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Introduction:
 The flatworms, Platyhelminthes, (from the Greek platy,meaning “flat” and
helminth-, meaning “worm”) are a phylum of relatively simple bilaterian,
unsegmented, softbodiedinvertebrates.
 They are acoelmates (having no body cavity), and have no specialized
circulatory and respiratory organs.
 The digestive cavity has only one opening for both ingestion (intake of
nutrients) and egestion (removal of undigested wastes).
TAXONOMIC POSITION:
Kingdom: Animalia
Phylum: platyhelminthes
Class: Trematoda
Sub-class: Diginea
Family: Fascioloidea
Genus: Fasciola
Species: Hepatica
 Fasciola hepatica, also known as the common liver fluke or sheep liver
fluke, is a parasitic flatworm, that infects the livers of various mammals,
including humans. F. hepatica is distributed worldwide, and causes great
economic losses in sheep and cattle.
 Discovery: Amongst the trematodes, this was the first to be discovered by
Jehan de Brie in 1379.
Life Cycle:
 F. Hepatica reproduces sexually, Cross fertilization takes place by
copulation within the bile duct.
 Digentic in nature i.e. life cycle is completed in two host i) primary
host-Sheep ii) secondary host-snail
Formation of egg capsules:
 Fertilization is internal and each fertilized egg is surrounded by yolk
cells from vitelline glands. The yolk cells provide yolk and shell
material. The shelled eggs are called capsules and are provided with a
lid or operculum.
Development:
 Zygote starts dividing while the eggs are still in the uterus. First division
produces a larger somatic cell and a smaller propagatory cell. Somatic
cell forms the larval ectoderm.
 Propagatory cell gives rise to 2 cells:- One forming the larval body and
the other forms the germ cells. Further development takes place in the
water. The embryo comes out of the gonopore and released into the
host intestine along with the bile juice.
Larval Stages:
 Miracidium Larva: It is the first larval stage in the life cycle of F. hepatica. Body is
oval and richly ciliated and covered with epidermal plates or cells arranged in five
rows. Anterior end is broad bearing an apical papilla.
 An apical gland is present at the anterior end. A pair of penetration glands is also
present whose ducts open near the apical papilla. The larva contains brain,larval eye
and pair of nephridia.
 Larva doesn’t feed and penetrate into the snail host.
 Larva passes into the digestive gland of the snail where it gives rise to the 2nd
Larvalstage called sporocyst larva in about 14 days.
Sporocyst Larva:
 It is the second larval stage. It looks like an elongated sac about 0.7mm
long and covered with a thin cuticle. Glands, brain,eyespot and oral
papilla have degenerated.
 Germ cells are also present. The germ cells give rise to the redia larva.
Each sporocyst produce 5-8 rediae.
Redia Larva:
 It is the third larval stage. Redia
emerges by rupture of sporocyst
larval wall. Redia is elongated
about 1.3 mm to 1.6mm in
length and cylindrical. A mouth
is situated at the anterior end
floowed by a muscular swelling
called collar.
 Protonephridia divide further
and the flame cells open
through a common excretory
pore.
 Its cavity has germ cells.
 During winter germ balls of
second generation develop into
next larval stage known as
cercaria larva.
Cercaria Larva:
 Around 14-20 cercaria larva are formed in each redia.
 Cercaria larva comes out through the birth pore and enters into snails
digestive gland.
 Anterior and ventral suckers are present. Rudimentary
digestive,excretory and genital system are also present.
 Flame cells occur in large numbers which joins to form an excretory
duct that bifurcates near the tail forming a pair of nephridiopore.
 Cystogenous gland cells are present within the body that secretes the
cyst of the metacercaria larve.
 In the water the larva looses it’s tail after 2-3 days and undergoes
encystment to give rise to the last larval stage, the metacercaria larva.
Metacercaria Larva:
 Metacercaria larva are rounded in structure, of about 0.2mm in
diameter.
 Cysts provide protection against desiccation.
 If the metacercariae are released into water they can live for a year,but
if they are formed on grass or vegetation they can survive only for a few
weeks.
Infection of the Primary Host:
 Metacercariae are not infective until 12 hours after encystment. The
larva enters along with the grass blades on which it is attached into the
sheep body.
 The cysts dissolve in the intestine to liberate the larvae.
