1. PARASITIC INFESTATIONS
OF THE BILIARY TRACT

2. Amoebiasis
Hydatidosis
Ascariasis
Fascioliasis
Clonorchiosis
Opisthorchiosis

3. FASCIOLIASIS
Etiology:
Zoonosis caused by trematode
◦ Fasciola hepatica
◦ Fasciola gigantica
Epidemiology
F. hepatica – temperate zones
F. gigantica – tropical zones
Now has become global in distribution

4. Epidemiologic pattern
◦ Cases imported by migration
◦ Autochthonous – isolated, sporadic
infection in areas where animal infestation
is present
◦ Endemic fascioliasis
◦ Epidemic fascioliasis – in animal endemic
and human endemic areas

5. Life cycle
F. hepatica flukes
are large, flat,
brown and leaf
shaped
25 -30 mm by 10-
15 mm
F. gigantica upto 75
mm

7. Adult flukes in common and hepatic
bile ducts of human or animal
Eggs – oval, yellowish brown; 130x60
microns
Eggs in tepid water  miracidia (9 to
14 days)
Miracidia  freshwater snails 
sporozoites and redia (4 to 7 weeks)
 free swimming cercaria 
watercress, water lettuce, alfalfa
(aquatic plants)

8. Life cycle
Consumption of Aquatic plants
contaminated with metacercaria 
excyst in the duodenum 
migrate through bowel wall and
peritoneal cavity 
Glisson capsule of liver (after 4 wks)

initiate larval, hepatic and invasive
stages of infection

9. Extrahepatic forms or ectopic
infections
Juvenile larva  adult flukes ( 3-5
months)
Adult fluke worms produce eggs in 4
months eggs traverse sphincter of
Oddi  intestine
Flukes live in biliary tracts between 9-
13.5 years
Women more affected; more
complications

10. Risk factors
Contaminated aquatic plant
consumption
Dietary habits
Geographic location
Treatment of contaminated plants with
high doses of KMnO₄ which decrease
metacercariae viability

12. CLINICAL FEATURES
Acute infection:
◦ 3-5 months
◦ Prolonged fever
◦ Hepatomegaly
◦ Abdominal pain
◦ Eosinophilia
◦ Acute cholecystitis like syndrome with
significant eosinophilia

13. Hyperbilirubinemia is absent in acute
phase
Anorexia, weight loss, nausea,
vomiting, urticaria
Lasts from migration of immature
larvae from duodenum to liver and
biliary duct

14. CHRONIC INFECTION
3-6 months after consumption of
metacercariae
Symptoms – biliary obstruction with
colicky pain in RUQ, epigastrium;
Extrahepatic cholestatic syndrome
Elevation of liver enzymes
Dilated CBD, parasites in GB and
CBD, stones in GB and bile duct
Hemobilia

15. Acute eosinophilic cholecystitis –
pruritis and intermittent jaundice
chronic granulomatous inflammation
Hepatic fibrosis
Cholangiocarcinoma

18. INVESTIGATIONS
USG Abdomen :
◦ Acute
Focal areas of increased echogenicity
Multiple nodular lesions
Single, complex mass in liver
Mimics malignancy
◦ Chronic
Less specific
Parasites in GB and CBD
Thickening of GB and CBD walls
Stones in CBD

19. COMPUTED TOMOGRAPHY
Multiple hepatic metastasis like
lesions
Change in position, attenuation, and
shape over time
Hepatomegaly
Subcapsular hematoma
Sub capsular Tract like hypodense
lesions

20. CT
Stages
◦ Early : contrast enhancement of Glisson
capsule
◦ Intermediate : subcapsular multiple
hypodense nodular areas, tortuous,
tunnel-like lesions
◦ Late stage : necrotic granuloma as a
single, non-contrast-enhanced hypodense
irregular mass in liver
◦ Liver calcification

21. LAB. DIAGNOSIS
Acute phase
◦ Antibodies against Cathepsin L1 by
ELISA
◦ Anti-parasitic trial
◦ Eosinophilia
Chronic phase
◦ Visualisation of parsitic egg in stool
◦ Sedimentation technique to concentrate
the eggs
◦ Serial stool specimens

22. SURGERY IN FASCIOLIASIS
Chronic phase – biliary obstruction with
choledocholithiasis
Incidentally found in cholecystectomy
specimens and T-tubes
ERCP – when there is biliary obstruction
In cholangitis – antiparasites,
percutaneous drainage and anti-biotics (
against E. faecalis, E. coli )
Incidental met. Like lesions in D-lap with
eosinophilia – consider fascioliasis

23. CHEMOTHERAPY
Triclabendazole
◦ Single dose of 10 mg/kg
◦ Better absorption with fatty meal
◦ Adverse effect – biliary colic;
antispasmodic to be administered
concurrently
◦ Other drugs
Bithionol
dehydroemetine
nitazoxanide

24. CLONORCHIASIS AND
OPISTHORCHIASIS
Clonorchiasis
◦ Clonorchis sinensis
◦ Chinese or oriental liver fluke
Opisthorchiasis
◦ Opisthorchis viverrini
◦ Opisthorchis felineus
Commonly found in oriental countries –
China, Laos, Thailand, Korea, Japan,
Taiwan
Eating raw and uncooked fish

26. Life cycle
Two intermediate hosts : Fresh water
snail & Fish
Human host  adult worms  eggs in
stools  water  fresh water snail 
miracidia  sporocyst, redia and
cercaria in snail  freshwater fish 
metacercariae in muscles of fish 
metacercarial cyst (acid resistant ) 
small intestine of human  Liver

