General Veterinary Parasitology and Helminthology 2016

VPA-211
MODULE-15: FAMILY - FASCIOLIDAE

Learning objectives

After reading this module the learner will understand the following

 Importance of liver fluke infection in cattle, sheep, goats and buffaloes, wild ruminants and
human beings.
 Life cycle, pathogenesis, clinical signs, diagnosis, treatment and control of liver fluke infection in
animals and man.
 Zoonotic significance

FASCIOLA SPP.
INTRODUCTION

Family: Fasciolidae

 Genus: Fasciola
 Species: Fasciola gigantica, Fasciola hepatica
 Common name: Liver fluke.
 Distribution: World wide. Commonest liver fluke in India.
 Disease: It causes fluke cirrhosis or liver rot, fascioliasis or fasciolosis or clay pipe cirrhosis, pipe
stem liver or gall stone formation.
 Host: Cattle buffalo, sheep, goat, and also in man.
 Location: Bile duct and Liver parenchyma.

Fasciola gigantica

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FASCIOLA SPP.
INTERMEDIATE HOST

Aquatic snail

 Lymnaea acuminata
 L.rufescens
 L.auricularia
 L.natalensis

Lymnaea Lymnaea auricularia

MORPHOLOGY OF FASCIOLA HEPATICA AND F.GIGANTICA

F.gigantica

 Leaf shaped large size. 25 - 75 mm in length, 12 mm in breadth and broader anteriorly than
posteriorly.
 Anterior cone is smaller. They have indistinct shoulder (not so prominent).
 Cuticle have spine (spinose tegment). The body is more transparent.
 The oral and ventral suckers are present. The ventral sucker situated at the level of shoulder and
is larger than oral sucker. The intestinal caeca is branched and diverticulated both externally and
internally.
 Two follicular branched testes placed in the middle region. Single branched ovary with a coiled
uterus lies anterior to the testes.
 Genital opening anterior to the ventral sucker. Numerous vitellaria placed laterally and 2
transverse vitellaine ducts.

F.hepatica

 OS and VS are same size.

 Prominent shoulder.
 Testes placed at the posterior region.

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 Comparatively smaller than
F. gigantica in size
 Presence of anterior cone and distinct shoulder.
 Intestinal caeca branched and diverticulated only externally.

Fasciola hepatica

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FASCIOLA SPP.
LIFE CYCLE

Fasciola-Egg

 Egg is composite egg. Large in

size. 156 - 197 X 90 - 104m.
 They are oval in shape and
yellowish tint with indistinct
operculum.
 They have yolk cells and germ
cells (hexagonal shape).
 The eggs are voided in the faeces
of the host.
 It survives 2 - 3 months in humid
faeces. But quickly destroy by
desiccation within few hrs /
days.
 Miracidium develop only after
the eggs have been laid
o Development in
invertebate host
o Development in
vertebrate host

FASCIOLA SPP.
DEVELOPMENT IN THE INVERTEBRATE HOST

 Eggs hatch in about 10 - 12 days at 26ºC. (depends on temperature) release miracidium.

 Miracidium is broad anteriorly, with small papiliform protrusion, tegument is ciliated and has a
pair of eyespot. (Within 3 hrs it should reach the snail.)
 Miracidium actively penetrate into acquatic snail (L.acuminata), casting off its ciliated covering
and develops into sporocyst. Each sporocyst gives rise to 1 - 6 rediae by polyembryony.
 Redia has a circular thickening behind the level of pharynx and a pair of blunt process at the
beginning of the posterior quarter. They are 1 - 3 mm long.
 Usually redia produce cercaria (daughter redia may develop under unfavorable condition).
 Cercaria is Gymnocephalus, there is no spine and eyespot but dark granular cystogenous glands in
the lateral part of body and long tail are present.
 Time taken for development of cercaria in the snail is 5-7 weeks under favourable condition.
Within few minutes to 2 hrs of the release of cercaria from snail settles on grass blades / other
plants just below the water level (submerged vegetation) casting off its tail and secrete a covering
by the cystogenous gland froms the spherical cyst is called as metacercaria.
 Small number may encyst on the surface of the water and sink into the bottom of the water.
Metacercaria is infective to D/H. They are pearly / milky white in colour with pinhead size.
 D/H acquire infection by ingestion of metacercaria along with herbage / drinking water.

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NOTE: Infection of snail with one miracidium can produce over 600 metacercaria.
They survive on the herbage for 4 – 6 weeks at R.H 70%. It survive for 270 – 340 days
on moist hay for 8 months and on silage for 35 – 57 days. Under normal condition 3 – 6
months but die quickly in hot and sunny days. This process of one embryo giving rise to
numerous offsprings is unique to trematode and is known as paedogenesis.

