Amebiasis Intestinalis

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? Intestinal Entamoeba histolytica amebiasis

Map Of Indonesia
Authors Section Editor Deputy Editor
Karin Leder, MBBS, Edward T Ryan, MD, DTMHElinor L Baron, MD, DTMH
Travel Indonesia FRACP, PhD, MPH, DTMH
Peter F Weller, MD, FACP
Bandung Disclosures
Conference
All topics are updated as new evidence becomes available and our peer review
process is complete.
Abdul Halim Literature review current through: Nov 2013. | This topic last updated: Sep 11,
2012.
Hotel Bandung
INTRODUCTION — Intestinal amebiasis is caused by the protozoan Entamoeba
histolytica. Most infection is asymptomatic; clinical manifestations include amebic
Malaysian Ringgit dysentery and extraintestinal disease [1]. Worldwide, approximately 40 to 50 million
people develop colitis or extraintestinal disease annually with 40,000 deaths [2].
Jakarta Hotels Extraintestinal manifestations include amebic liver abscess and other more rare
manifestations such as pulmonary, cardiac, or brain involvement; these are
Bandung Hotels discussed separately. (See "Extraintestinal Entamoeba histolytica amebiasis".)
There are three species of intestinal amebae with identical morphologic

Indonesia Travel characteristics: E. histolytica, E. dispar, and E. moshkovskii [3]. E. dispar and E.
Guide moshkovskii are non-pathogenic and do not cause clinical disease; all symptomatic
disease is caused by E. histolytica. Alternative diagnostics based on the genetic,
Indonesia Online antigenic, biochemical, and pathogenic differences between the three species have
been developed to help differentiate between them in clinical specimens [3]. (See
"Nonpathogenic enteric protozoa" and 'Diagnosis' below.)
EPIDEMIOLOGY — Amebiasis occurs worldwide; the prevalence is

disproportionately increased in developing countries because of poor socioeconomic
conditions and sanitation levels. Infection with E. dispar and E. moshkovskii occurs
approximately ten times more frequently than infection with E. histolytica [3,4].
Areas with high rates of amebic infection include India, Africa, Mexico, and parts of
Central and South America. The overall prevalence of amebic infection may be as
high as 50 percent in some areas [3]. The seroprevalence of E. histolytica in one
Mexican study was 8.4 percent [5]. In another series from urban Bangladesh,
children had a 4.2 percent prevalence rate of E. histolytica infection [6].
In developed countries, amebiasis is generally seen in migrants from and travelers to

endemic areas. E. histolytica is not a common cause of travelers' diarrhea, and
gastrointestinal infection is uncommon in travelers who have spent less than one
month in endemic areas. In one prospective study of German travelers to the
tropics, only 0.3 percent had pathogenic E. histolytica infection [7]. Institutionalized
patients and sexually-active homosexuals are also at increased risk of infection [8].
In the United States and Europe, homosexual males are principally colonized with
nonpathogenic E. dispar; in these regions, HIV-infected patients are not at
increased risk for intestinal or extraintestinal amebiasis [3,9]. In Japan and Taiwan,
however, E. histolytica is much more prevalent amongst male homosexuals.
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Invasive, extraintestinal amebiasis (eg, hepatic abscesses) are more frequent in

The use of UpToDate is subject to the Subscription Close
HIV-infected patients in these
and License countries [3,10].
Agreement.
Transmission — The parasite exists in two forms, a cyst stage (the infective form),
and a trophozoite stage (the form that causes invasive disease) (figure 1). Infection
occurs following ingestion of amebic cysts; this is usually via contaminated food or
water but can be associated with venereal transmission through fecal-oral contact
[8].
Cysts can remain viable in the environment for weeks to months, and ingestion of a
single cyst is sufficient to cause disease. The cysts pass through the stomach to
the small intestine where they excyst to form trophozoites. The trophozoites can
invade and penetrate the mucous barrier of the colon causing tissue destruction and
increased intestinal secretion, and can thereby ultimately lead to bloody diarrhea.
PATHOGENESIS — The host-parasite interaction is complex, and the virulence of

different strains of E. histolytica is variable [11,12]. Colitis results after penetration of
the trophozoite through the intestinal mucous layer, which otherwise acts as a
barrier to invasion [1]. The trophozoite is able to kill both epithelial cells and
inflammatory cells, which is thought to occur through a number of different
mechanisms including:
Secretion of proteinases by the trophozoites

