Pyogenic and amebic liver infections and infestations are described. Pyogenic liver abscesses are usually caused by bacteria spreading from another infected site via the bloodstream and are typically treated with antibiotics and drainage. Amebic liver abscesses are caused by the parasite Entamoeba histolytica and present with right upper quadrant pain, fever, and tenderness. Diagnosis involves blood tests and imaging, and treatment consists of antiparasitic medications and sometimes drainage. Hydatid cysts are caused by the tapeworm Echinococcus granulosus and seen endemic areas; they may cause liver masses, pain, or allergic reactions.

1. LIVER INFECTIONS AND
INFESTATIONS
DR. BARUN KUMAR

2. AT A GLANCE
I.INFECTIONS
A. PYOGENIC LIVER ABSCESS
II. INFESTATIONS
A. AMOEBIC LIVER ABSCESS
B. HYDATID DISEASE
C. LIVER FLUKE DISEASE
A)FASCIOLA HEPATICA
B) CLONORCHIS SINENSIS
C) BILIARY ASCARIASIS

3. PYOGENIC LIVER ABSCESS
• Once considered invariably fatal, has now
became a perfectly treatable disease with
following advances:
a) Antimicrobial therapy
b) Surgical drainage
c) USG/ CT scan
d) percutaneous drainage procedures

4. ETIOLOGY
MOST FREQUENT CAUSES OF PYOGENIC LIVER ABSCESS
A. Hepatobiliary
Benign
Lithiasis, Cholecystitis, Biliary-enteric anastomosis
Endoscopic biliary procedures, Percutaneous biliary procedures
Malignant
B. PORTAL
Benign
Diverticulitis
Anorectal suppuration ,Pelvic suppuration
Postoperative sepsis
Intestinal perforation ,Pancreatic abscess , Appendicitis
Malignant – gastric, colonic Ca
C.ARTERIAL
Endocarditis ,Vascular sepsis ,Ear, throat, nose infection
Dental infection
D.TRAUMATIC
Benign - Open or closed abdominal trauma
Malignant- Chemoembolization
Percutaneous ethanol injection or radiofrequency
E.CRYPTOGENIC
F. DIRECT EXTENSION FROM A NEARBY NIDUS OF INFECTION

5. PATHOGENESIS
• Liver is subjected to a heavy load of bacteria on a
continuous basis through portal blood
• Development of abscess occurs when liver fails to clear
it
• The primary cause being obstruction in biliary tree and
infection
• Immunosuppression and particularly diabetes has been
shown to have great association
• RIGHT LOBE has been shown to preferentially involved
(75%):
a) laminar flow to the right lobe from portal vein
b) large mass

6. MICROBIOLOGY
• Most common organism: E.COLI & KLEBSIELLA PNEUMONIAE
• STAPH AUREUS: monobacterial, systemic sepsis, diabetic
• Klebsiella asso with gas forming abscess
• Enterococci and streptococcus viridans
• Uncommon: pseudomonas, enterobacter proteus, other
anaerobes
• Fungal and mycobacterial : immunocompromised
• Depends on the mode of infection
BILIARY TRACT: gram neg with anaerobic (polymicrobial)
SYSTEMIC INFECTIONS: single organsim

7. CLINICAL FEATURES
• The classical triad is of FEVER (96%) + JAUNDICE
(20%)
+ RUQ PAIN (53%) AND TENDERNESS (40-70%)
(triad seen only in 10% of cases)
• Other symptoms depends on complications or
etiology such as involvement of diaphragm may
lead to cough, or rupture will lead to sepsis and
peritonitis
• Endogenous endoophthalmitis: specific to
klebsiella hepatic abscess

8. LABORATORY DIAGNOSIS
• Leucocytosis
• raised liver enzymes and bilirubin
• Elevated pt/inr and hpoalbuminemia (chronicity)
PLAIN X-RAY : reflects sub diaphragmatic pathology
or any lung involvement
ULTRASONOGRAPHY :
 round to oval area with less echogenecity
 Sensitivity of 80-95%
 Guided aspiration can be done

