A brief description of trematodes of family Fasciolidae, their morphology, pathogenesis, clinical signs, diagnosis, treatment and control.

1. Dr. Ishfaq Maqbool
Ph. D. scholar
Veterinary Parasitology
GADVASU

2. Phylum: Platythelminthes
Class: Trematoda
Sub-class: Digenea
Family: Fasciolidae
Genus: Fasciola
Fasciolopsis
Fascioloides
Parafasciolopsis

3.  Large flukes present in bile ducts and intestine of
mammals
 Cuticle is spined, suckers closely approximated,
caeca long, simple or much branched
 Testis as well as ovaries are branched
 Eggs are thin shelled and operculated

4.  3-5 cm long and 1 cm wide.
 Cuticle is spiny
 At anterior end there is a cone like projection
followed by broad shoulders.
 The oral sucker at the anterior tip while the
ventral sucker at the level of shoulder.
 Intestinal caeca are branched.
 Testis are branched and tandemly placed.
 Ovary is branched and anterior to the testis.
 The field between the ovary and the ventral
sucker occupied by uterine coils which leads to
the genital pore.
 Vitelline glands are scattered at the lateral field

5.  Bigger than Fasciola hepatica (5-7cm in
length).
 At anterior end cone is less prominent
than Fasciola hepatica.
 Cuticle spiny.
 Internal morphology is same as Fasciola
hepatica.

7. .
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Egg

8.  Egg: Yellowish brown in colour, oval operculated.
 Bile imparts the yellow colour to the egg.
 Hatching depends on atmospheric temp.
 At room temperature, majority of eggs hatch within 10-12days.
 Miracidium hatches only if stimulated by light and if water surround
the egg
 After hatching the miracidae stages comes out
 Moves vigoursly in water to detect fresh water snail, by chemotaxis.
Parasite Intermediate host
Fasciola hepatica Lymnaea truncatulla
Fasciola gigantica L.accuminata, L.auricularia,
L.rufescens

9.  After contact has been made, usually with the foot
of the snail, they burrow using enzymes and then
lose their ciliated outer layer to form sporocyst.
 Each sporocyst give rise to 5-8 rediae stages
 Redial stages has a oral aperture, pharynx and sac
like gut. There is a pair of blunt process behind
the body.
 There is a birth pore through which several
Gymnocephalous cercariae released in the
atmosphere.
Miracidium
Rediae

10.  Gymnocephalus cercariae are liberated from the
body of snail which adheres on the solid surface and
the grass blade, it then losses its tail and secretes a
protective cyst wall.
 This encysted cercaria is called as metacercariae
 Infection to the definitive host is through ingestion of
metacercaria while grazing on low line pasteur
 Metacercariae which are settle at the bottom of
lake/pond gets stirred up & swallowed up along with
drinking water when larger host like cattle & buffalo
enter.
Cercariae
Metacercariae

11.  Excystation in Small Intestine due to action of bile and acid pepsin
 Immature flukes emerges
 Penetrate the mucosa and the wall of intestine.
 Enter peritoneal cavity, goes to liver
 Penetrate liver capsule (4-6 days post infection)
 Some flukes reach liver via hepatoportal circulation.
 However most common route is peritoneal cavity.
 After entering liver, immature flukes migrates in the liver parenchyma for 5-6
weeks.
 Eventually assemble in bile duct, matures, lays egg.
 Adult flukes are sluggish, feed on bile duct mucosa, blood & bile
 Survive for many years in sheep but not in cattle

12.  Prepatent period: 8 weeks
 Undeveloped egg to miracidium: 9 days
 Entry in snail to exist of cercaria: 5 weeks
 Ingestion of metacercariae to formation of egg 6-12 weeks.
 Egg to egg: 14 ½ weeks.

13.  Atmospheric temperature:
 10-26ºC optimum temperature.
 Below 12ºC, no development of miracidium.
 At 12ºC -20ºC, increase in development inside egg.
 For egg at 12ºC- 60 days for eggs to hatch
 15ºC- 42 days for eggs to hatch
 26º C– 27ºC – 12 days for eggs to hatch
 Above 27ºC : Snail mortality and larval stages can`t survive in the
snail.

14. 2. Snail Ecology:
 Lymnaea spp. of snail act as intermediate host.
 Ubiquitous and amphibious in nature
 Longevity of snail is 12 months
 Snail hibernation results in arrested development of developing stages
 Size of snails plays important role and not number.
 Summer infection of Snails important

15. 3. Longevity of metacercariae :
 Under lab condition survives one year
 Only 5% remains infective during suitable atm. temp. & moisture and
can survive for 3-4 months.
 As time passes, metacecariae drop down from grass blade.
 Silage:1-2 months
 Hay: 8 months
 Water: 3-4months

16.  Depends on number of infective stage ingested.
 Not much damage to intestine and peritoneal cavity due to migration
of immature stages
 Principle lesion produced in the liver parenchyma or bile ducts.
 2 disease entities:
 Acute fasciolosis: Less common. Seen in sheep during August & September,
since large no. of metacercariae are present on pasture during the month of June &
July.
 Chronic fasciolosis: Common in cattle and buffalo, seen during the month of
November & March.

