local names, definition, etiology,epidemiology lifecycle, pathogenesis, clinical findings, necropsy finding, diagnosis,treatment, control and prevention
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Fasciolosis
1. Faculty of Veterinary Science
Infectious Diseases II
(Parasitic Diseases)
FASCIOLOSIS
21st ,May ,2016
2. Fasciolosis
Synonyms: Liver fluke disease, liver rot, pipe
stem liver.
It is characterized by both acute and chronic
form of disease caused by large fluke parasitic
in the bile ducts liver mammals characterized
by loss of appetite, debility, jaundice, anemia,
and bottle jaw.
3. Etiology
The disease is caused by Fasciola hepatica and
F.gigantica.the common parasite is F.gigantica
but in the upper hill region F.hepatica may be
recovered from the liver. Its leaf shaped,
broader anteriorly than posteriorly with
anteriorly cone shaped projection fallowed by
pair of broad shoulders.
5. Epidemiology
The parasite has cosmopolitan’s distribution
but more common at places where water
lodging remains for many months. F.gigantica
is found in Asia, Africa, Australia, and India
and F.hepatica is found in European country
and South and North America, high altitude of
Asia and Africa.
6. In India fasciola is mainly caused by F.gigantica
but F.hepatica also present at high altitude and
hilly area. A. P. W. Thomas discovered this
trematode in 1883. Fluke occur in the bile duct
of sheep, goat, ox and other ruminants, pigs,
rabbit, elephants, horse, dog, cat, kangaroo and
man. Disease is more common in cattle and
buffalo and sheep. In case of horse and man,
these fluke are present in lungs. However in goat,
horse and pig the incidence of disease is low.
7. It is transmitted through the snail of Lymnea
Spp. (L.trunneculata, L.aunculata).
10. Pathogenesis
Life cycle of parasite is indirect. Eggs come
faeces and hatch in the environment to
release to the miracidium that penetrate
inside the snail and undergoes asexual
reproduction to develop sporocyst and radiae.
They leave snail in 5-8 weeks from the time of
infection in the form of cercariae. Cercariae
immediately convert in metacercariae. Which
may survive for 4-6 months depending about
humidity.
11. Metacercarie are ingested by definitive host and
excyst in small intestine. Immature larvae
penetrate the lumen and come in peritoneal
cavity than goes to liver capsule to damage liver
parenchyma during movement, where it live and
migrate at places for 6-8 weeks then reaches to
bile ducts. By the time it become mature and
start laying eggs. During migration of larvae
damage parenchyma take place. Adult parasite
sucks blood and it hinders in normal flow of bile
to disturb the digestion.
12. Hepatic damage and loss of enzyme production
also contribute the pathogenesis by disturbing
the digestion.
13. Clinical findings
Disease of entity can be divided into an acute and
chronic form.
Acute
Acute form mostly encounters in sheep and occurs
after 5-6 weeks of ingestion. It occurs because of
liver parenchyma damage by moving immature
fluke causing traumatic hepatitis. The liver is very
much enlarged and become inefficient to cause
anorexia and distended abdomen with painful to
touch due to hepatitis
14. There is hypoprotenemia leading to edema of
dependent parts. Sometimes rupture of liver
capsule and hemorrhage into the peritoneal
cavity may occur. In acute cases the animal
dies suddenly with blood stained froth
appearing at the nostril and anus.
15. Sub-acute
This type of disease occurs in all species of
animals.
In sheep and cattle weight loss, pale mucus
membrane and submandibular edema are
commonly observed.
16. Chronic
Chronic form mostly occur in cattle and buffalo.
There are digestive disturbances such as
sometimes constipation and other time diarrhea.
There is marked decrease in milk yield, anaemia
weight loss, lack of vigor, paler mucus membrane,
anorexia, and edema of dependent part and
edema in intermandibular space called as bottle-
jaw. Skin becomes dry and wool brittles and
falling out in patches. Prostration occurs in
severely affected animals
18. Necropsy findings
Necropsy is characterized by appearance of
damaged and swollen of liver, sub scapular
hemorrhage, calcification of bile duct (clay-
pipe like appearance) and presence of large,
leaf-like fluke in bile ducts and liver.
19.
20. Diagnosis
Although history and symptoms provide clue,
confirmation can be made by faecal
examination for detection of typically elliptical
eggs, having less distinct embryonic mass,
operculum and yellow in colour. Hematology
will reveal hypercytic, normochromic,
anaemia and eosinophilia. Serological test like
double immunodifusion, ELISA, AGPT are also
helpful in diagnosis. Necropsy finding clearly
elucidate adult parasite in the bile ducts.