9. LABORATORY DIAGNOSIS contd,
CT SCAN:
Sensitivity of 95-100%
• Diag multiple small abscesses
• The PORTAL VENOUS PHASE using intravenous
contrast material gives the best differentiation
between the liver and the abscess, with the
periphery of the PLA having contrast enhancement
as opposed to non-enhancement of the central
portion.
• Diagnosis of etiology and other intra-abdominal
pathology

11. Echo-poor area in the right lobe of
liver
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12. Multiple abscess in the right lobe of
liver
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13. Multiloculated abscess in the right
lobe
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14. Multiloculated tubercular liver abscess
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15. TREATMENT
• The modality of choice is percutaneous drainage with
antibiotic coverage.
A. ANTIBIOTICS
 Should be started as soon as diagnosis is suspected
 Broad coverage for gram neg and anaerobes
( 3rd gen cephalosporin with metronidazole)
 Aspiration should be done and sent for culture and
sensitivity
 Fungal and mycobacterial culture in immuno-compromised
states
 Switch over to monotherapy after sensitivity reports
 Usual recommendation is to continue for 2 weeks after
clinical improvement

16. TREATMENT
B. Percutaneous drainage :
• Treatment of choice
• Usg/ ct guided
• Single aspiration/ indwelling catheter
• Relative contraindications: presence of ascites,
coagulopathy, proximity to vital structures
C. SURGICAL DRAINAGE:
• Reserved for patients requiring surgery for primary
pathology
• Open/ laparoscopic
D. ANTIBIOTIC ALONE:
not recommended for large abscesses, carries high mortality

17. TREATMENT
E. Repeated aspiration
• 60-90% success rates in comparision with
catheter
F. HEPATIC RESECTION
• Infected hepatic malignancy
• Hepatolithiasis
• Intrahepatic biliary strictures

18. AMEBIC LIVER ABSCESS
• There has been numerous citings of bloody and mucus diarrhoea
with ball-like masses in as early as Bhrigu-sanhita
• Amebiasis is infection with intestinal pathogen Entameba
histolytica (tissue lysing ameba)
• Most Infection are asymptomatic
• Can cause disease ranging from Dysentry to extaintestinal
infectons like liver absess
• Most of asymptomatic infection is due to E.dispar
• Third most common cause of death due to parasite
• Endemic area Mexico,India & tropical regions of Africa,South and
Central America

19. LIFE CYCLE AND TRANSMISSION
• E. histolytica exists in two stages
multinucleate cyst Motile Trophozoite

21. LIFE CYCLE AND TRANSMISSION
 E. histolytica are most common in areas where poor
sanitation and crowding compromise the barrier to
contamination of food and drinking water
 Infection is acquired by ingestion of cysts in faecally
contaminated water or food or rarely ,through oral-anal
sexual contact(MSM)
 Cysts are resistant to the acid in the stomach

22. PATHOGENESIS
Virulent factors of E.histolytica are:
1. Galactose/ N-acetyl galactosamine (Ga1NAc):
responsible for adhesion to colonic cells
2. Cysteine proteases: responsible for extracellular
degradation and spread. Also inactivates complement
C3
3. Induces both humoral and cell mediated response
4. Infection gives partial immunity to further infecton
5. Deep seated FLASK-SHAPED ulcers with normal
intervening mucosa in colon

23. CLINICAL MANIFESTATIONS
• INTESTINAL AND EXTRAINTESTINAL MANIFESTATIONS
• INTESTINAL is chiefly blood and mucus diarrhoea with
colicky abdominal pain
• AMEBIC LIVER ABSCESS is the most common extra-
intestinal manifestations
• Colonic and liver abscess rarely occur simultaneously
• The classical presentation of ALA are right upper –
quadrant pain ,fever and liver tenderness
• Its acute in nature lasting < 10 days
• With chronic presentation wt. loss and anorexia are
prominent
• ANCHOVY-SAUCE like pus

24. .• Most commonly in right lobe (postero-superior area)
• Left lobe abscess are more prone to rupture
• Rt-sided pleural effusion and atelectesis are common
in cases of ALA
• In 10% rupture of abscess through diaphragm may
cause pleuro-pulmonary amebiasis
• Sudden onset cough,pleuritic chest pain and
shortness of breath are suggestive symptom
• Hepatobronchial fistula is dramatic complication in
which pt has complaint of cough with content of liver
abscess
• Liver abscess may rupture into pericardial cavity and
can cause pericarditis with 30% mortality due to
cardiac temponade