28. Metacercariae navigate through
ampulla of vater  mature into adult
worms in bile ducts
Live for 45 years in liver
1000-2500 eggs/day
Reside in medium to small
intrahepatic bile ducts, extrahepatic
ducts, GB and pancreatic duct

29. CLINICAL FEATURES
Mostly asymptomatic
5%-10% - non specific symptoms
◦ Fever
◦ Rash
◦ Malaise
◦ RUQ pain
◦ Flatulence
◦ Fatigue

30. Clonorchis sinensis
◦ Acute : asymptomatic and non-specific
symptoms
◦ Chronic:
Recurrent cholangitis
Cholecystitis
Obstructive jaundice
Hepatomegaly
Cholelithiasis
Multiple hepatic tumours
Cholangiocarcinoma

31. Opisthorchis viverrini:
◦ Acute : 5-10% have non-specific
symptoms
◦ Chronic:
Hepatomegaly
Intrahepatic duct stones
Recurrent suppurative cholangitis
Cholangiocarcinoma

32. Opisthorchis felineus:
◦ Raw, salted and frozen fish consumption
◦ Acute
High grade fever
Nausea and vomiting
Abdominal pain
Malaise, arthralgia and lymphadenopathy
Eosinophilia with Increased LFT
◦ Chronic
Liver abscess and suppurative cholangitis

33. CHOLANGIOCARCINOMA AND
FLUKES
O. viverrini ( More common )
C. sinensis
Secretion of parasite proteins with
mitogenic properties into bile ducts
Ov-GRN-1
Inflammation around biliary tree;
epithelial hyperplasia; metaplasia of
mucin-producing cells and periductal
fibrosis

34. DIAGNOSIS
Eggs in stool sample
Serology : Ov-CP-1 based ELISA ,
doesn’t distinguish recent or past
infection
USG : Intrahepatic duct dilation;
increased periductal echogenicity; GB
sludge
PCR to detect adult parasite DNA in
stool samples

35. Treatment
Praziquantel
O. viverrini – single dose (40-50
mg/kg)
C. sinensis – 25 mg/kg three times at
5 hour intervals in 1 day

36. BILIARY ASCARIASIS
Ascaris lumbricoides
Roundworm – 20-30 cm in length
Tropical and sub-tropical regions
Poor socioeconomic conditions
Source of infection -Fecal
contamination of soil and farms
Symptoms – when worms enter biliary
tree

37. Adult worm of A. lumbricoides

38. Life cycle
Adult worm in human intestine 
Female lay eggs 
Feces  warm moist soil 
maturation mature egg  human
ingestion
Hatch in duodenum larvae 
penetrate mucosa  portal venous
blood  liver  right heart  pulm.
Capillary bed  trachea 
esophagus  Jejunum

40. Pathology
Ascaris reach duodenum
◦ Increased load in jejnum
◦ Increased intestinal motility
One or two worms enter biliary system
via ampulla of vater
Part of worm may remain in intestine
Common in women and pregnant
women (progesterone)
Common after cholecystectomy,
sphincterotomy, choledochostomy

41. Impacted worm  sphincter of oddi
spasm  biliary colic
Suppurative cholangitis 
cholangiohepatic abscess
Acalculous cholecystitis, empyema,
perforation of bile duct
Acute pancreatitis
Ductal stricture and stones ( dead
worms)

42. Clinical features
Children ; 2-8 yrs
Adults in endemic areas – 35 yrs
(mean)
Women > men
History of previous biliary surgery
Vomiting of worms
Worms in stools

43. Sudden severe upper abdominal pain
RUQ tenderness and guarding
Low grade fever
Jaundice is usually absent
Complications
◦ Early
Acute suppurative cholangitis
Hepatic ascariasis
Acute pancreatitis
◦ Late- calculi and strictures

44. Diagnosis
Stool analysis for ova and dead
worms
Leukocytosis – suppurative
complications
Hyperbilirubinemia – hepatopancreatic
ascariasis
Elevated liver enzymes in cholangitis
S. amylase elevation

45. Imaging
Abdominal radiographs – worms can
be seen
USG – dilated bile ducts containing
linear or round areas of increased
echogenicity;GB sludge, movement of
worms in biliary system; alternating
echogenic and echolucent strips
CT is less sensitive
Endoscopy – worm in duodenum;
protruding from ampulla of water

46. MRCP – useful in pancreaticobiliary
ascariasis
ERCP – diagnostic and therapeutic
EUS
PTC – in cases of failed ERCP

47. Management
Conservative
Endoscopic extraction
Surgical intervention

48. Conservative
Spontaneous return to duodenum in
98% of children
Parenteral analgesics and
antispasmodics – relax sphincter
NGA
IV fluids
Piperazine citrate through nasobiliary
catheter

49. Oral anti-helminthics:
◦ Albendazole 400 mg/day for 1 day
◦ Mebendazole 100 mg BD for 3 days and
◦ Pyrantel palmoate 11mg/kg single dose

50. Endoscopic interventions
ERCP with sphinterotomy and removal
of worms
Extracted from papillary opening using
dormia basket
Endoscopic papillary balloon dilatation
Requires multiple sessions
Indications:
◦ Severe persistent pain unresponsive to
antihelminthics
◦ Symptoms or USG abnormalities persist 2
wks after conservative line
◦ Increasing jaundice

51. Surgical
PTC – in failed ERCP with cholangitis
Indications of surgery
◦ Intrahepatic duct worms, stones, strictures
and abscess
◦ Gall bladder ascariasis
◦ Procedure:
Longitudinal choledochotomy
Lap. Cholecystectomy with CBD exploration
Choledochoscopy
T-tube intra and post-operatively