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University of Duhok
College of Health Sciences
Dep. of Medical Laboratories
Parasitology Theory
3rd stage
Lecture 11
Lecturer: Dr. Shameeran S. Ismael
BVM & S, M.Sc Medical Microbiology(Parasitology),
PhD Molecular Parasitology
Class Trematoda
Introduction to Trematodes
• Flattened dorsoventrally, leaf like un-segmented
worms
• Body cavity is absent
• Hermophrodites, except Shistosoma species
(sexes are separated)
• Most flukes have two suckers for attaching to the
host, one close to the mouth (dorsal sucker) and on
the ventral side (ventral sucker).
• Digestive system is simple, the
oral opening leading to a
pharynx, oesophagus & pair of
branched intestinal caeca
which end blindly.
• Excretory system includes:
flame cells, capillaries,
collecting tubules and an
excretory bladder
• The body is covered with tegument, which may
partially or completely covered with spines, tubercles
or smooth
• All member are oviparous.
• Infective stage is usually a encysted metacercria,
except for Schistosoma species is cercaria
• Have indirect life cycle
• Intermediate host is snail
Trematode Reproduction
Male reproductive system:
• Usually have two testes (number may vary)
• Vas efferent leaves each testis and forms the
vas deferens.
• The vas deferens gives rise to a seminal vesicle
which stores sperm
• the muscular cirrus pouch stores the male
copulatory organ called the cirrus.
Female reproductive system
• Usually a single rounded ovary but in some
species may be lobulated or branched.
• A short oviduct leads from the ovary and has a
sphincter called the ovicapt which regulates the
passage of ova.
• Vitellaria or vitelline glands are important
because they contribute yolk to the eggs.
• Where the oviduct and the vitelline duct join
there is a expansion which forms the ootype.
• Mehlis glands surround the ootype and in
combination with the ootype and vitelline glands
forms the oogenotop or egg forming apparatus.
• Beyond this, the duct expands to form the uterus
and on to the genital pore.
Trematode stages:
• Egg
• Miracidium
• Sporocyst (mother and daughter)
• Redia (redia1 and redia2)
• Cercaria
• Metacercaria and
• Adult
Trematodes
Stages of
. Fasciola hepatica
1
Fasciola hepatica (Distomum hepaticum),
also known as the common liver fluke, is a parasitic
flatworm of the class Trematoda, phylum
Platyhelminthes that infects the livers of various
mammals, including humans. The disease caused by
the fluke is called fascioliasis (also known as
fasciolosis).
Fasciola hepatica
Kingdome: Animalia
Phylum: Platyhelminthes
Class: Trematoda
Order: Echinostomadia
Super family: Fasciolidea
Family: Fasciolidae
Genus: Fasciola
Species: Fasciola hepatica
Common name: Liver fluke or hepatic fluke
Final host: human
Intermediate host: Snails of genus Lymnaea
Site of infection: Bile duct- gall bladder & sometimes in
the peritoneal cavity
Life cycle: Indirect
Infective stage: Encysted metacercaria
Rout of infection: By ingestion of contaminated grasses
or drinking of water with encysted metacercaria
Disease: Fascioliasis
Adult liver flukes have a flat body, an oval shape, and
large up to 30 mm long and 15 mm wide. Pink-grayish
to dark red color.
 The anterior end is conical in shape & with two clear
shoulders and the posterior end is some time rounded.
Liver flukes have two suckers (Dorsal and ventral
suckers)
Morphology
 The body surface is covered with numerous spines
(spiny tegument).
 The most characteristic features is the extensive
branching of intestine, testis & vitellain gland
Eggs:
• Oval in shape & large
• Yellowish in color
• Operculated
• Un-embryonated eggs
Miracidia
Cercariae Metacercariae
Redia
Life Cycle
Fasciola hepatica has an indirect life
cycle with snails as intermediate hosts, typically from
the genus Lymnaea.
Adult flukes lay eggs in the bile ducts of their hosts.
These eggs reach the gall bladder and are passed with
feces
Out side the host, eggs hatch and miracidium release
in 7 to 15 days. These larvae can survive for weeks off
a host provided there is enough humidity. They die
quickly in a dry environment. Miracidia can swim and
penetrate actively into the snails where they remain for
4 to 8 weeks and develop successively
to sporocysts, rediae and cercariae, the usual larval
stages of most fluke species.
Mature cercariae leave the snail, attach to the
vegetation, lose their tail and become
encysted (metacercariae), which are infective for the
final host. Such cysts can survive for months in the
vegetation.