 In the duodenum, the parasite breaks free and burrows through the
intestinal lining into the perioteneal cavity.
 It infects the liver and metamorphoses to adult in 5-6 weeks. It then
enters the bile duct and attains sexual maturity and within 11-13 weeks
it starts laying eggs.
Pathology:
 Infection begins when metacercaria, infected aquatic vegetation is
eaten or when water containing metacercariae are drunk.
 Both F. hepatica and F.gigantica can cause fasciolosis.
 In cattle and sheep, classic signs of fasciolosis include persistent
diarrhea, chronic weight loss, anemia and reduced milk production. F.
hepatica can cause sudden death in both sheep and cattle,due to
internal hemorrhage and liver damage.
Diagnosis:
 Specific diagnosis depends on finding eggs in the stool an enzyme
linked immunosorbent assay (ELISA) test is available as well. ELISA
tests are available commercially and can detect anti-hepatica
antibodies in serum and milk.
Treatment:
 Antihelminthic drugs like hexachloroethane, carbon tetrachloride,
tetrachloroethane and emetine hydrochloride, etc., are effectively used
for the treatment of disease caused by F. hepatica.
Prophylaxis:
 Fasciolosis is an important cause of both production and economic
losses in the dairy and meat industry.
 The best way to prevent Fasciolosis is by reducing the lymnaeid snail
population or separating livestock from areas with these snails.
Significance:
 The concept of product life-cycle highlights that sooner or later all
products die and that if management wishes to sustain its revenues, it
must replace the declining products with the new ones. The product
life-cycle concept indicates as to what can be expected in the market for
a new product at various stages. i.e., introduction, growth, maturity
and decline. Thus, the concept of product life-cycle can be used as a
forecasting tool. It can alert management that its product will
inevitably face saturation and decline, and the host of problems these
stages pose. The product life-cycle is also a useful framework for
describing the typical evolution of marketing strategy over the stages of
product life-cycle. This will help in taking sound marketing decisions
at different stages of the product life-cycle.
Conclusion:
 Fasciola hepatica infection should be considered in the differential
diagnosis of patients with hepatic or biliary disease and/or acute
pancreatitis associated with eosinophilia.

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LIFE CYCLE OF FASCIOLA HEPATICA.pptx

  • 1.
  • 2. Introduction:  The flatworms, Platyhelminthes, (from the Greek platy,meaning “flat” and helminth-, meaning “worm”) are a phylum of relatively simple bilaterian, unsegmented, softbodiedinvertebrates.  They are acoelmates (having no body cavity), and have no specialized circulatory and respiratory organs.  The digestive cavity has only one opening for both ingestion (intake of nutrients) and egestion (removal of undigested wastes). TAXONOMIC POSITION: Kingdom: Animalia Phylum: platyhelminthes Class: Trematoda Sub-class: Diginea Family: Fascioloidea Genus: Fasciola Species: Hepatica  Fasciola hepatica, also known as the common liver fluke or sheep liver fluke, is a parasitic flatworm, that infects the livers of various mammals, including humans. F. hepatica is distributed worldwide, and causes great economic losses in sheep and cattle.  Discovery: Amongst the trematodes, this was the first to be discovered by Jehan de Brie in 1379.
  • 3. Life Cycle:  F. Hepatica reproduces sexually, Cross fertilization takes place by copulation within the bile duct.  Digentic in nature i.e. life cycle is completed in two host i) primary host-Sheep ii) secondary host-snail Formation of egg capsules:  Fertilization is internal and each fertilized egg is surrounded by yolk cells from vitelline glands. The yolk cells provide yolk and shell material. The shelled eggs are called capsules and are provided with a lid or operculum. Development:  Zygote starts dividing while the eggs are still in the uterus. First division produces a larger somatic cell and a smaller propagatory cell. Somatic cell forms the larval ectoderm.  Propagatory cell gives rise to 2 cells:- One forming the larval body and the other forms the germ cells. Further development takes place in the water. The embryo comes out of the gonopore and released into the host intestine along with the bile juice.
  • 4.
  • 5.
