Fascioliasis

(Assignment)

Submitted to: Dr. M. Abdul Hafeez

Submitted by: Adeel Mumtaz Abbasi

2019-MPhil-1123
 Fascioliasis
Fascioliasis is an infectious disease caused by Fasciola parasites, which are flat worms referred
to as liver flukes. The adult (mature) flukes are found in the bile ducts (the duct system of the
liver) of infected people and animals, such as sheep and cattle. In general, fascioliasis is more
common in livestock and other animals than in people.

Epidemiology

Fasciola hepatica is found in focal areas of more than 70 countries, in all continents except
Antarctica. It is found in parts of Latin America, the Caribbean, Europe, the Middle East, Africa,
Asia, and Oceania. Fasciola gigantica is found in fewer geographic regions. Human cases have
been reported in the tropics, in parts of Africa and Asia, and also in Hawaii.

Etiology

The trematodes Fasciola hepatica (also known as the common liver fluke or the sheep liver
fluke) and Fasciola gigantica are large liver flukes (F. hepatica: up to 30 mm by 15 mm; F.
gigantica: up to 75 mm by 15 mm), which are primarily found in domestic and wild ruminants
(their main definitive hosts) but also are causal incedents of fascioliasis in humans.

Morphology
Fasciola hepatica is one of the largest flukes of the
world. Adult Fluke Leaf like shape, Length - 30 mm
, Width - 13 mm Aprox. It has powerful oral suckers
located at te end of cone-shaped projection at the
anterior end. A marked widening of the body at the
base of the oral cone gives the worm the
appearance of having shoulders. The tegument is
covered with large, scale like spines. Eggs are
operculated and measure approx. 130µm to 150
µm in length and 65-90 width.
Life Cycle

Immature eggs are discharged in the biliary ducts and passed in the stool . Eggs become
embryonated in freshwater over ~2 weeks ; embryonated eggs release miracidia ,
which invade a suitable snail intermediate host . In the snail, the parasites undergo
several developmental stages (sporocysts , rediae , and cercariae ). The cercariae
are released from the snail and encyst as metacercariae on aquatic vegetation or other
substrates. Humans and other mammals become infected by ingesting metacercariae-
contaminated vegetation (e.g., watercress) . After ingestion, the metacercariae excyst in
the duodenum and penetrate through the intestinal wall into the peritoneal cavity. The
immature flukes then migrate through the liver parenchyma into biliary ducts, where they
mature into adult flukes and produce eggs . In humans, maturation from metacercariae
into adult flukes usually takes about 3–4 months; development of F. gigantica may take
somewhat longer than F. hepatica.
Pathogenesis
After the larvae (metacercariae encysted on the vegetation) ingested, a symptomless
incubation period starts, lasting for a few days to a few months. This is followed by an acute
and a chronic clinical phase.

Acute phase. The acute phase, lasting 2-4 months, begins when the immature worms
penetrate the intestinal wall and the peritoneum, the protective membrane surrounding the
internal organs . From here, they puncture the liver's surface and eat their way through its
tissues until they reach the bile ducts. This invasion kills the liver's cells and causes intense
internal bleeding.

Chronic phase. The chronic phase begins when the worms reach the bile ducts, where they
mature and start producing eggs. These eggs are released into the bile and reach the intestine,
where they are evacuated in faeces, thereby completing the transmission cycle.

Signs & Symptoms

Fasciolosis ranges in severity from a devastating disease in sheep, alpacas, and llamas to an
asymptomatic infection in cattle. The course usually is determined by the number of
metacercariae ingested. Acute disease occurs 2–6 wk after the ingestion of large numbers of
metacercariae over a short period.In sheep, acute fasciolosis occurs seasonally and is manifest
by a

 Distended, painful abdomen;

 Anemia; and sometimes sudden death occurring 2–6 wk after infection.

The acute syndrome can be complicated by concurrent infections with Clostridium novyi,
resulting in “black disease” (clostridial necrotic hepatitis).

Chronic fasciolosis can be seen in all seasons but manifests primarily in late fall and winter. It
occurs as a result of ingesting moderate numbers of metacercariae over longer periods of
time;

 Signs include anemia, unthriftiness, submandibular edema, and

 Reduced milk production, but even heavily infected cattle may show no clinical signs
although their immunity to other pathogens (eg, Salmonella spp) may be reduced.
 Heavy chronic infection is fatal in sheep, alpacas, and llamas.
 Sheep do not appear to develop resistance to infection, and chronic liver damage is
cumulative over several years. In cattle, a partial acquired resistance develops
beginning 5–6 mo after infection.
Lesions
Severity depends on the number of
metacercariae ingested, the phase of
development in the liver, and the species
of host involved. During the first phase,
immature, wandering flukes destroy liver
tissue and cause hemorrhage. The second
phase occurs when the flukes enter the
bile ducts, where they ingest blood and
damage the mucosa with their cuticular
spines. In acute fasciolosis, damage is
extensive; the liver is enlarged and friable with fibrinous deposits on the capsule. Migratory
tracts can be seen, and the surface has an uneven appearance. In chronic cases, cirrhosis
develops. The damaged bile ducts become enlarged, or even cystic, and have thickened,
fibrosed walls.

In cattle but not sheep, the duct walls

become greatly thickened and often
calcified. Aberrant migrations occur
more commonly in cattle, and
encapsulated flukes may be found in
the lungs. Tissue destruction by
wandering flukes may create a
microenvironment favorable for
activation of clostridial spores.

Diagnosis
Fascioliasis may be suspected on the basis of the clinical picture
supported with the history of grazing near ponds or lakes,
supposedly the habitat involving snails. Whenever liver blockage
coincides with a history of watercress consumption, fascioliais should
be suspected. Specific diagnosis depends on finding eggs in the faeces.
Some concentrations techniques of detecting eggs in fecces are very
helful like floatation and sedimentation methods.

Fig - Fasciola hepatica egg in an unstained wet mount (400x

magnification): F. hepatica eggs are broadly ellipsoidal,
operculated, and measure 130–150 μm by 60–90 μm.
Treatment
• Triclabendazole @ 20 mg/kg body weight in two divided doses 12-24 hours apart.

• Clorsulon @ 7mg/kg

Control
– Treat the herd with suitable Anthelmintics.
– Control measures for F hepatica ideally should involve reduction of the intermediate host snail
population,
– prevention of livestock access to snail-infested pasture.

In practice, only the first of these is used in most cases. Although molluscicides can be used to
reduce lymnaeid snail populations, Copper sulfate, if applied before the snail population multiplies
each year, is effective but toxic to sheep, which must be kept off treated pasture for 6 wk after
application. Prevention of livestock access to snail-infested pasture is frequently impractical
because of the size of the areas involved and the consequent expense of erecting adequate
fencing.

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References

Centre For Disease Control and Prevention CDC

https://www.cdc.gov/parasites/fasciola/gen_info/faqs.html

MSD Veterinary Manual https://www.msdvetmanual.com/digestive-system/fluke-infections-in-

ruminants/fasciola-hepatica-in-ruminants

World Health Organization

https://www.who.int/foodborne_trematode_infections/fascioliasis/en/

Vetstream https://www.vetstream.com/treat/bovis/bug/fasciola-hepatica

Veterinary Clinical Parasitology 8th Edition