After ingestion of metacercaria, excystation occur
young immature flukes release and within a few hours
they cross the intestinal wall and get into the peritoneal
cavity where they migrate towards the liver, which they
reach in about 3 weeks.
To reach the bile duct they have to cross the hepatic
tissue, a particularly harmful process for the host that
lasts 6 to 8 weeks. Once in the bile ducts they complete
their development to adult flukes and start producing
eggs.
In GIT there is a little damage is caused by juveniles
penetrating the intestinal wall and juveniles migrating
through the liver tissues and crossing the wall of
the bile ducts cause the major harm. This process
destroys the tissues and causes bleeding. The spines in
the surface of the flukes irritate the tissues that
become inflamed. All this leads to cell death
and fibrosis. Affected livers increase in size and
become fragile. Some flukes can become encapsulated
in the liver tissues and build cysts as large as walnuts.
The bile ducts are also damaged: they become
thickened and can be calcified and even obstructed.
Pathogenesis
1.Acute disease
Acute type occurs 2-6 wks after ingestion of large No.
of metacercaria (over 2000)
Sudden death due to massive invasion of liver by
young fluke with acute hepatic insufficient and
hemorrhage in peritoneal cavity
2.Sub-acute disease occurs 6-10 wks after ingestion of 500-
1500 metacercaria, Cause cholengitis
3.Chronic or latent phase, it’s occurs 4-5 months after the
ingestion of moderate No. (200-500) of metacercaria
Develop slowly due to mature liver fluke in bile duct which
cause cholongitis, bilary obstruction, destruction of hepatic
tissue, fibrosis and hemorrhagic anemia
Clinical signs
 Pallor of mucus membrane
 Rapid loss of weight
 Abdominal pain
 Ascites
 Dyspnoeic
Diagnosis
•History (Present of snail in area)
•Clinical signs, based on emaciation, diarrhea, bottle jaw,
sudden death
•Laboratory diagnosis, by fecal examination for detection
of characteristic eggs (oval in shape, yellowish and
operculated)
•Wash Aquatic Vegetables in 6% Vinegar for 5-10
minutes
•Control of the snail vectors
• Health education.
• People must be aware of how infection might
occur.
Control
Thanks for attention,,,

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Introduction to class Trematoda and Fasciola hepatica

  • 1. University of Duhok College of Health Sciences Dep. of Medical Laboratories Parasitology Theory 3rd stage Lecture 11 Lecturer: Dr. Shameeran S. Ismael BVM & S, M.Sc Medical Microbiology(Parasitology), PhD Molecular Parasitology
  • 3. Introduction to Trematodes • Flattened dorsoventrally, leaf like un-segmented worms • Body cavity is absent • Hermophrodites, except Shistosoma species (sexes are separated) • Most flukes have two suckers for attaching to the host, one close to the mouth (dorsal sucker) and on the ventral side (ventral sucker).
  • 4. • Digestive system is simple, the oral opening leading to a pharynx, oesophagus & pair of branched intestinal caeca which end blindly. • Excretory system includes: flame cells, capillaries, collecting tubules and an excretory bladder
  • 5. • The body is covered with tegument, which may partially or completely covered with spines, tubercles or smooth • All member are oviparous. • Infective stage is usually a encysted metacercria, except for Schistosoma species is cercaria • Have indirect life cycle • Intermediate host is snail
  • 6. Trematode Reproduction Male reproductive system: • Usually have two testes (number may vary) • Vas efferent leaves each testis and forms the vas deferens. • The vas deferens gives rise to a seminal vesicle which stores sperm • the muscular cirrus pouch stores the male copulatory organ called the cirrus.
  • 7. Female reproductive system • Usually a single rounded ovary but in some species may be lobulated or branched. • A short oviduct leads from the ovary and has a sphincter called the ovicapt which regulates the passage of ova. • Vitellaria or vitelline glands are important because they contribute yolk to the eggs. • Where the oviduct and the vitelline duct join there is a expansion which forms the ootype.
  • 8. • Mehlis glands surround the ootype and in combination with the ootype and vitelline glands forms the oogenotop or egg forming apparatus. • Beyond this, the duct expands to form the uterus and on to the genital pore.
