but are rather long, thin, and rounded in
shape. There is an oral sucker surrounding the mouth and a ventral sucker located just slightly below the oral
sucker. The adult male averages 1.5 cm in length and is wider than the female, having a ventral fold that wraps
around the female when they mate (Figure 59). The adult female averages 2 cm in length and is very thin.
The eggs of each species are distinct, and can be distinguished by size, spine morphology, and sometimes
specimen type (Figure 60). The size range for eggs of S. haematobium is 110 to 170 μm long by 40 to 70 μm
wide and they have a sharply pointed terminal spine. They are fully embryonated without an operculum. The size
range for the eggs of S. japonicum is 70 to 100 μm long by 50 to 65 μm wide, and they have a small lateral spine
that is sometimes difficult to detect .
S. mekongi eggs are smaller than those of S. japonicum, ranging in size from 50 to 65 μm long by 30 to 55 μm
wide. They are fully embryonated without an operculum and have a small lateral spine. The size range for eggs of
S. mansoni is 115 to 180 μm long by 40 to 75 μm wide, and they have a large lateral spine. S. mansoni eggs are
unoperculate, immature when released, and take up to 8 to 10 days to develop a miracidium. S. intercalatum eggs
are fully embryonated without an operculum, have a terminal spine, and range in size from 140 to 240 μm long by
50 to 85 μm wide. S. intercalatum eggs resemble those of S. haematobium and can be differentiated by ZiehlNeelsen acid-fast positivity. In addition, S. intercalatum eggs are only found in feces, not in urine specimens
One of the main differences in the schistosomes from other trematodes is that instead of being hermaphroditic,
there are separate male and female adult worms. In human infection, the adult worms live in either the veins that
supply the intestine (S. japonicum and S. mansoni) or the veins that supply the urinary bladder (S. haematobium).
The eggs are passed from the body in either the feces or the urine. To reach the inside of the intestine or bladder,
the eggs must penetrate the tissue from the veins. This is accomplished via a spine that is distinctive among the
major species. The embryonated egg will release the miracidium (Figure 62) once it reaches freshwater, and will
enter the snail host, where it will develop into the infectious cercaria. The freeswimming cercariae are capable of
penetrating through the human skin directly and do not encyst on aquatic vegetation or other aquatic wildlife
(Figure 63). The cercariae penetrate the host tissue until they reach a vein; then they travel to capillaries near the
lungs and then to the portal vein of the liver, where they mature. When they are mature, the adult males will pair
with the females and then travel to the veins of either the intestine or thebladder, where the eggs are produced.
Pathology and spectrum of disease
Infection with only a small number of worms may be asymptomatic. Quite often, penetration of the skin by
the cercariae causes localized swelling and itching. The migration of the larvae through the body may cause
transient symptoms of fever, malaise, cough (when they migrate in the lungs), or hepatitis (when in the liver).
The adults are able to acquire some host antigens on their outer surface, and so may not elicit an immune
response, although the eosinophil count may be high.
Severe tissue damage, with associated pain, fever, and chills, may occur when the eggs travel through the
tissue to reach the intestine or bladder. There may also be bloody diarrhea or blood in the urine (hematuria).
Necrosis, lesions, and granulomas may develop, as well as obstruction of the bowel or ureters. Penetration of
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human skin by the cercariae of blood flukes that commonly infect other mammals or aquatic birds may cause a
schistosomal dermatitis known as “swimmer’s itch.” Erythema, edema, and intense itching may develop that
usually disappear within 1 week. The cercariae of these species are not able to complete the life cycle by
entering the human bloodstream, and are destroyed by the host immune system.
Figure 59: Mating of Schistosoma mansoni male and femaleWorms.
Figure 60, Schistosoma mansoni egg. B, Schistosoma japonicum egg. C, Schistosoma haematobium egg.
Figure 61 :S. japonicum egg. Figure 62 :S. mansoni miracidium.
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Laboratory diagnosis
The standard method of diagnosis is by the detection of characteristic eggs in feces or rectal biopsy, for S.
japonicum, S. mekongi, S. mansoni, and S. intercalatum (and perhaps S. haematobium if these worms have
migrated to a bladder vein that is close to the intestine); and in urine (usually concentrated before examination)
or bladder tissue biopsy for S. haematobium.
A wet mount with/without iodine from a sedimentation or concentration method can be examined for eggs.
Figure provides images of three different schistosome eggs. To optimize recovery of S. haematobium in urine,
the specimen should be collected between noon and 2 pm. There are some antibody-based assays that are
available for diagnosis of schistosomal IgG antibody (enzyme immunoassay [EIA], enzyme-linked
immunosorbent assay [ELISA], and immunoblot), but these methods cannot distinguish between current and
previous infections. This type of assay may, however, be useful for travelers who have returned from endemic
areas.
Several nucleic acid-based testing methods have been developed that demonstrate high sensitivity and
specificity using genomic or mitochondrial sequences. In addition, schistosome DNA has been identified in
patients’ plasma using real-time polymerase chain reaction (PCR).
Therapy
The drug of choice for treatment of schistosome infections is praziquantel, given in two or three doses in a
day. Infection with S. mansoni may require a larger dose than that for the other species.
Prevention
Because human infection is by direct penetration of the cercariae, prevention of schistosome infection is more
difficult to achieve. Educational programs are required to help people in endemic areas understand how to help
prevent infection.
Sanitary conditions need to be improved with proper disposal not only of human wastes but also that of
domestic animals (in areas with S. japonicum and S. mekongi). A safe water supply for bathing and washing
Figure 63: S. mansoni cercaria.
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clothes is also necessary. Various snail control methods have been tried, but these methods are very costly and
would need to be repeated on a regular basis to have the desired effect.
Table Body Sites and Parasite Recovery (Trophozoites, Cysts, Oocysts, Spores, Adults, Larvae, Eggs,
Amastigotes,Trypomastigotes)
Site Parasites
Blood
Red cells
Plasmodium spp.
Babesia spp.
White cells Leishmania spp.
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