  • 6. Larval Stages:  Miracidium Larva: It is the first larval stage in the life cycle of F. hepatica. Body is oval and richly ciliated and covered with epidermal plates or cells arranged in five rows. Anterior end is broad bearing an apical papilla.  An apical gland is present at the anterior end. A pair of penetration glands is also present whose ducts open near the apical papilla. The larva contains brain,larval eye and pair of nephridia.  Larva doesn’t feed and penetrate into the snail host.  Larva passes into the digestive gland of the snail where it gives rise to the 2nd Larvalstage called sporocyst larva in about 14 days.
  • 7. Sporocyst Larva:  It is the second larval stage. It looks like an elongated sac about 0.7mm long and covered with a thin cuticle. Glands, brain,eyespot and oral papilla have degenerated.  Germ cells are also present. The germ cells give rise to the redia larva. Each sporocyst produce 5-8 rediae.
  • 8. Redia Larva:  It is the third larval stage. Redia emerges by rupture of sporocyst larval wall. Redia is elongated about 1.3 mm to 1.6mm in length and cylindrical. A mouth is situated at the anterior end floowed by a muscular swelling called collar.  Protonephridia divide further and the flame cells open through a common excretory pore.  Its cavity has germ cells.  During winter germ balls of second generation develop into next larval stage known as cercaria larva.
  • 9. Cercaria Larva:  Around 14-20 cercaria larva are formed in each redia.  Cercaria larva comes out through the birth pore and enters into snails digestive gland.  Anterior and ventral suckers are present. Rudimentary digestive,excretory and genital system are also present.  Flame cells occur in large numbers which joins to form an excretory duct that bifurcates near the tail forming a pair of nephridiopore.  Cystogenous gland cells are present within the body that secretes the cyst of the metacercaria larve.  In the water the larva looses it’s tail after 2-3 days and undergoes encystment to give rise to the last larval stage, the metacercaria larva.
  • 10.
  • 11. Metacercaria Larva:  Metacercaria larva are rounded in structure, of about 0.2mm in diameter.  Cysts provide protection against desiccation.  If the metacercariae are released into water they can live for a year,but if they are formed on grass or vegetation they can survive only for a few weeks.
  • 12. Infection of the Primary Host:  Metacercariae are not infective until 12 hours after encystment. The larva enters along with the grass blades on which it is attached into the sheep body.  The cysts dissolve in the intestine to liberate the larvae.  In the duodenum, the parasite breaks free and burrows through the intestinal lining into the perioteneal cavity.  It infects the liver and metamorphoses to adult in 5-6 weeks. It then enters the bile duct and attains sexual maturity and within 11-13 weeks it starts laying eggs. Pathology:  Infection begins when metacercaria, infected aquatic vegetation is eaten or when water containing metacercariae are drunk.  Both F. hepatica and F.gigantica can cause fasciolosis.  In cattle and sheep, classic signs of fasciolosis include persistent diarrhea, chronic weight loss, anemia and reduced milk production. F. hepatica can cause sudden death in both sheep and cattle,due to internal hemorrhage and liver damage.
  • 13. Diagnosis:  Specific diagnosis depends on finding eggs in the stool an enzyme linked immunosorbent assay (ELISA) test is available as well. ELISA tests are available commercially and can detect anti-hepatica antibodies in serum and milk. Treatment:  Antihelminthic drugs like hexachloroethane, carbon tetrachloride, tetrachloroethane and emetine hydrochloride, etc., are effectively used for the treatment of disease caused by F. hepatica. Prophylaxis:  Fasciolosis is an important cause of both production and economic losses in the dairy and meat industry.  The best way to prevent Fasciolosis is by reducing the lymnaeid snail population or separating livestock from areas with these snails.
  • 14. Significance:  The concept of product life-cycle highlights that sooner or later all products die and that if management wishes to sustain its revenues, it must replace the declining products with the new ones. The product life-cycle concept indicates as to what can be expected in the market for a new product at various stages. i.e., introduction, growth, maturity and decline. Thus, the concept of product life-cycle can be used as a forecasting tool. It can alert management that its product will inevitably face saturation and decline, and the host of problems these stages pose. The product life-cycle is also a useful framework for describing the typical evolution of marketing strategy over the stages of product life-cycle. This will help in taking sound marketing decisions at different stages of the product life-cycle. Conclusion:  Fasciola hepatica infection should be considered in the differential diagnosis of patients with hepatic or biliary disease and/or acute pancreatitis associated with eosinophilia.