Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Parasitic infestations of the biliary tract


Published on

  • Login to see the comments

Parasitic infestations of the biliary tract

  2. 2. Amoebiasis Hydatidosis Ascariasis Fascioliasis Clonorchiosis Opisthorchiosis
  3. 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. 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. 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
  6. 6. 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)
  7. 7. 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
  8. 8. 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
  9. 9. Risk factors Contaminated aquatic plant consumption Dietary habits Geographic location Treatment of contaminated plants with high doses of KMnO₄ which decrease metacercariae viability
  10. 10. CLINICAL FEATURES Acute infection: ◦ 3-5 months ◦ Prolonged fever ◦ Hepatomegaly ◦ Abdominal pain ◦ Eosinophilia ◦ Acute cholecystitis like syndrome with significant eosinophilia
  11. 11. 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
  12. 12. 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
  13. 13. Acute eosinophilic cholecystitis – pruritis and intermittent jaundice chronic granulomatous inflammation Hepatic fibrosis Cholangiocarcinoma
  14. 14. 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
  15. 15. COMPUTED TOMOGRAPHY Multiple hepatic metastasis like lesions Change in position, attenuation, and shape over time Hepatomegaly Subcapsular hematoma Sub capsular Tract like hypodense lesions
  16. 16. 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
  17. 17. 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
  18. 18. 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
  19. 19. 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
  20. 20. 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
  21. 21. 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
  22. 22. 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
  23. 23. CLINICAL FEATURES Mostly asymptomatic 5%-10% - non specific symptoms ◦ Fever ◦ Rash ◦ Malaise ◦ RUQ pain ◦ Flatulence ◦ Fatigue
  24. 24. Clonorchis sinensis ◦ Acute : asymptomatic and non-specific symptoms ◦ Chronic: Recurrent cholangitis Cholecystitis Obstructive jaundice Hepatomegaly Cholelithiasis Multiple hepatic tumours Cholangiocarcinoma
  25. 25. Opisthorchis viverrini: ◦ Acute : 5-10% have non-specific symptoms ◦ Chronic: Hepatomegaly Intrahepatic duct stones Recurrent suppurative cholangitis Cholangiocarcinoma
  26. 26. 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
  27. 27. 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
  28. 28. 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
  29. 29. Treatment Praziquantel O. viverrini – single dose (40-50 mg/kg) C. sinensis – 25 mg/kg three times at 5 hour intervals in 1 day
  30. 30. 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
  31. 31. Adult worm of A. lumbricoides
  32. 32. 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
  33. 33. 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
  34. 34. 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)
  35. 35. 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
  36. 36. 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
  37. 37. Diagnosis Stool analysis for ova and dead worms Leukocytosis – suppurative complications Hyperbilirubinemia – hepatopancreatic ascariasis Elevated liver enzymes in cholangitis S. amylase elevation
  38. 38. 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
  39. 39. MRCP – useful in pancreaticobiliary ascariasis ERCP – diagnostic and therapeutic EUS PTC – in cases of failed ERCP
  40. 40. Management Conservative Endoscopic extraction Surgical intervention
  41. 41. Conservative Spontaneous return to duodenum in 98% of children Parenteral analgesics and antispasmodics – relax sphincter NGA IV fluids Piperazine citrate through nasobiliary catheter
  42. 42. Oral anti-helminthics: ◦ Albendazole 400 mg/day for 1 day ◦ Mebendazole 100 mg BD for 3 days and ◦ Pyrantel palmoate 11mg/kg single dose
  43. 43. 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
  44. 44. 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