L14: Liver Flukes Flashcards
What are Fasciola
F. hepatica and F. giganitca
infects animal definitve host cause ruminant faciolisais or liver rot disease
veterinary + medical importance
humans are accidental definitive cause fasciolsis zoonosis, worldwide
where do liver flukes live
bile ducts, gall bladder, liver tissue of vertibrate hosts
Comapre F.hepatica and F. gigantica
F.hapatica
sheep liver fluke
infects domestic aniamsl
worldwide
temperate countries
F. giganitca
definitive hosts are cattle, camel, water buffalo sometimes goat, sheep, donkeys
tropical and subtropical
Africa, South Asia, Far east
Faciola life cycle
Immature eggs are discharged in the biliary ducts and
passed in the stool
2. Eggs become embryonated in freshwater over ~2 weeks
3. Embryonated eggs release miracidia
4. Miracidia invade snail intermediate hosts. In the snail,
parasites undergo several developmental stages from
sporocysts (4a) to rediae (4b) to cercariae (4c)
5. Cercariae are released from the snail and encyst as
metacercariae on aquatic vegetation or other substrates
6. Mammalian definitive hosts become infected by ingesting
metacercariae-contaminated vegetation (e.g., watercress).
7. After ingestion, the metacercariae excyst in the duodenum
and penetrate through the intestinal wall into the peritoneal
cavity.
8. 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 longer than F.
hepatica
Fasciolosis in animals
feed of epitherlial cells and suck blood
infection depends on number of metacercariaes ingested
acute + subacute
in sheep and camelides, >2000 metacear in short period or less in sort
traumatic haptiis as immune flukes go to river => distended abdomen, anemia, death
chronic
common in cattle, reduced milk, anemica,
develop partial acquired resistance so even chronic not really fatal but other animals do not
Fasciolosis in humans
suck on blood, asymptomatic heavy infection => acute with serious liver damage
acute
migratory, invase, larval
inflammation, tissue destruction, toxic/allergic reaction
nonspecific sympmtms, headache, backache..
juveniles get lost and it become ectopic
chronic
bilairy/adult
months or years after due to mechanical damage, liver and bile ravaged, diarrhoea, anemia, portal vessel atrophy
metabolic product => inflammatory => secondary condition => death
What is Clonorchis sinesis
Chinese/oritenal small liver fluke
def hosts are humans, dogs, carnivrious fish
first intermediate: snails, many species
second: freshwater fish
causes clonorchiasis
Life cycle of C. sinensis
- C. sinensis eggs are discharged in the biliary ducts and in
the stool in the embryonated state - Eggs are ingested by a suitable snail intermediate host.
Eggs release miracidia (2a), which develop through
sporocysts (2b) rediae (2c) and cercariae (2d) stages - The cercariae are released from the snail and, after a
short period of free-swimming in water, they encounter,
and penetrate the flesh of freshwater fish, where they
encyst as metacercariae - Infection of humans and other definitive hosts occurs by
ingestion of infected, undercooked, salted, pickled, or
smoked freshwater fish - After ingestion, the metacercariae excyst in the
duodenum - Freed metacercariae migrate through the biliary tract
into the biliary ducts where they become sexually mature
adult flukes and reside. Maturation takes ~1 month.
Explain Clinical presentation of Clonorchiasis
Most infections are light and asymptomatic, and symptoms are very rare and are related to the worm burden
* Common symptoms include weakness, weight loss, diarrhoea, anemia, edema, secondary bacterial infections,
abdominal pain, and inflammatory symptoms associated with the worm’s metabolic products
* In endemic areas, chronic and heavy infections (up to thousands of worms) can cause:
✓ Liver damage
✓ Hepatitis & liver cirrhosis
✓ Damage to the bile ducts resulting in jaundice
✓ Gall stones & biliary obstruction
✓ Recurrent cholangitis and pancreatitis
✓ hemorrhage
* Hepatomegaly and cancer of the bile duct (choloangiocarcinoma) may develop
* Unlike Fasciola, Clonorchis does not invade liver tissues. Therefore, it does not cause extensive liver necrosis
* Clonorchiasis is rarely fatal
Diagnosis of Fascioliasis & Clonorchiasis diagnosis
eggs in chronic infection in poop, bule, diodental
immunodiagotic serum antibiotic for acute
but cross reactivity may happen for Fascioli and Clonor
Treatment for Fascioliasis & Clonorchiasis
F
prazi doesnt work, use antheleminitcs for animals
for humans use triclabendzole
drug resistance
C
prazi is only recommended
what is Dicrocoelium dendriticum
small, lancet fluke, common in ruminants maybe sheep / cattles
intermedia: snails
inter 2: ants of Formica genus
Life Cycle of Dicrocoelium dendriticum
- Embryonated eggs containing miracidia are shed in feces of
definitive hosts, which are typically ruminants - Eggs are then ingested by the first intermediate host (snails).
When the miracidia hatch (2a), they migrate through the gut wall
and settle into the adjacent vascular connective tissue, where
they become mother sporocysts (2b). The sporocysts migrate to
the digestive gland where they give rise to several daughter
sporocysts. Inside each daughter sporocyst, cercariae are
produced (2c) - Cercaria migrate to the respiration chamber. Their presence here
irritates the snail and mucus is secreted around them. Infected
snails expel these masses of mucus and cercariae as a slime ball
in grass - Ants (second intermediate hosts) feed on these slime balls.
Ingested cercariae become free in the intestine and migrate to
the hemocoel where they become metacercariae - When the infected ant is eaten by a suitable definitive host, the
metacercariae excyst in the small intestine. - The worms migrate to the bile duct where they mature into
adults - Humans can serve as definitive hosts after ingesting infected ants
(e.g., on contaminated food items)
Dicrocoelium dendriticum clinical presentation
cows, sheep goat no immunity, heavy infections can happen => cirrohissi => thick bile ducts
alpaca
acute decline , anemia => cirrhosis, absess, granulomas
liver spoilt bad for buisness
Dicrocoelium dendriticum: Clinical presentation in humans
accidental defeintive host, low number of fukes, low symptoms
if intense => liver absses, GIT stress, colecysists
