Amebiasis Intestinal dan

Extraintestinal
Oleh :dr Tities A Indra SpPD

November 2017
FK Trisakti
 INTRODUCTION
• Amebiasis  a common intestinal protozoal infection
that may also cause systemic manifestations.
• Amebiasis is a parasitic infection caused by the protozoa
 Entamoeba histolytica.
• Amebiasis  the third leading parasitic cause of death
worldwide
• About 90% of infections asymptomatic
• 10%  a spectrum of clinical syndromes ranging from
dysentery to abscesses of the liver or other organs
 Life cycle
Infection by Entamoeba histolytica

1. Occurs by ingestion of mature cysts in fecally contaminated

food, water, or hands
2. Excystation occurs in the small intestine and
3. Trophozoites are released, which migrate to the large
intestine
4. Trophozoites multiply by binary fission and produce cysts ,
which are passed in the feces

Because of the protection conferred by their walls, the cysts

can survive days to weeks in the external environment and
are responsible for transmission. (Trophozoites can also be
passed in diarrheal stools, but are rapidly destroyed once
outside the body, and if ingested would not survive exposure
to the gastric environment.)
• In. many cases, the trophozoites remain confined to the
intestinal lumen ( A: non-invasive infection) of
individuals who are asymptomatic carriers, passing cysts
in their stool.
• In some patients the trophozoites invade the intestinal
mucosa ( B : intestinal disease), or,
• Pass through the bloodstream, extraintestinal sites such
as the liver, brain, and lungs (C : extra-intestinal
disease), with resultant pathologic manifestations.
The invasive and noninvasive forms represent two
separate species, respectively E. histolytica and E.
dispar, however not all persons infected with E.
histolytica will have invasive disease. These two species
are morphologically indistinguishable.
.

The parasite has 2 forms:

