Class Trematoda. Tapeworms as parasites of human being

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Theme:
Medical helmintology. Tapeworms as
parasites of a human being.
Class Trematoda.

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Medical Helminthology
CLASSIFICATION OF MEDICALLY IMPORTANT
WORMS
Phylum 1. Plathyhelminthes:
- Class Trematoda (flatworms, flukes)
- Class Cestoidea (tapeworms)
Phylum 2. Nemathelminthes:
- Class Nematoda (roundworms)

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According to the way of development helminths are
classificated into geohelminthes and
biohelminthes:
• Geohelminthes develop without intermediate host.
Soil is the environment for their egg's development.
Humans are infected through dirty fruits and
vegetables, which contain geohelminthe's eggs (for
example, Ascaris lumbricoideus).
• Biohelminthes have complete life cycle with definitive
and intermediate hosts. There are feeding connections
between definitive and intermediate hosts (for
example, Taenia solium).

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General characteristics of Plathelminthes:
All Plathelminthes are dorso-ventrally-flattened,
acoelomate soft-bodied, bilaterally symmetrical
animals with an obvious head-end.
1. They have a definite head at the anterior end.
2. Only internal space consists of the digestive cavity.
They have not an anus (waste material is egested
through the mouth).
3. They have a series of tubules that constitute their
excretory system - protonephridia.
4. Most platyhelminth species are hermaphrodites,
containing both male and female reproductive
organs.

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Class Trematoda (Flukes). General description:
1.Flattened dorsoventrally (leaf-like).
2. Unsegmented body.
3. Body is covered by cuticle.
4. Organs of fixation: oral sucker, ventral sucker.
5. Organs and systems: digestive system, excretory
system, nervous system.
6. Reproduction: Trematodes are hermaphrodites,
except genus Schistosoma.
6. The life cycle is passed in two hosts (alternation of
hosts) and has sexual and asexual stages.

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Life cycle stages of Trematodes in general:
Life cycle
stage
Description Reproduction
Adult Lives in the definitive host. Usually hermaphro-
dites but sexes separate in some species. Has
mouth and gut though may also absorb nutrients
across the body surface. Motile. Produces eggs.
Yes. Usually sexual
reproduction but
may be
parthenogenic.
Egg Contains the miracidium. May hatch in the environ-
ment or within gut of the first intermediate host.
No
Miracidiu
m
Infective stage. Covered in cilia, motile, invades the
first intermediate host.
No
Sporocyst Lacks a mouth and gut; absorbs nutrients across
body wall. Reproduces asexually within first
intermediate host.
Yes. Asexual reproduc-
tion to form daughter
sporocysts or rediae.
Redia Has a mouth and gut. Motile. Reproduces
asexually within first intermediate host. Evidence
of caste system in some species.
Yes. Asexual
reproduction to form
daughter rediae or
cercariae.
Cercaria Infective stage. Usually motile with a propulsive
‘tail’. Often leaves first intermediate host and inva-
des second intermediate host or definitive host.
No
Metacerca
ria
Infective stage. Not motile once encysted and
covered with protective wall. Develops in the envi-
ronment or within the second intermediate host.
No

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FASCIOLA HEPATICA
• Disease: “fascioliasis” or “liver rot”.
• Distribution: Worldwide
• Localization: bile ducts, gallbladder, and
pancreas
• Morphology: large size (3-5 cm), conical form
of the body; possess sucking disks (oral and
abdominal) that provide them motion.
Multibranched uterus is situated under the
abdominal sucking disk. Testis are branched
too and situated in the middle part of the body.

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FASCIOLA HEPATICA

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• Final host:
herbivorous mammals
(sheeps, horses,
cattle) and humans.
• Intermediate host:
the snail Limnea
truncatula.
• Transmission: fecal-
oral (ingestion of
water , some non-
water plants and
vegetables, which
contain
metacercariae).
• Invasive stage:
metacercaria
(adolescaria).

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FASCIOLA HEPATICA
• Clinical disease: parasites obstruct bile ducts
and lay eggs within them, leading to
cholelithiasis (gallstones). Biliary obstruction
can occur, sometimes causing biliary cirrhosis.
• Diagnosis: immature eggs in feces. An egg
has large sizes, thin membrane, yellow color
and small cover in one pole.
• Prevention: involves not eating semi-aquatic
plants (eg. water cress), not drinking fresh
water from open waters.