25. DIAGNOSIS
• Hemogram : leucocytosis without
eosinophilia, anemia
• CHEST X-RAY : right lung atelectasis, pleural
effusion
• ULTRSONOGRAPHY: has low specificity (40%)
usual presentation is hypoechoic ,non-
homogenous cystic spaces in right lobe
• CT-SCAN : offers no diagnostic superiority in
terms of specifity. Of use in close diagnosis.

26. Ct scan liver with ALA in Rt lobe

27. DIAGNOSIS
SEROLOGY: reactive in invasive Amoebiasis
• 1 Indirect Heamagglutination assay ( IHA )
• 2 ELISA
• 3 Latex agglutination test
• 4 gel diffusion
• 5 Counter current Imunoelectrphoresis
• Serological tests remain positive for several years ever
after successful treatment
GALLIUM SCAN: differentiation of amebic from
pyogenic liver abscess

28. TREATMENT
CHEMOTHERAPY:
 Start with monotherapy with METRONIDAZOLE (800mg thrice
daily for 10 days or 500mg IV QDS)
 In cases where improvement is not seen within 3 days,
alternate chemotherapy or surgical means
 EMETINE HYDROCHLORIDE: intramuscular or deep
subcutaneous injection @ 1mg/kg/day not exceeding
60mg/day ( contraindicated in renal, cardiac and muscular
disease)
 CHLOROQUINE: 1 g (600-mg base) per day for 2 days followed
by 500 mg (300-mg base) per day for 2 to 3 week
 DILOXANATE FUROATE: added after treatment of liver abscess
for eradication of intestinal amebiasis

29. TREATMENT
ASPIRATION/DRAINAGE:
Therapeutic aspiration has not been proved superior or very effective in
management of amebic liver abscess
Its use has been reserved for the following situations:
1.Amebic serology is inconclusive, delayed, or unavailable, and the main
differential diagnosis is a pyogenic liver abscess.
2.A therapeutic trial with antiamebic drugs is deemed inappropriate (as
in pregnancy).
3.There is suspicion of secondary infection of the liver abscess; this is
estimated to occur in 15% of cases
4. When fever and pain persist for more than 3 to 5 days after starting
appropriate therapy, aspiration may provide symptomatic relief.
5. Rupture is suspected to be imminent in an extremely large abscess,
especially if pericardial

30. PYOGENIC VS AMEBIC LIVER ABSCESS
CLINICAL FEATURES PYOGENIC LIVER ABSCESS AMOEBIC LIVER ABSCESS
AGE >50 20-40
M:F RATIO 1.5:1 >10:1
SOLITARY VERSUS MULTIPLE SOLITARY 50% SOLITARY 80%
LOCATION USUALLY RIGHT LOBE USUALLY RIGHT LOBE
TRAVEL IN ENDEMIC AREAS NO YES
DIABETES MORE COMMON UNCOMMON
ALCOHAL USE COMMON COMMON
JAUNDICE COMMON UNCOMMON
ELEVATED ALKALINE
PHOSPHATASE
COMMON COMMON
POSITIVE BLOOD CULTURE COMMON POSITIVE AMEBIC
SEROLOGY

31. HYDATID CYST OF LIVER
• There are 3 known form echinococcosis
E. Granulosus- cystic
E. Multiocularis- alveolar
E. Vogeli/oligarthus-polycystic
• INTERMEDIATE HOST: sheep DEFINATIVE: dog
• Humans are accidental host
• Infective form : eggs from faeces of dog
• Eggs hatch in duodenum to release oncopheres
which settles in liver

32. Life cycle of E.granulosus

33. CLINICAL FEATURES
• The chief complains ranges from RUQ pain ,
fever to jaundice or allergic reactions.
• The examination findings are a palpable liver
mass with or without features of jaundice
• Chest signs might be present depending on
whether there is any thoracic involvement
• It might even present as pyogenic liver
abscess, if infected, most common cause of
which is cysto-biliary communication.