FASCIOLA SPP.
DEVELOPMENT IN THE VERTEBRATE HOST

 Following ingestion of metacercaria excystation occurs in the duodenum. Within 24 hrs of

infection, the majority of immature trematodes occur in abdominal and peritoneal cavity.
 By 4 - 6 days after infection, majority will penetrate the liver capsule and found migrating in the
liver parenchyma. Young fluke may reach the liver through blood stream but it is unusual. Usual
route is via peritoneal cavity and migration in the liver may occurs upto 5 - 6 weeks.
 From 7th week onwards they enter the bile duct and reach the sexual maturity, some flukes may
be seen in gall bladder also. During 8th week of infection eggs are passed in the faeces. Prepatent
period is normally 8 - 12 week.
 Occasionally in cattle, the immature flukes may be found in the other organs, such as in lungs and
in the pregnant animals, the parasite may occur in the foetus.
 Minimum period of completion of one life cycle (egg to egg) is 17 - 18 weeks in F.gigantica, under
favourable condition.
The longevity of Fasciola in untreated sheep may be years; in cattle, it is less than one year.

Metacercaria

FASCIOLA SPP.
PATHOGENESIS

 The pathogenesis depends on the number of metacercaria ingested

 They are two forms of this disease.
o Acute fasciolosis
o Chronic fasciolosis

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FASCIOLA SPP.
ACUTE FASCIOLOSIS

 This is due to the Immature fluke

 It is a less common form compared to chronic form in sheep
 The condition usually results in Traumatic hepatitis which is mainly due to the migration of
immature flakers.
 By about 6-8th week after infection, extensive destruction of liver parenchyma with hemorrhage
 If the number of parasites are more, it results in rupture of the liver capsule with hemorrhages in
peritoneal cavity. In such animals death occurs in a few days time from the onset of clinical signs.
 Liver is enlarged, pale in color with hemorrhagic tracts on the liver surface.
 In less acute sub acute forms the liver is covered with migratory tracts with early fibrosis
 Sub acute form is common in animals of all ages
 A complication of acute fasciolosis is the occurrence of black’s disease – A condition caused by the
anaerobic bacteria Clostridium novyi which are mainly seen in the anaerobic lesions caused by
the immature trematodes.

Acute Fasciolosis Fasciolosis in lung

Acute Fasciolosis in lung Fasciolosis in Heart

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Fasciolosis in Heart

FASCIOLA SPP.
CHRONIC FASCIOLOSIS

 This is due to the activity of the Adult flukes.

 Most common form seen in sheep, cattle and other ruminants.
 The normal sequlae is hepatic fibrosis
 The chronic form is always associated with the presence of adult flukes in liver of like duct.
 The condition may result in hyperplasic cholangitis in the liver and bile duct due to the presence
adult flukes.
 In such cases, the bile duct wall epithelium gets thickened giving the appearance of pipe stem
liver and resulting in a condition called clay pipe cirrhosis or pipe stem liver

Chronic Fasciolosis Sheep died due to fasciolosis

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FASCIOLA SPP.
CLINICAL SIGNS

 The disease is common in animals of all the age groups.

 Affected animals shows anorexia, looks weak, emaciated.
 The most important sign is the appearance of odema especially in the sub mandibular region is
referred commonly as bottle jaw (jowl odema) caused due to loss of proteins/ hypoalbuminaemia
or loss of absorption of proteins by the host.
 In some cases especially in acute fasciolosis there will be diarrhea followed by constipation.
 Fasciolosis affected calf with sub mandibular swelling

FASCIOLA SPP.
DIAGNOSIS

 By clinical symptoms
 Weather based forecasting
 By examination of the dung sample for the presence of fasciola egg.
 Immunological test.

Fasciola Egg

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FASCIOLA SPP.
TREATMENT AND CONTROL

Treatment

 Oxyclozanide – 15 – 20 mg/kg b.w orally

 Rafoxanide – 10 mg / kg bw orally
 Nitroxynil – 10 mg/ kg B.W s/c
 Diamphenithide – ideal for fasciolosis
 Triclabendazole -10 mg/kg bwt

Control

 Eradication of Intermediate host– molluscide – CuSO4 7 H2O, Baylucide

 Treatment of infected animal -segregate
 Flukicides- twice a year trichlobendazole, oxyclozanide to healthy animal . Of all the drugs above,
Triclabendazole is considered as the drug of choice for fasciolosis since it was found to be effective
against both immature and adult stages of Fasciola species. In addition to treatment with
flukicidal drugs, the flock should be moved to snail free pasture. The control include snail control
in the endemic areas with efficient water management system. More over new water bodies /
check dams, reservoir created should be made snail free. This may be acheived by application of
herbal molluscidal drugs in the new areas.

FASCIOLOPSIS BUSKI
INTRODUCTION

Definite Host Man and pigs

Location Small intestine of man & pig

Common names Intestinal fluke of man.

FASCIOLOPSIS BUSKI
INTERMEDIATE HOST

 Planorbis sp, Segmentina sp,

 Water plants -- water calotrop, water chesnut.

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MORPHOLOGY OF FASCIOLOPSIS BUSKI
Fasciolopsis buski

 Largest fluke 3 – 7.5 by 0.8 – 2 cm.

 Body is oval shaped and shoulders are absent.
 Cuticle is spiny.
 Ventral sucker is larger than the oral sucker.
 Intestinal caeca simple.
 Testes in the posterior third of the body are branched and
lie in tandem position.
 Ovary is branched anterior to testes in the middle region,
vitellaria occupy lateral fields.