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OPISTHORCHIS FELINEUS
• Small biliary fluke, causing Opisthorchiasis.
• Distribution: Siberia.
• Morphology: flat, the length of the body 4-13
mm. In the middle part of the body there is a
branched uterus. Behind it there is a round
ovary. There is a roseolla-like testis in the
back of the uterus - a diagnostic sign of this
worm.

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OPISTHORCHIS FELINEUS

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The life-cycle of Opistorchus felineus
Final host: carnivorous
mammals and humans.
Intermediate hosts: 1)
snail Bithynia leachi
genus; 2) fish.
Transmission: ingestion
of contaminated raw,
frozen, dried, pickled,
and salted fish, which
contains metacercariae.
Invasive stage:
metacercariae in fish
muscles.
Localization: bile ducts,
gallbladder, liver.

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OPISTHORCHIS FELINEUS
• Clinical disease: cholecystitis and
cholelithiasis, hepatic colic, cirhosis. Clinical
picture is very similar to Clonorhis infection.
Infection can lay dormant for several years
before presenting clinically.
• Diagnosis: immature eggs in feces, in fluid
from biliary drainage, or duodenal aspirate.
Eggs are 15-30 mcm in sizes, have oval form
and yellow color. The outer membrane is thick,
and there is a cover in the front of the egg.
The internal structure of the egg is
microgranular.
• Prevention involves not eating undercooked
or contaminated raw, frozen, dried, pickled,
and salted fish; eradication of snail hosts when

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CLONORCHIS SINENSIS - BILIARY
(LIVER) FLUKES
• CLONORCHIS
SINENSIS – oriental
small biliary (liver) fluke,
causes Clonorchiasis.
• Distribution: endemic in
Far East, China, Japan,
and Vietnam.
• Morphology: the adult
worms are 1 to 2 cm; the
eggs are small, brownish.
• Localization: bile ducts,
gallbladder, and
pancreas.

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CLONORCHIS SINENSIS

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The life cycle of CLONORCHIS SINENSIS
• Transmission: fecal-oral
(ingestion of contaminated
raw, frozen, dried, pickled,
and salted fish).
• Infective stage:
metacercariae.
• Final hosts: carnivorous
mammals and humans.
• Intermediate hosts: 1-
snail (miracidium,
sporocyst, rediae,
cercariae); 2 - fish
Cyprinidae genus- the
family that includes carp
and goldfish
(metacercariae).

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CLONORCHIS SINENSIS
• Clinical disease: cholecystitis and
cholelithiasis, hepatic colic, associated
with profound weight loss and diarrhea. An
individual fluke may live for 15-30 years in
the liver. In humans a heavy infestation of
liver flukes may cause cirrhosis of the liver
and death.
• Laboratory diagnosis: immature eggs in
feces
• Prevention: adequate cooking of fish and
proper disposal of human waste

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DICROCOELIUM LANCEATUM
• Disease: Dicrocoeliasis
• Distribution: Worldwide.
• Localization: bile ducts, gallbladder and liver of
mammals (cattle, horses). Very rare in humans.
• Morphology: the worms are 1 cm long with lanceolate
form of the body; the intestine (gut) has two
nonbranched channels which are situated in the lateral
sides of the body. Two round testis are situated in the
front of the body - the diagnostic sign of this worm.

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DICROCOELIUM LANCEATUM

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The life-cycle of DICROCOELIUM
LANCEATUM
• Final host: herbivorous
mammals (cattle, horses).
• Intermediate hosts: 1) the
snail of Zebrina and Helicela
genus, 2) ants Formica genus.
• Transmission: ingestion of
plants with the ants, which
contain metacercariae.
• Diagnosis: immature eggs in
feces. An egg have oval form,
smooth membrane, brown
color, a cover is present in the
front end.
• Prophylactics: eradication of
the snails, ants when
possible; dehelmithization of
cattle.

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LUNG FLUKE: PARAGONIMUS WESTERMANI
• Disease:
paragonimiasis
• Distribution: Far East,
Central America, Africa,
and India.
• Morphology: an egg-
like form of the body,
from 7,5 to 16 mm.

