Amobiasis

Introduction
Several

protozoan species in the genus

Entamoeba colonize humans, but not all
of them are associated with disease.
Entamoeba histolytica is well recognized
as a pathogenic ameba, associated with
intestinal and extraintestinal infections.
The other species are important because
they may be confused with E. histolytica in
diagnostic investigations

Geographic Distribution:
Worldwide,

with higher incidence of

amebiasis in developing countries.
In industrialized countries, risk groups
include:
Male

homosexuals
Travelers
Recent immigrants
Institutionalized populations

Life cycle
1.
2.

3.
4.
5.

Cysts and trophozoites are passed in feces

Cysts are typically found in formed stool,
whereas trophozoites are typically found in
diarrheal stool. Infection by entamoeba
histolytica occurs by ingestion of mature cysts
In fecally contaminated food, water, or hands.
Excystation occurs in the small intestine and
trophozoites are released,
Which migrate to the large intestine. The
trophozoites multiply by binary fission and
produce cysts

eC
E. H ycle
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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 passed in the stool 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

1.

2.

3.

Noninvasive infection of individuals who

are asymptomatic carriers, passing cysts
in their stool.
In some patients the trophozoites invade
the intestinal mucosa (intestinal
disease).
Through the bloodstream, extraintestinal
sites such as the liver, brain, and lungs
(extraintestinal disease), with resultant
pathologic manifestations.

f
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Life C
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Clinical Features:
1.
2.

A wide spectrum, from asymptomatic infection ("luminal

amebiasis"),
Invasive intestinal amebiasis:
1.
2.
3.
4.
5.

3.

Dysentery
Colitis
Appendicitis
toxic megacolon
amebomas),

Invasive extraintestinal amebiasis

1.
2.
3.
4.
5.

liver abscess
Peritonitis
pleuropulmonary abscess
cutaneous
genital amebic lesions

Laboratory Diagnosis:
Differentiation

is possible, but not always

easy, based on morphologic
characteristics of the cysts and
trophozoites.
The nonpathogenic Entamoeba dispar,
however, is morphologically identical to E.
histolytica, E. polecki and differentiation
must be based on isoenzymatic or
immunologic analysis.

Laboratory Diagnosis:
Microscopic

identification of cysts and

trophozoites in the stool is the common method
for diagnosing E. histolytica.
This can be accomplished using:
Fresh

stool: wet mounts and permanently stained

preparations (e.g., trichrome).
Concentrates from fresh stool: wet mounts, with or
without iodine stain, and permanently stained
preparations (e.g., trichrome). Concentration
procedures, however, are not useful for
demonstrating trophozoites.
In addition, E. histolytica trophozoites can also be
identified in aspirates or biopsy samples obtained
during colonoscopy or surgery

Diagnostic findings:
1.
2.
3.
4.
5.

Microscopy
Immunodiagnosis
Molecular methods for discriminating
between E. histolytica and E. dispar
Morphologic comparison with other
intestinal parasites
Bench aid for E. histolytica

Treatment:
1.

For asymptomatic infections:

1.
2.
3.

2.

Iodoquinol
Paromomycin
Diloxanide furoate (not commercially available in
the U.S.) are the drugs of choice.

For symptomatic intestinal disease, or

extraintestinal, infections (e.g., hepatic
abscess), the drugs of choice are;
1.
2.

Metronidazole or tinidazole
Immediately followed by treatment with iodoquinol,
paromomycin, or diloxanide furoate.

Giardiasis

Causal Agent:
Giardia

intestinalis is a protozoan flagellate

(Diplomonadida).
This protozoan was initially named Cercomonas
intestinalis by Lambl in 1859 and renamed
Giardia lamblia by Stiles in 1915, in honor of
Professor A. Giard of Paris and Dr. F. Lambl of
Prague.
However, many consider the name, Giardia
intestinalis, to be the correct name for this
protozoan. The International Commission on
Zoological Nomenclature is reviewing this issue.

Life Cycle:

Life Cycle:

Life Cycle:
1.

2.

3.

Cysts are resistant forms and are responsible

for transmission of giardiasis. Both cysts and
trophozoites can be found in the feces
(diagnostic stages)
The cysts are hardy and can survive several
months in cold water. Infection occurs by the
ingestion of cysts in contaminated water, food,
or by the fecal-oral route (hands or fomites)
In the small intestine, excystation releases
trophozoites (each cyst produces two
trophozoites)

Life Cycle:
4.

5.

Trophozoites multiply by longitudinal

binary fission, remaining in the lumen of
the proximal small bowel where they can
be free or attached to the mucosa by a
ventral sucking disk
Encystation occurs as the parasites
transit toward the colon. The cyst is the
stage found most commonly in
nondiarrheal feces

Geographic Distribution:

Worldwide, more prevalent in warm

climates, and in children.

Clinical Features:
1.
2.

3.

The spectrum varies from asymptomatic

carriage to severe diarrhea and malabsorption.
Acute giardiasis develops after an incubation
period of 1 to 14 days (average of 7 days) and
usually lasts 1 to 3 weeks.
Symptoms include:
1.
2.
3.
4.

4.

Diarrhea
Abdominal pain
Bloating
Nausea, and vomiting.

In chronic giardiasis the symptoms are

recurrent and malabsorption and debilitation
may occur.

Laboratory Diagnosis:

1.

2.
3.

4.

Giardiasis is diagnosed by the identification of

cysts or trophozoites in the feces, using direct
mounts as well as concentration procedures.
Repeated samplings may be necessary.
In addition, samples of duodenal fluid (e.g.,
Enterotest) or duodenal biopsy may
demonstrate trophozoites.
Alternate methods for detection include antigen
detection tests by enzyme immunoassays, and
detection of parasites by immunofluorescence.

Treatment

1.

2.

Several prescription drugs are available

to treat giardiasis including
metronidazole and tinidazole.
Nitazoxanide has provided some
encouraging results in the management
of giardiasis in children.