Fasciolopsis Buski

FASCIOLOPSIS BUSKI
LIFECYLE

 Eggs are similar to Fasciola gigantica like thin shelled, oval, operculate, brown colored.
 This cercariae encysts on the tubers or the nuts of the plants which are eaten raw by the humans.
 These possibly also other plants may carry the infection to pigs.

FASCIOLOPSIS BUSKI
PATHOGENESIS

 The parasite is chiefly of importance as a cause of disease in man.

 It attaches itself to the intestinal mucosa causing a local inflammation or deep ulcerative lesions
in heavy infections.
 It produces abdominal pain, diarrhoea, oedema and ascites.

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FASCIOLOPSIS BUSKI
CLINICAL SIGNS, DIAGNOSIS, TREATMENT AND CONTROL

Clinical signs

 common in children.
 Human – Abdominal pain, diarrhea, edema, ascites.

Diagnosis

Based on clinical signs, eggs in faces.

Treatment

 Niclosamide – 60 mg /kg BW orally.

 Praziquantel – 20 mg /Kg BW orally.

Control

 Intermediate host control.

 Proper disposal of faeces of human and pig .
 Proper cooking.

DICROCOELIUM DENDRITICUM
INTRODUCTION

Definite host Cattle, sheep and goat .

Location Bile duct .

Common name Lancet flukes/blade/needle fluke.

DICROCOELIUM DENDRITICUM
INTERMEDIATE HOST

 Land snail - Macrochalamys cassida

 Ant – Formica fusca

MORPHOLOGY OF DICROCOELIUM DENDRITICUM

Dicrocoelium dendriticum

 Small fluke, 1.6 – 1 by 0.15 – 0.25 cm.

 Body is elongate, lanceolate shape with smooth cuticle.
 Oral sucker is smaller than the ventral sucker.
 Intestinal caeca are simple, not reaching the posterior end of the body.

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 Testes are slightly lobed and are tandem in position just below the ventral sucker
 Ovary is posterior to testes.
 Uterus is quite distinct (filled with brown eggs) and coiled occupying the posterior part of the
body.
 Vitelline glands are restricted to mid lateral region.

Dicrocoelium dendriticum

DICROCOELIUM DENDRITICUM
LIFECYCLE

 Eggs are small dark brown, operculate.

 Usually with one side flattened.
 It contains miracidium (embryonated).
 Redia stage absent.

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DICROCOELIUM DENDRITICUM
PATHOGENESIS

 Extensive cirrhosis and scarring of liver surface.

 Bile ducts are distended in fibrosis in portal triads, marked proliferation of bile duct epithelium.
 In severe cases, edema, anemia and emaciation common in hill region – dicrocoeliosis.

DICROCOELIUM DENDRITICUM
TREATMENT

 Hetolin- 19-22 mg/kg BW orally.

 Albendazole - 7.5 mg/kg BW orally .
 Fenbendazole - Large doses 150 mg/kg BW orally.

DICROCOELIUM DENDRITICUM
CONTROL

 Snail control.
 Ant control .
 Treatment .

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MODULE-17: FAMILY-OPISTHORCHIIDAE

Learning objectives

After reading this module, the learner will understand the following

 Importance of morphology, life cycle, pathogenesis, clinical signs, diagnosis, treatment and
control of Ophistorchiid flukes.

OPISTHORCHIS TENUICOILLIS
INTRODUCTION
Host Dog, cat, fox, pig and man
Location Bile duct, rarely in intestine and pancreatic ducts
Common name Liver fluke of dogs and cats

OPISTHORCHIS TENUICOILLIS
INTERMEDIATE HOST

 Normally, two intermediate hosts present in Opisthorchis tenuicollis . These are

o Bithynia sp.
o Cyprinid fish

OPISTHORCHIS TENUICOILLIS
MORPHOLOGY

 Small fluke (translucent body), reddish when fresh.

 Elongate body and narrow anteriorly.
 Suckers weakly developed.
 Pharynx, Oesophagus present and intestinal caeca extend almost to the posterior end.
 Testes spherical / slightly lobed, diagonal, in the posterior half of the body.
 Ovary small, slightly lobed and is anterior to the testes.
 Uterus situated between ventral sucker and the ovary.
 Vitellaria present as series of transversely arranged follicle and occupy the middle third of the
lateral fields.
 The excretory bladder is typically ‘ Y ‘ – shaped.

OPISTHORCHIS TENUICOILLIS
PATHOGENESIS

 Marked proliferation of bile duct epithelium. Severe inflammation of bile duct.

 Tumor formation in liver - carcinoma of liver

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OPISTHORCHIS TENUICOILLIS
CLINICAL SIGNS, DIAGNOSIS, TREATMENT AND CONTROL

 Clinical signs
o Abdominal pain, diarrhoea.
 Diagnosis
o Eggs in faeces.
 Treatment
o Praziquantel.
o Albendazole.
 Control
o Feeding only cooked fish to dog and cats

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