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• Mode of
transmission:
ingestion of
metacercaria in
crabs or crayfish.
• Final hosts:
carnivoirous
mammals, pigs,
humans.
• Intermediate
hosts: 1) snail
(sporocyst, redia,
cercaria); 2) crabs
or crayfish
(metacercaria).
• Infective stage:
metacercariae

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• Clinical disease: a chronic cough with bloody
sputum, dyspnoa, pleuritic chest pain, and
pneumonia.
• Laboratory diagnosis: eggs in sputum or feces.
• Prevention: cooking crabs and crayfish properly.
LUNG FLUKE

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Schistosomiasis:
Distribution
• Schistosoma haematobium, S. mansoni
infections: in sub-Saharan Africa.
• S. mansoni remains endemic in parts of
Brazil, Venezuela and the Caribbean.
• S. japonicum still occurs in China, Indonesia &
the Philippines.

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Schistosomiasis distribution

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BLOOD FLUKES - genus
SCHISTOSOMA
• Schistosoma mansoni and
Schistosoma japonicum
cause Hepatosplenic
schistosomiasis.
• Schistosoma haematobium
causes Urinary
schistosomiasis.
• Localization: venous vessels
of bowel, liver, and bladder.
• Morphology: atypical
trematodes which the adult
female nesting within a
specialized groove in the body
of the larger male.

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• Male/female pair
copulate throughout
life-produce eggs
• Females resides in
canal-Important for
maturation
• Some differences
among species
• Worm pairs can live for
more than 10 years in a
host
•Pair migrate back
against the blood flow
to the mesenteries
around the intestine.

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BLOOD FLUKES
• Infective stage for
definitive host:
cercariae.
• Definitive host:
man.
• Intermediate host:
snail.
• Mode of
transmission:
penetration of skin
by cercarie.

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Cercaria in a water
 It is composed of a body
125 µm long by 25 µm
in diameter to which a
200 µm long tail is
attached.
 First escape into the
hemolynph and then
through the snail’s
integument
 Swim into the
surrounding water to
find their definitive host
 Swims by alternating
side-to-side rhythmic
contractions

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How do you get schistosomiasis ?
In a canal of the
Nile, just
southwest of Cairo,
Egypt
In a storage
reservoir just
outside of Belo
Horizonte, Brazil

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In endemic areas, most at risk are school-age children,
women, and those involved in occupations such as
irrigation, farming and fishing.

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BLOOD FLUKES
• Clinical manifestations of Hepatosplenic
Shistosomiasis: eosinophilia, polyps in colon,
fever, anorexia, weight loss, anemia, portal
hypertension; cirrhosis of liver; pruritic skin
rash. Eggs go back through portal circulation to
liver, causing hepatomegaly, liver tenderness.
• Clinical manifestations of Urinary
Schistosomiasis: eosinophilia, hematuria,
terminal dysuria (pain, difficulty at the end of
urination); obstructed urine flow.

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The abdomen of an 11-year-old boy with intestinal schistosomiasis
with the size and extent of the liver and spleen marked, indicating the
severity of infection. The disease has caused a stunting of the boy's
growth, he is only 120cms tall and weighs 22 kg.

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Morphology of the Eggs of the 3 Key Schistosomes
that Infect Humans
S. manosni egg: prominent lateral
spine ovoid (140X61µ)
S. haematobium egg:
prominent terminal spine, ovoid
(150X62µ)
S. japonicum egg: lateral spine
obscured, round (100X60µ)

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BLOOD FLUKES
• Laboratory diagnostics of Hepatosplenic
Schistosomiasis: eggs with lateral spine in feces
• Laboratory diagnostics of Urinary
Schistosomiasis: eggs with terminal spine in urine
• Prevention: involves proper disposal of human waste
and eradication of the snail host when possible.
Swimming in endemic areas should be avoided.
• How can I prevent schistosomiasis?
– Avoid swimming or wading in fresh water when you
are in countries in which schistosomiasis occurs.
– Swimming in the ocean and in chlorinated
swimming pools is generally thought to be safe.

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Control programmes
• Large scale population based chemotherapy;
• Environmental modification
• Controlling snail habitat,
• Use of molluscicides;
• Behavioral modification;
• Difficult and costly to sustain.

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The lecture is over,The lecture is over,
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