17.  Large number of immature stage in subst. of liver
 Death of host in 4-6 weeks P.I due to destruction of liver parenchyma
 Haemorrhagic tracts in liver
 Liver becomes enlarged, pale and friable
 Fibrinous clots on surface of liver & peritoneal cavity.
 Generally left lobe commonly affected.
 At proximal end, hemorrhagic tract & immature flukes present,
followed by zone of hemorrhages and zone of reddish grey material of
inflammatory cells

18.  Immature flukes (0.7 – 2mm) can be squeezed from the cut surface.
 In massively infected animal large number of metacercariae may
rupture the liver capsule leading heavy bleeding in the peritoneal
cavity and death

19.  Mainly two types of lesion produced
 1. Hepatic Fibrosis
 2. Hyperplastic cholangitits
 Hepatic Fibrosis:
 Due to migration of immature fluke in liver parenchyma
 Migratory tract, area of haemorrhages and necrosis
 Thrombus formation
 Area of coagulative necrosis
 Healing by regeneration of parenchyma
 Marked fibrosis
 FCT matures
 Scarring and distortion of hepatic parenchyma.
 FCT proliferation divides liver in to small lobule

20. 2. Hyperplasic cholangitits
 Presence of adults flukes in the bile duct cause irritation to bile duct
epithelium.
 Causes of irritation is due to:
a) Spines on cuticle and suckers
b) Release of toxic metabolites of parasites
c) Retention of bile
 Inflammation, Hyperplasia and Denudation of bile duct epithelium
which is replaced by FCT

21.  In large ruminants, Calcification of fibrotic lesion (calicification of
bile duct).
 Clay Pipe Liver or Pipe Stem liver: Protrusion of Bile duct out from
the surface of liver giving appearance of Stem of Clay pipe .
 Microscopically, lesions can be described as hyperplastic cholangitits
with progress biliary cirrhosis.
 Occasionally, eggs of Fasciola trapped in tertiary bile duct causes
granulomatous lesions.
 Rarely flukes may settle in Subcutaneous tissues or lungs enclosed in
cyst with yellowish brown cheesy material.

22.  Seen in sheep due to presence of Clostridium novyi in intestine.
 Clostridium novyi carried by the immature flukes to the liver where
are of coagulative necrosis are produced
 These anaerobes multiply and produce disease called as the Black
disease.

23.  Two types of clinical findings:
 Anaemia
 Hypoproteinaemia
 Anemia is due to
 Haematophagous activity of adult
flukes (0.5 ml/day) and
hemorrhagic tracts by immature
flukes
 Initially anemia is initially
normochromic normocytic and
later hypochromic macrocytic
 Hypoproteinaemia (Hypoalbuminaemia):Due to
 1. Destruction of hepatic parenchyma by
immature fluke
 Liver is principle site of synthesis of
albumin.
 Due to migration of flukes synthesis
affected.
 2. Preferential use of aminoacids for synthesis of
globulin results in hypoalbuminaemia.

24. 1. Acute Fasciolosis:
 No specific symptom.
 Sudden death.
 Blood tinged from nostrils,
mouth as well as bloody
discharge from anus.
3. Chronic Fasciolosis
Anaemia
Pale mucus membrane
Anorexia
Emaciation
Edema of dependent part “Bottle Jaw
condition”
Skin becomes dry and rough
Wool falls off in patches
Irregular peristalsis (Diarrhoea or
constipation)
2. Sub Acute Fasciolosis:
•Anorexia
•Disinclination to move
•Distention of abdomen
•Pain on palpation
•If not treated on time, animal
may die due to infection.

25.  Chronic Fasciolosis:
 S.S.E (stool sample examination) for detection of Fasciola egg.
 Acute Fasciolosis:
 Based of symptoms in endemic areas
 Incase of death, perform Post Mortem
 On necropsy, liver shows traumatic hepatitis with migratory
tracts.
 Cut liver into thin slices, place in Luke warm saline, Flukes will
wriggle out

26.  Sheep is most susceptible to Fasciola infection because they donot
develop protective immunity against subsequent infection.
 Cattle and Buffalo: Immunity develops
 In C & B vaccination can be targeted but not in Sheep and goat.
 Experimental feeding of irradiated metacercaria to showed
encouraging results.
 No commercial vaccine available till date.