  • 9. Trematode stages: • Egg • Miracidium • Sporocyst (mother and daughter) • Redia (redia1 and redia2) • Cercaria • Metacercaria and • Adult
  • 12. Fasciola hepatica (Distomum hepaticum), also known as the common liver fluke, is a parasitic flatworm of the class Trematoda, phylum Platyhelminthes that infects the livers of various mammals, including humans. The disease caused by the fluke is called fascioliasis (also known as fasciolosis).
  • 13. Fasciola hepatica Kingdome: Animalia Phylum: Platyhelminthes Class: Trematoda Order: Echinostomadia Super family: Fasciolidea Family: Fasciolidae Genus: Fasciola Species: Fasciola hepatica Common name: Liver fluke or hepatic fluke Final host: human
  • 14. Intermediate host: Snails of genus Lymnaea Site of infection: Bile duct- gall bladder & sometimes in the peritoneal cavity Life cycle: Indirect Infective stage: Encysted metacercaria Rout of infection: By ingestion of contaminated grasses or drinking of water with encysted metacercaria Disease: Fascioliasis
  • 15. Adult liver flukes have a flat body, an oval shape, and large up to 30 mm long and 15 mm wide. Pink-grayish to dark red color.  The anterior end is conical in shape & with two clear shoulders and the posterior end is some time rounded. Liver flukes have two suckers (Dorsal and ventral suckers) Morphology
  • 16.  The body surface is covered with numerous spines (spiny tegument).  The most characteristic features is the extensive branching of intestine, testis & vitellain gland
  • 17.
  • 18.
  • 19. Eggs: • Oval in shape & large • Yellowish in color • Operculated • Un-embryonated eggs
  • 21. Life Cycle Fasciola hepatica has an indirect life cycle with snails as intermediate hosts, typically from the genus Lymnaea. Adult flukes lay eggs in the bile ducts of their hosts. These eggs reach the gall bladder and are passed with feces
  • 22. Out side the host, eggs hatch and miracidium release in 7 to 15 days. These larvae can survive for weeks off a host provided there is enough humidity. They die quickly in a dry environment. Miracidia can swim and penetrate actively into the snails where they remain for 4 to 8 weeks and develop successively to sporocysts, rediae and cercariae, the usual larval stages of most fluke species.
  • 23. Mature cercariae leave the snail, attach to the vegetation, lose their tail and become encysted (metacercariae), which are infective for the final host. Such cysts can survive for months in the vegetation. After ingestion of metacercaria, excystation occur young immature flukes release and within a few hours they cross the intestinal wall and get into the peritoneal cavity where they migrate towards the liver, which they reach in about 3 weeks.
  • 24. To reach the bile duct they have to cross the hepatic tissue, a particularly harmful process for the host that lasts 6 to 8 weeks. Once in the bile ducts they complete their development to adult flukes and start producing eggs.
  • 25.
  • 26. In GIT there is a little damage is caused by juveniles penetrating the intestinal wall and juveniles migrating through the liver tissues and crossing the wall of the bile ducts cause the major harm. This process destroys the tissues and causes bleeding. The spines in the surface of the flukes irritate the tissues that become inflamed. All this leads to cell death and fibrosis. Affected livers increase in size and become fragile. Some flukes can become encapsulated in the liver tissues and build cysts as large as walnuts. The bile ducts are also damaged: they become thickened and can be calcified and even obstructed. Pathogenesis
  • 27. 1.Acute disease Acute type occurs 2-6 wks after ingestion of large No. of metacercaria (over 2000) Sudden death due to massive invasion of liver by young fluke with acute hepatic insufficient and hemorrhage in peritoneal cavity
  • 28. 2.Sub-acute disease occurs 6-10 wks after ingestion of 500- 1500 metacercaria, Cause cholengitis 3.Chronic or latent phase, it’s occurs 4-5 months after the ingestion of moderate No. (200-500) of metacercaria Develop slowly due to mature liver fluke in bile duct which cause cholongitis, bilary obstruction, destruction of hepatic tissue, fibrosis and hemorrhagic anemia
  • 29. Clinical signs  Pallor of mucus membrane  Rapid loss of weight  Abdominal pain  Ascites  Dyspnoeic
  • 30. Diagnosis •History (Present of snail in area) •Clinical signs, based on emaciation, diarrhea, bottle jaw, sudden death •Laboratory diagnosis, by fecal examination for detection of characteristic eggs (oval in shape, yellowish and operculated)
  • 31. •Wash Aquatic Vegetables in 6% Vinegar for 5-10 minutes •Control of the snail vectors • Health education. • People must be aware of how infection might occur. Control