- a motile form, called the trophozoite, and
- a cyst form
- The trophozoite of E histolytica inhabits
the large intestine to produce lesions of
amebic colitis.
–Invasion of the colonic mucosa leads to
dissemination of the organism to
extracolonic sites, predominantly the liver.
 Infections due to E histolytica
• Intestinal disease
– Asymptomatic infection
– Symptomatic noninvasive infection
– Acute proctocolitis( inflammation of the rectum and colon )
– Fulminant colitis (coming on suddenly with great severity ) with
perforation
– Toxic megacolon (dialated colon )
– Chronic nondysenteric colitis
– Ameboma (an inflamed, tumor like, spreading nodule )
– Perianal ulceration
• Extraintestinal disease
– Liver abscess
– Pleuropulmonary disease
– Peritonitis
– Pericarditis
– Brain abscess
– Genitourinary disease
 Pathophysiology
• Fecal-oral route
• Excystation in the small bowel and invasion of the
colon by the trophozoites.
• Invasive disease begins with the adherence of E
histolytica to colonic mucins, epithelial cells, and
leukocytes.
• Adherence of the trophozoite is mediated by a
galactose-inhibitable adherence lectin.
 Cont ..
• After adherence, trophozoites :
– invade the colonic epithelium to produce the
ulcerative lesions typical of intestinal amebiasis .
– lyse the target cells by using lectin to bind to the
target cells' membranes and using the parasite's
ionophore like protein to induce a leak of ions (i.e,
Na+, K+, Ca+) from the target cell cytoplasm.
• An extracellular cysteine kinase causes
proteolytic destruction of the tissue, producing
flask-shaped ulcers
Cont ..
– Spread of amebiasis to the liver occurs via the
portal blood.
– Trophozoites ascend the portal veins to produce
liver abscesses filled with acellular
proteinaceous debris. This material has the
appearance of anchovy paste.
– The trophozoites of E histolytica lyse the
hepatocytes and the neutrophils. This explains
the paucity (smallness of quantity ) of
inflammatory cells within the liver abscesses.
 Diagnosis
• The incubation period  commonly 2-4 weeks
• Amebiasis is more severe in very young patients, in
elderly patients, and in patients receiving
corticosteroids.
• The clinical spectrum of amebiasis ranges from
asymptomatic infection to fulminant colitis and
peritonitis to extraintestinal amebiasis, most
commonly amebic liver abscess
 Cont ..
Amebic colitis : -
– gradual in onset, with symptoms presenting over 1-2 weeks,
– Diarrhea is the most common symptom.
– cramping abdominal pain, watery or bloody diarrhea, and weight
loss.
– Fever is noted in 10% of patients.
• Fulminant (coming on suddenly with great severity )amebic
colitis : -
– is a rare complication of amebic dysentery (<0.5%).
– It presents with a rapid onset of severe bloody
diarrhea, severe abdominal pain, and high fever.
– Children younger than 2 years are at increased risk.
– Intestinal perforation is common.
Cont ..
– presents with fever and a constant, dull, upper right
abdominal or epigastrium pain.
– Involvement of the diaphragmatic surface of the liver
may lead to right-sided pleuritic pain or referred
shoulder pain.
Associated GI symptoms : -
– occur in 10-35% of patients and include nausea,
vomiting, abdominal distention, diarrhea, and
constipation.
– May present with vague abdominal discomfort,
weight loss, and anemia.
Cont ..
• Patients may develop toxic megacolon, which is
typically associated with the use of corticosteroids.
• Chronic amebic colitis is clinically similar to
inflammatory bowel disease. Recurrent episodes of
bloody diarrhea and vague abdominal discomfort
develop in 90% of patients with chronic amebic
colitis who have antibodies to E histolytica.
• Amebic colitis should be ruled out prior to treatment
of suspected inflammatory bowel disease because
corticosteroid therapy worsens amebiasis.
 Cont..
• Amebic liver abscess is the most common
form of extraintestinal amebiasis.
– It results from spread of the organisms from the
intestinal submucosa to the liver via the portal
system.
– Approximately 40% of patients who have amebic
liver abscess do not have a history of prior bowel
symptoms.
– 5% of patients with symptomatic intestinal
amebiasis and is 10 times as frequent in men as
in women.
Cont...
– Pleuropulmonary amebiasis is most commonly the
result of contiguous spread from a liver abscess
rupturing through the right hemidiaphragm.
– cough, pleuritic pain, and dyspnea.
– Hepatobronchial fistula expectoration of sputum
resembling anchovy paste. The trophozoites of E
histolytica may be found in the sputum sample.
– Amebic peritonitis is generally secondary to a
ruptured liver abscess. Left lobe liver abscesses are
more likely to rupture. Patients present with fever and
rigid distended abdomen.
– Roughly 2-7% of liver abscesses rupture into the
peritoneum.
Cont..
Amebic pericarditis : -
– caused by a rupture of the left liver lobe abscess
and occurs in 3% of patients with hepatic
amebiasis. It presents with chest pain and the
features of congestive heart failure.
Cerebral amebiasis : -
– abrupt onset and rapid progression to death in 12-
72 hours.
– presents with altered consciousness and focal
neurologic signs.
– CT scanning reveals irregular lesions without a
surrounding capsule.
– Tissue biopsy :- trophozoites.
Genitourinary involvement : -
– may cause painful genital ulcers or fallopian tube
amebiasis.
Physical
Acute amebic colitis : -
– lower quadrant abdominal tenderness.
– Fever is noted in only a minority of patients.
– Dehydration is uncommon.
– Occult blood is nearly always present in stools.
Amebic liver abscess : -
- fever and tender hepatomegaly.
- Right lower intercostal tenderness, particularly
posteriorly.
- Breath sounds may be diminished at the right lung base,
and rales may be heard.
- hepatomegaly, weight loss, and anemia.
Pleuropulmonary amebiasis:-
– produce findings of right-sided pleural effusions,
empyema, pneumonia, and lung abscess.
 Cont ..
Amebic peritonitis : -
• present with fever and a tender, rigid, and distended
abdomen.
Amebic pericarditis : -
• presents with features of congestive heart faliure.
• pericardial friction rub may be audible.
Cerebral amebiasis : -
presents with altered consciousness and focal neurologic
signs.
CT scanning reveals irregular lesions without a
surrounding capsule or enhancement.
Genital ulcers :-
punched-out appearance and profuse discharge.
 Laboratory Studies
Stool
Light microscopy:
• Examination of a fresh stool smear for
trophozoites that contain ingested RBCs.
• Routine microscopy cannot distinguish the E
dispar (nonpathogenic amebae) from E
histolytica.
• PCR-based diagnostic tests
• Other stool tests
– The stool samples are always heme positive.
– Fecal leukocytes may be absent.
 Serum tests