23. Refoxanide @ 7,5 mg/kg body weight
Clioxanide @ 20-40 mg/kg body weight
Dianiphenenthial @ 100 mg/kg body weight
Oxylozanide @ 10 mg/kg body weight
Albendazole @ 15 mg/kg body weight
Fendendazole @ 20 mg/kg body weight
Closental @ 10 mg/kg body weight
Triclalbendazole @ 12 mg/kg body weight
24. Control
Control of the disease can be achieved by
regular prophylactic treatment at least two
times in a year during months of February-
March and September-October. Therapeutic
treatment as and when required should be
carried out to minimize the chance of spread
of disease to other contact animals.
Management practices particularly in aspect
of hygiene should be regularly monitored.
25. If possible attempt should be made for
disruption of meracedia, as it may be most
suitable aspect of disease control. Control of
snails may be achieved by CuSO4, other
molluscicide and by the ducks that feed on
snails. Vaccination are been tried but still at
experimental stage.
26. Conclusion
Fasciolosis is a common fluke infestation of
domestic animal that causes heavy production
losses. An intermediate host, snail is required
for compilation of life-cycle. Disease is
clinically manifested by loss of appetite,
weight, jaundice, anaemia, and reduce milk
yield. Regular deworming decreases the
burden of disease in domestic animals.
Editor's Notes
Hepatica – 20-30 mm long and 13 mm wide
Gigantica – 25-75 mm long and 12 mm wide
Adults are hermaphroditic and can produce thousands of eggs in a day
F. hepatica – Europe, America (specifically the south and west), Australia – more temperate areas
F. gigantica – Asia and Africa – more tropical areas (NOTE: this map seems to have gotten it backwards…all my other sources say it’s the other way around)
2.4 million people infected
180 million people are at risk
A lot of cases are probably not reported, especially in Africa (note question marks)
This is mostly in the developing countries, and not developed ones, as a neglected disease, it has largely been eliminated from the developed world and so is largely forgotten in the developing world
Fluke eggs are contained in the feces of the infected organism.
Once it gets into the water by fecal contamination or washed out by heavy rains, the embryo (miracidium) begins to develop (and not before, though it can last for a while in the feces)
The eggs hatch to release larvae (called miracidium)
The larvae have to find a host immediately because they cannot survive longer than 24 hours on their own, so they infect snails (usually the Lymnaea)
Inside the snail, they transform into a sporocyst and migrate to the digestive gland, also known as the liver
when they hatch, they produce larvae (rediae) that are much more active than the sporocyte and so damage the liver considerably more.
Once fully developed into the third stage within the snail liver (cercariae), these organisms then escape inot the water
These cercariae encyst 1-2 minutes to 2 hours onto aquatic plants and develop into metacercariae.
Humans and animals are infected by eating these plants uncooked;
the immature flukes are released from the metacercariae cysts within an hour in the small intestine.
The flukes penetrate the intestinal wall and travel throught the abdominal cavity to the liver
It usually takes the flukes 4-6 days to reach the liver; after they do, the burrow into the liver where they grow in size
7 weeks into the infection, the flukes reach the bile ducts in the liver where they grow and mature into adults
8 weeks into the infection, eggs are found in the bile and then feces of the infected organism
NOTE: the more flukes that infect, the longer it takes them to mature
Chronic phase: can develop months to years after the initial infection
reach bile ducts – can get thickening and calcification of said ducts,
inflammation leads to thickening of ducts and gallbladder,
fibrosis – which is the creation of excess connective tissue in an attempt to heal
eventual blockage due to parasites or parasite fragments which results in biliary colic pain – similar to having a stone in your gall bladder
can also cause jaundice and anaemia
This is why they call it liver rot
It is assumed that humans are not the ideal host, because a lot of the flukes die in the liver parenchyma without reaching the bile ducts.
Very low mortality rate in humans- if they do die (a few cases have been reported) it’s usually because the bile duct is blocked
However, they can die of complications, such as bleeding from the haemmorhaging
Most physical immune barriers (mucus membranes, skin, gastric acid, body temperature) aren’t effective against Fasciola
- they are ingested usually
- gastric acid helps the worms excyst from the metacercariae
Best test: Detecting eggs in stools is the best but this is difficult and unreliable in humans
- humans are not the ideal host and so flukes may exist but if they don’t grow to maturity, then they won’t release eggs
ultrasound, CT scans and MRI – these are very expensive though
Immunoserological tests(like some of the papers we’ve read) used to find it in your blood