27.  Consumption of metacercariae through uncooked/unwashed leafy
vegetables.
 Fluke settles in S/C tissue and lungs, forming a granulomatous mass.
 Symptoms: Gastrointestinal problems such as nausea, vomiting, and
abdominal pain/tenderness. Fever, rash, and difficulty breathing may
occur.
 Inflammation of the liver, gallbladder, and pancreas also can occur.
 Treatment: Bithionol@50mg/kg body weight every alternate days for
15 days

28.  1.Carbon tetrachloride given orally @ 1-3ml in sheep/goat and
1-5 ml in large ruminant.
 Should be given in gelatin capsule or should be mixed with Liq.
Paraffin oil in equal quantity.
 Effective against adult flukes
 Use discontinued, since it is Hepato and nephrotoxic.
 Chances of toxicity reduced when given deep i/ m injection but
there is formation of abscess at the site of injection.

29.  Hexachlorethane given @ 220-400mg/kg body weight against Adult flukes
 Hexachlorophene given orally or s/c @15-20mg/kg against adult flukes.
 Hetol@150mg/kg body weight against chronic fasiciolosis
 Bitihonol @ 40mg/kg body weight effective against chronic fasciolosis.
 Oxyclozanide @15mg/kg body weight in chronic cases. In acute cases increase the dose
3 times.
 Rafoxinide @ 7.5mg/kg body weight
 Nitroxynil: 10mg/kg body weight given S/c
 Oxyclozanide @15mg/kg body weight
 Diamphenethide @ 100mg/kg body weight
 Albendazole @7.5 mg/kg body weight
 Oxyfendazole @5 mg/kg body weight
 Drug of Choice TRICLABENDAZOLE@10-12mg/kg body weight

30. Prevention:
 Prevent the animal from grazing on infected pastures.
 Destruction of snails:
 Molluscide: Copper Sulphate i.e. CuSO4
 Destruction of snails on wet pasteur: 1-2% Cuso4 is sprayed or 1
part of CuSO4 mixed with 4 parts of sand and sprayed on pasteur
10-30 kg/ha.
 Destruction of snails in water body:
 In stagnant water, CuSO4 should be added to make the final conc.
1:50,000 to 1:1,00,000

31.  For flowing water: CuSO4 should be placed in non metallic boxes having pores in it.
 These boxes should be placed at the origin of the streams so that it can kill the snails
several km. down the stream.
 If CuSO4 is not available then Cupentachlorophenate can be used @ 10lbs/acres.
 This molluscicide treatment should be repeated every 3-4 months.
2. Biological control: Birds like Free-ranging ducks or geese
 Echinostome flukes: Ability of larval echinostomes to aggressively displace other
larval flukes from their snail hosts and parasitic castration of snails by larval
echinostomes( E. revolutum)
 Prophylaxis : No chemoprophylaxis
 Treatment: Frequent deworming (Pre-monsoon, monsoon, post monsoon)

32.  Occurs in elephant
 Severe submandibular and ventral
abdominal oedema
 Anaemia and Hypoproteinaemia
 Other features same as ovine fasciolosis
 Nitroxynil (10mg/kg) used for treatment

33.  Found in cattle, horse, sheep and pigs of north
America and in cattle, sheep and deer in Europe.
 Oval and round posterior end, no anterior cone like
projection
 Eggs with protoplasmic appendage at the pole
opposite the operculum
 Intermediate host: snails of Fossaria spp., Lymnaea
spp. and Stagnicola spp.

34.  Deer: Family Cervidae normal host.
 Young flukes migrate extensively and then encapsulated with 2-3 flukes per
capsule. Capsules connected to bile duct, eggs passed in faeces.
 Bovidae: Cattle, Bison, Yak are aberrant hosts
 Closed cysts, No eggs in faeces and no signs of ill health.
 Sheep: Also aberrant host. Uninterrupted migration and no encapsulation
which is fatal.
 Treatment: Oxyclozanide@13-28.5 mg/kg
 Rafoxanide@12-25mg/kg
 albendazole@15-35mg/kg is 90% effective

35.  Small intestine of Man, pig.
 The largest one of human trematodes.
 No shoulders
 Unbranched intestinal caeca.
 The ventral sucker is near by the much smaller oral
sucker.
 Branched, tandem testes are located in the posterior half
of the body, ovary in right of midline.
 Intermediate hosts: Planorbis and Segmentina snail
which feed on certain plants: water calthrap, Trapa
natans and T. bicornis; and water chestnut, Eliorchis
tuberosa fertilised by human night soil
130-140×80-85µ(the largest helminth egg).

36.  Enteritis or ulcerative lesions due to the attachment of the adults manifests
abdominal discomfort, nausea, vomiting and diarrhea.
 Malnutrition results from the worms sharing food with the host and diarrhea .
Manifests anaemia, oedema of leg and face even ascites.
 Treatment
 The treatment of the patients, carriers and pigs
 Drug of choice is praziqantel. Also 1g of hexaresorcinol is highly effective.
Other effective drugs include hexachloroparaxylol, bithionol , Tetrachloroethylene,
Niclosamide
 Prevention
 (1) Health education, (2) Deal with night soil.
 (3) Avoid feeding pigs on raw water plants

37. Gall bladder of elk, deer and wild goat in
Russia and Poland
Spiny cuticle
Planorbis snail as intermediate host
Heavy infections are lethal to elk