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Page 1: Parasitic infestations of the biliary tract

PARASITIC INFESTATIONS OF THE BILIARY TRACT

Page 2: Parasitic infestations of the biliary tract

AmoebiasisHydatidosisAscariasisFascioliasisClonorchiosisOpisthorchiosis

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FASCIOLIASISEtiology:

Zoonosis caused by trematode◦Fasciola hepatica◦Fasciola giganticaEpidemiology

F. hepatica – temperate zonesF. gigantica – tropical zones

Now has become global in distribution

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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

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Life cycleF. hepatica flukes

are large, flat, brown and leaf shaped

25 -30 mm by 10-15 mm

F. gigantica upto 75 mm

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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)

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Life cycleConsumption 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

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Extrahepatic forms or ectopic infectionsJuvenile 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

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Risk factorsContaminated aquatic plant

consumptionDietary habitsGeographic location

Treatment of contaminated plants with high doses of KMnO₄ which decrease metacercariae viability

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CLINICAL FEATURESAcute infection:

◦3-5 months◦Prolonged fever◦Hepatomegaly◦Abdominal pain◦Eosinophilia ◦Acute cholecystitis like syndrome

with significant eosinophilia

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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

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CHRONIC INFECTION 3-6 months after consumption of

metacercariaeSymptoms – biliary obstruction with

colicky pain in RUQ, epigastrium;Extrahepatic cholestatic syndromeElevation of liver enzymesDilated CBD, parasites in GB and

CBD, stones in GB and bile ductHemobilia

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Acute eosinophilic cholecystitis – pruritis and intermittent jaundice

chronic granulomatous inflammation

Hepatic fibrosisCholangiocarcinoma

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INVESTIGATIONSUSG 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

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COMPUTED TOMOGRAPHYMultiple hepatic metastasis like

lesionsChange in position, attenuation,

and shape over timeHepatomegaly Subcapsular hematomaSub capsular Tract like

hypodense lesions

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CTStages

◦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

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LAB. DIAGNOSISAcute 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

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SURGERY IN FASCIOLIASISChronic phase – biliary obstruction with

choledocholithiasisIncidentally found in cholecystectomy

specimens and T-tubesERCP – when there is biliary obstructionIn cholangitis – antiparasites,

percutaneous drainage and anti-biotics ( against E. faecalis, E. coli )

Incidental met. Like lesions in D-lap with eosinophilia – consider fascioliasis

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CHEMOTHERAPYTriclabendazole

◦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

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CLONORCHIASIS AND OPISTHORCHIASISClonorchiasis

◦Clonorchis sinensis◦Chinese or oriental liver fluke

Opisthorchiasis ◦Opisthorchis viverrini◦Opisthorchis felineusCommonly found in oriental countries

– China, Laos, Thailand, Korea, Japan, Taiwan

Eating raw and uncooked fish

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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

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Metacercariae navigate through ampulla of vater mature into adult worms in bile ducts

Live for 45 years in liver1000-2500 eggs/dayReside in medium to small

intrahepatic bile ducts, extrahepatic ducts, GB and pancreatic duct

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CLINICAL FEATURESMostly asymptomatic5%-10% - non specific symptoms

◦Fever◦Rash ◦Malaise◦RUQ pain◦Flatulence ◦Fatigue

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Clonorchis sinensis◦Acute : asymptomatic and non-

specific symptoms◦Chronic:

Recurrent cholangitis Cholecystitis Obstructive jaundice Hepatomegaly Cholelithiasis Multiple hepatic tumours Cholangiocarcinoma

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Opisthorchis viverrini:◦Acute : 5-10% have non-specific

symptoms◦Chronic:

Hepatomegaly Intrahepatic duct stones Recurrent suppurative cholangitis Cholangiocarcinoma

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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

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CHOLANGIOCARCINOMA AND FLUKES O. viverrini ( More common ) C. sinensisSecretion of parasite proteins

with mitogenic properties into bile ducts

Ov-GRN-1Inflammation around biliary tree;

epithelial hyperplasia; metaplasia of mucin-producing cells and periductal fibrosis

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DIAGNOSISEggs in stool sampleSerology : 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

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TreatmentPraziquantelO. viverrini – single dose (40-50

mg/kg)C. sinensis – 25 mg/kg three

times at 5 hour intervals in 1 day

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BILIARY ASCARIASISAscaris lumbricoidesRoundworm – 20-30 cm in lengthTropical and sub-tropical regionsPoor socioeconomic conditionsSource of infection -Fecal

contamination of soil and farmsSymptoms – when worms enter

biliary tree

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Adult worm of A. lumbricoides

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Life cycleAdult 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

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PathologyAscaris 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 intestineCommon in women and pregnant

women (progesterone)Common after cholecystectomy,

sphincterotomy, choledochostomy

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Impacted worm sphincter of oddi spasm biliary colic

Suppurative cholangitis cholangiohepatic abscess

Acalculous cholecystitis, empyema, perforation of bile duct

Acute pancreatitisDuctal stricture and stones

( dead worms)

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Clinical featuresChildren ; 2-8 yrsAdults in endemic areas – 35 yrs

(mean)Women > menHistory of previous biliary surgeryVomiting of wormsWorms in stools

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Sudden severe upper abdominal painRUQ tenderness and guardingLow grade feverJaundice is usually absentComplications

◦Early Acute suppurative cholangitis Hepatic ascariasis Acute pancreatitis

◦Late- calculi and strictures

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Diagnosis Stool analysis for ova and dead

wormsLeukocytosis – suppurative

complicationsHyperbilirubinemia –

hepatopancreatic ascariasisElevated liver enzymes in

cholangitisS. amylase elevation

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Imaging Abdominal radiographs – worms can

be seenUSG – 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 sensitiveEndoscopy – worm in duodenum;

protruding from ampulla of water

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MRCP – useful in pancreaticobiliary ascariasis

ERCP – diagnostic and therapeutic

EUSPTC – in cases of failed ERCP

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ManagementConservativeEndoscopic extractionSurgical intervention

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ConservativeSpontaneous return to duodenum

in 98% of childrenParenteral analgesics and

antispasmodics – relax sphincterNGAIV fluidsPiperazine citrate through

nasobiliary catheter

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Oral anti-helminthics:◦Albendazole 400 mg/day for 1 day◦Mebendazole 100 mg BD for 3 days

and◦Pyrantel palmoate 11mg/kg single

dose

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Endoscopic interventionsERCP with sphinterotomy and removal of

wormsExtracted from papillary opening using

dormia basketEndoscopic papillary balloon dilatationRequires multiple sessionsIndications:

◦Severe persistent pain unresponsive to antihelminthics

◦Symptoms or USG abnormalities persist 2 wks after conservative line

◦ Increasing jaundice

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SurgicalPTC – in failed ERCP with cholangitisIndications 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