34. COMPLIACTIONS
1. Secondary infection
2. Pressure effect leading to compressive
hepatocyte damage and fibrosis ( asso with
budh-chiarri syndrome and spleenomegaly)
3. RUPTURE
a) Internal rupture: penetration of bile between
pericyst and endocyst
b) Free rupture- intraperitoneal or intrathoracic
c) Communicant rupture

35. .
Peritoneal seeding in the region of the transverse
mesocolon in a patient with a history of surgery for
hepatic hydatid disease

36. INVESTIGATIONS
USG
• Most imp single diagnostic tool
• Pathognomic US findings are
1)unmistakable daughter cyst(rosette) within main
cyst cavity
2) detachment of the membrane of the cyst
3)agglomeration of daughter cyst in dependent
portion of a HC
4)calcification of the cyst wall

37. WHO-IWGE CLASSIFICATION

38. .• CT
SCAN
 CT
yields the
most
accurate
info
regarding
the no,
position
and cyst
characteris
tics(volume
and density
as well as
the extent
of
intraabdom
inal extent

39. IMMUNODIAGNOSIS
A.PRIMARY TESTS
casoni test : has historical value
a) ELISA
b)indirect hemagglutination antibody test
c)latex agglutination test
d) immunoflorense antibody test
e)immuno electrophoresis
B. SECONDARY TESTS
a) Detection of precipitation line (arc 5)
b) Identification of immunoglobin-G subclasses
c) Immunoblotting
d)Polymerase chain reaction
The secondary tests should always be used for extra-hepatic localisation
or calcified cyst

40. TREATMENT
A. CHEMOTHERAPY
• Drugs : albendazole and mebendazole
• Dose: albendazole-(10-15mg/kg/day) with fat rich meal
mebendazole-(40-50mg/kg/day) in 3 divided dose
if ABZ is not tolerated
• Indication :
a)inoperable case
b)multiple cyst in 2 or more organ
c) multiple small(>5cm) liver cyst
d)recurrent hydatidosis

41. .
B. PAIR (Puncture, Aspiration, Injection, Re-
aspiration)
Injection with 95% ethanol or hypertonic saline
Indications for PAIR in Patients with:
• Non-echoic lesion ≥ 5 cm in diameter (CE1m and l)
• Cysts with daughter cysts (CE2), and/or with
detachment of membranes (CE3)
• Multiple cysts if accessible to puncture
• Infected cysts
• Also in patients where surgery is contraindicated

42. C.SURGICAL PROCEDURES
I.CONSERVATIVE
1.Deroofing+omentoplast
y+wound drainage
2. Partial pericystectomy
3. Pericystic cystectomy
4.Marsupialisation
5.Partial hepatectomy
II.RADICAL
1.Closed cystectomy
2.Open cystectomy
3.Near total open cystectomy
4.Sub-adventitial cystectomy
5.Anatomic and non-anatomic
liver resection
6.Completion of cystecto-
pericystectomy
7.Total cysto-pericystectomy

43. LIVER FLUKE DISEASE
• TREMATODE parasite F.HEPATICA
(temperate) and F.GIGANTICA (tropical) are
the cause of fascioliasis where cattle and
sheep are raised and human eat raw
watercress.
• Europe, middle east and asia are the
endemic zones
I. FASCIOLIASIS

44. MORPHOLOGY AND LIFE CYCLE

45. PATHOLOGY
• primary infection is in liver parenchyma causing
greyish nodules and dense fibrosis
• The parasite then enters bile radicals causing to
and fro movements and causing extensive
damage to biliary epithelium and fibrosis.
• Association with cholangiocarcinoma has been
shown
• Migration to other organs have been seen like in
urinary tract (hematuria), peritoneum, muscle,
brain and subcutaneous tissue.