– Antibody tests:
– Indirect hemagglutination antibody (IHA)
test
– Detection of immunoglobulin M (IgM)
antibodies
– ELISA for Ab detection (most sensitive test)

– Sigmoidoscopy or biopsy of symptomatic

sick patients.
Imaging Studies
Chest radiography : -
–elevated right hemidiaphragm and a
right-sided pleural effusion in patients
with amebic liver abscess.
–Ultrasonography (amebic liver abscess
)
–cerebral amebiasis, CT shows irregular
lesions without a surrounding capsule
–MRI
 Other Tests
– Leukocytosis without eosinophilia is observed
in 80% of cases.
– Mild anemia may be noted.
Liver function tests : -
– elevated alkaline phosphatase levels (in 80% of
patients),
– elevated transaminase levels,
– mild elevation of serum bilirubin level,
– Erythrocyte sedimentation rate is elevated.
 Treatment
• Medical Care
– Luminal agents that are minimally absorbed by the GI
tract (eg, paromomycin, iodoquinol, diloxanide
furoate) are best suited for such therapy.
– Metronidazole is the mainstay of therapy for invasive
amebiasis.
– Tinidazole for intestinal or extraintestinal amebiasis
 Metronidazole (Flagyl)
– Kills trophozoites of E histolytica in intestine and
tissue.
– Does not eradicate cysts from intestines.
• Adult
– Intestinal amebiasis:
PO: 500-750 mg PO tid for 5-10 d; alternatively, 2 g PO
qd for 3 d or a single dose of 50 mg/kg
IV: 500 mg IV q6h for 5-10 d
Amebic liver abscess: 500 mg IV q6h for 10 d
• Pediatric
– 35-50 mg/kg/d PO/IV divided q8h for 10 d
 Surgical Care
Surgical intervention :-
– perforated amebic colitis, massive GI bleeding, or toxic
megacolon.
– Amebic liver abscess generally responds to medical
therapy alone and drainage is seldom necessary.
– When necessary, imaging-guided percutaneous
treatment (needle aspiration or catheter drainage) has
replaced surgical intervention as the procedure of choice
for reducing the size of an abscess.
Indications for drainage : -
– Presence of left-lobe abscess (>10 cm in diameter)
– Rupture and
– abscess that does not respond to medical therapy within
3-5 days
 Complications
– Bowel perforation
– GI bleeding
– Stricture formation
– Fistula formation
– Intussusception
– Secondary bacterial infection of amebic
liver abscess (uncommon)
– Peritonitis
– Pericarditis
– Empyema
– Brain abscess
 Mortality/Morbidity
• Mortality rate in patients with uncomplicated amebic
liver abscess is less than 1%.
• Fulminant amebic colitis has a mortality rate of more
than 50%.
• Pleuropulmonary amebiasis has a mortality rate of 15-
20%.
• Amebic pericarditis has a case fatality rate of 40%.
• Cerebral amebiasis is highly fatal, with a 90% death rate.
Increased severity of amebiasis is noted :
• in children (especially neonates),
• women who are pregnant or postpartum, individuals
who use corticosteroids,
• individuals with malignancy, and
• malnourished individuals.
 Patient Education
- Educate patients about the prevention :
- avoiding drinking contaminated water and
avoiding eating raw fruits and salads,
which are difficult to sterilize.
- Bottled water may be used during such
travel.
- Eating only cooked food in endemic areas
minimizes risk.