7. Pathophysiology
•
•
•
Ingestion contaminated water or food
containing E. histolytica cysts infective cyst form of the parasite
survives passage through the stomach
and small intestine.
Excystation occurs in the bowel
lumen, where motile and potentially
invasive trophozoites are formed.
In most infections the trophozoites
aggregate in the intestinal mucin layer
and form new cysts, resulting in a selflimited and asymptomatic infection.
In some cases, adherence to and lysis of the
colonic epithelium, mediated
by the galactose and N-acetyl-Dgalactosamine (Gal/GalNAc)–specific lectin,
initiates invasion of the colon → neutrophils
responding to the invasion contribute to
cellular damage.
Once the intestinal epithelium is invaded,
extraintestinal spread to the peritoneum,
liver, and other sites may follow.
8. CLINICAL MANIFESTATION
PYOGENIC
AMEBIC
Nonspesific, fever (absent in 30%), chills, RUQ
pain (45%), malaise, weight lose
More severe RUQ pain, fever 90% cases
Dominate by underlying disease : appendicitis,
diverticulitis, biliary disease
Recent travel to endemic area, but maybe remote
Comorbid common : DM, malignancy, alcholism,
cardiovascular, chronic renal disease
Previous colonic amebiasis (only 5-15%),
concurrent hepatic abcess & amebic dysenteri
are unusual
Eosinophilia, high bilirubin, blood culture + 50%,
aspirates + bacteria 75-90%
Most aspiration does not yield an organism
(tropozoite < 20%); odorless, serologic + only
invasive amebiasis, negative asymptomatic
carrier, gel diffusion precipitin (best test)
9. Laboratory &
Diagnostic
• Routine lab not diagnostic
for both abcess : WBC (↑),
anemia (normocytic
normochromic), sed rate (↑)
• LFT nonspesific : 90% high
AP, AST/ALT ↑ but to a lesser
degree, low albumin (<2mg%)
poor prognostic
10. • CXR : 50-80% abnormal (RLL
atelectasis, R pleural eff, R
hemidiaphragm elevation)
• U/S initial test of choice :
noninvasive, high sensitivity
80-90%; to distinguish cyst
from solid lesion/visualizing
biliary tree
• CT (IV contrast) : smaller
abcess, asses peritoneal
cavity
11. ASPIRATE
• Pyogenic (multipel abcess,
coexistent biliary disease,
intraabdominal
inflammatory process)
• Non amebic
• Amebic aspiration : pyogenic
can’t be roled out, respond to
amebic therapy has not
occurred within 24-48 hours,
abcess is large (size greater
than 5 cm) & painful
• Surgical drainage of amebic
abcess : located in left lobe,
respon therapy is not dramatic
in 4-5 days
12. PYOGENIC
PYOGENIC
• Antibiotic : aminoglicoside/
cephalosporin (gram -),
clindamycin/metronidazole
(anaerobes),
penicillin/ampicillin
(enterococci)
• Surgery percutaneus
drainage : conservative
measure fail, to treat primary
intraabdominal lesion
76% cure rate, 60% either alone
TREATMENT
AMEBIC
AMEBIC
• Metronidazole drug active
against extraintestinal form
of amebiasis : 750mg TID x
10 days
• Eradicates intestinal form :
iodoquinol 650mg TID x 20
days
• Consider aspiration if failing
therapy
13. CoMPLICATION & PROGNOSIS
PYOGENIC
AMEBIC
Untreated 100% mortality
Rapid clinical improvement is observed in less
than 1 week with antiamebic drug therapy alone
Ruptur into peritoneal cavity : subphrenic,
perihepatic, subhepatic abscesses or peritonitis;
metastatic ruptur emboli (lung, brain)
similar
Left lobe abscess : cardiac tamponade,
pericarditis
Abscess in dome of liver or complicated by
bronchopleural fistula
Depends on rapidity diagnosis & underlying
illness
Generally do well with treatment
Morbidity high (50%), mortality 5-10% (prompt
recognation & adequate AB) higher in multipel
abscesses
Morbidity 4.5%, mortality 2.2%
14. Independent risk factors predicting a higher
mortality
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–
–
–
–
–
Bilirubin level greater than 3.5 mg/dL
Encephalopathy
Volume of abscess cavity greater than 500 mL at presentation
Serum albumin less than 2 g/dL
Hemoglobin less than 8 g/dL
Multiple abscesses