46. CLINICAL FEATURES
• The principal mode of infection is contaminated water as
opposed to the popular conception of eating watercress.
ACUTE PHASE: RUQ pain,hepatomegaly, fever, vomiting,
diarrhoea, and allergic reactions may develop.
• the investigation of choice being CT SCAN which shows
hypodense lesions arranged in a “tracklike” fashion
CHRONIC PHASE: (>4 months)
• adult flukes in the biliary system
• Recurrent episodes of biliary colic, cholangitis and
cholecystitis.
• USG may show motile images in bile duct and gallbladder
during this stage

47. DIAGNOSIS
• HEMATOLOGY : eosinophilia, anemia, LFT with
cholestasis features
• Specific IgG antibodies to fasciola antigen has
been found positive in 97% of cases.
• STOOL EXAMINATION: detection of ova in stool
through concentration method or filteration-
ninhydrin method.
• IMAGING : already described

48. TREATMENT
• The drug of choice is triclabendazole, 10 mg/kg
orally, repeated after 12 hours
It can be used even in the presence of biliary
obstruction. Cure rates of 90% have been reported
with no significant drug-related side effects.
• Bithionol is an alternative; available as 200-mg
tablets, the daily dose is 30 mg/kg/day, to a total
therapeutic dose of 150 mg/kg
• SURGERY is reserved for cases with biliary
obstruction

49. II. CLONORCHIASIS
• 10-25 mm flat trematode which generaly inhabit
intrahepatic biliary radicals, occasionaly travels to
common bile duct and rarely can be found in
pancreatic duct.
• Infective form: cyst from infected fish
• Intermediate host : Hydrobiid snail
• Additional intermediate host: cyprinoid fish
• Definative host: human

50. PATHOLOGY
• Inflammatory changes in bile duct due to irritant effect
on biliary epithelium.
• Inflammation leads to metaplasia and then
adenomatous hyperplasia
• Stagnation of bile leads to bacterial infection,
cholangitis, and cholangiohepatitis.
• In late stages, ductal fibrosis and stricture formation
• Association with cholangiocarcinoma has been
documented.
• Propensity for Calcium bilirubinate stones formation
increases.

51. CLINICAL FEATURES, DIAGNOSIS, TREATMENT
• The classic symptom complex associated with
clonorchiasis is the occurrence of recurrent pyogenic
cholangitis.
• Diagnosis is by eggs in the stool or duodenal aspirate
• Severity of infection is determined by the no of eggs
per gram of stool
• Elevated eosinophil count
• Praziquantel is the drug of choice. The dosage
schedule is usually 25 mg/kg/day for 1 or 2 days
• Surgey needed for stone and stricture

52. III. BILIARY ASCARIASIS
• Asia , africa and central america
• Worm enters into cbd through ampulla of vater
• CLINICAL FEATURES
I. Uncomplicated biliary ascariasis
II. Complicated biliary ascariasis
A. Early complications
1. Acute cholecystitis
2. Acute suppurative cholangitis
3. Hepatic invasion with or without abscess
4. Hemobilia
5. Acute pancreatitis
B. Late complications
1. Biliary calculi
2. Granulomatous strictures of the bile ducts
3. Hepatic granuloma

53. DIAGNOSIS
• STOOL MICROSCOPY : ova or remains of dead
worm
• Leucocytosis with eosinophilia (generally<5%)
• Bilirubinemia greater than 3.5 mg/dL is
uncommon
• IMAGING :
Real time USG: shows live worm (bulls eye sign)
CT : offers no extra advantage
ERCP : has more of a therapeutic role in acute
setting

54. TREATMENT
ACUTE STAGE:
• Parenteral antispasmodic drugs to relax the sphincter
of Oddi, analgesics for the relief of biliary colic,
nasogastric decompression, and intravenous fluids.
• Worm returns to duodenum in >90% of cases
• Antihelminthic drugs avoided in acute setting
• Albendazole (400 mg/day for 1 day) OR mebendazole
(100 mg twice daily for 3 days) and pyrantel pamoate
(single dose of 11 mg/kg to a maximum of 1 g

55. .
• Failure of conservative management warrants
ERCP removal of dead worms
• However if ERCP fails or facilities not available,
surgery is indicated.
SURGERY :
• Initial operative cholangiogram helps in planning
• Worm removed after choledochotomy and the
biliary tree then flushed with normal saline
• Another intraoperative cholangiogram done to
check for residual worms
• The bile duct then closed over a wide bore T-tube
• Simultaneous removal of all worms from intestine
done via enterostomy

56. THANK
YOU
.