Lysis of target cells via a contact-dependent mechanism
Killing of mammalian cells by apoptosis (programmed cell death)
Formation of amebapores, a family of small peptides that can form pores in
lipid bilayers, resulting in cytolysis of infected cells
Changes in intestinal permeability, probably via disruption of tight-junction
proteins
The pathogenicity of amebic trophozoites is facilitated by adherence to colonic

epithelial cells via a specific lectin (the galactose/N-acetylgalactosamine lectin) [13].
Mammalian cells without N-terminal galactose or N-acetylgalactosamine residues
are resistant to adherence by amebic trophozoites, which is consistent with an
important role for the lectin in adhesion. This lectin also plays a role in immunity,
since mucosal immunity against the lectin seems to mediate some degree of
protection from invasive disease following colonization. One study from Bangladesh
showed that children with a mucosal IgA response against the lectin had 86 percent
fewer new infections during a one year period than children without this response
[14], and when reinfected had a lower incidence of infection and disease over a four
year follow-up period [15]. Other amebic molecules such as
lipophosphopeptidoglycan, peroxiredoxin, arginase, and lysine, and glutamic acid-
rich proteins are also implicated in the pathogenesis of amoebiasis [16].
CLINICAL MANIFESTATIONS — The majority of entamoeba infections are

asymptomatic; this includes 90 percent of E. histolytica infections and all E. dispar
infection and E. moshkovskii infections [3]. Factors that influence whether infection
leads to asymptomatic or invasive disease include the E. histolytica strain and host
factors such as genetic susceptibility, age, and immune status [3,17]. Risk factors
for severe disease and increased mortality include young age, pregnancy,
corticosteroid treatment, malignancy, malnutrition, and alcoholism.
Clinical amebiasis generally has a subacute onset, usually over one to three weeks.
Symptoms range from mild diarrhea to severe dysentery-producing abdominal pain
(12 to 80 percent), diarrhea (94 to 100 percent), and bloody stools (94 to 100
percent) to fulminant amoebic colitis. Weight loss occurs in about half of patients
[18]. Fever occurs in 8 to 38 percent [19]. Amebic dysentery is diarrhea with visible
blood and mucus in stools and the presence of hematophagous trophozoites

(trophozoites with ingested red blood cells) in stools or tissues [20]. Fulminant
colitis with bowel necrosis leading to perforation and peritonitis has been observed in
approximately 0.5 percent of cases; associated mortality rate is more than 40
percent [21]. Toxic megacolon can also develop.
Amebic colitis has been recognized in asymptomatic patients. Among 5193

asymptomatic individuals in Japan undergoing colonoscopy for evaluation of positive
fecal occult blood tests, for example, four were found to have amebic ulcerative
lesions in the cecum or ascending colon [22].
Rarely, intestinal amebiasis may present as a chronic syndrome of diarrhea, weight

loss, and abdominal pain without dysentery, lasting for years and mimicking
inflammatory bowel disease.
Uncommonly, localized colonic infection resulting in a mass of granulation tissue

forming an ameboma can occur, mimicking colon cancer [23,24]. Patients with
amebomas usually are found to have a tender palpable mass. Other rare
complications of amebiasis include perianal cutaneous amebiasis and rectovaginal
fistulae [25].
DIAGNOSIS — Diagnostic techniques include microscopy, antigen detection,

serology, molecular techniques, and colonoscopy with histological examination.
Culture techniques are limited to research settings.
Diagnosis is best accomplished by the combination of serology or antigen testing

together with identification of the parasite in stool or extraintestinal sites (such as
liver abscess pus).
Stool microscopy — The demonstration of cysts or trophozoites in the stool

suggests intestinal amebiasis, but microscopy cannot differentiate between E.
histolytica and E. dispar or E. moshkovskii strains. In addition, microscopy requires
specialized expertise and is subject to operator error [26].
Organism excretion can vary; a minimum of three specimens on separate days

should be sent to detect 85 to 95 percent of infections. Specimens can be
concentrated and stained with iodine to detect cysts. To look for trophozoites, a
saline wet mount and a fresh smear stained with iron hematoxylin and/or Wheatley's
trichrome should be performed; fixation with polyvinyl alcohol for delayed staining is
often useful.
Stool specimens are frequently positive for blood in the setting of invasive intestinal
amebic disease. The presence of ingested erythrocytes is not pathognomonic for E.
histolytica infection (picture 1); ingested erythrocytes may also be observed with E.
dispar. Fecal leukocytes are not always present since white cells may be destroyed
by the organisms.
Antigen testing — Antigen detection is sensitive, specific, rapid, easy to perform,

and can distinguish between E. histolytica and E. dispar. Stool and serum antigen
detection assays that use monoclonal antibodies to bind to epitopes present on
pathogenic E. histolytica strains (but not on nonpathogenic E. dispar or E.
moshkovskii strains) are commercially available for diagnosis of E. histolytica
infection [27-29]. Antigen detection kits using enzyme linked immunosorbent assay
(ELISA), radioimmunoassay or immunofluorescence have been developed [30-33].
Antigen detection has many advantages, including ease and rapidity of the tests,
capacity to differentiate between strains, greater sensitivity than microscopy, and
potential for diagnosis in early infection and in endemic areas (where serology is
less useful).
The TechLab E. histolytica stool antigen test is an ELISA test that is specific for E.
histolytica. The assay detects the E. histolytica-derived Gal/GalNAc lectin in stool
specimen; it has a sensitivity of 87 percent and a specificity of >90 percent
compared with culture [32,34,35]. A study comparing the TechLab E. histolytica-
specific antigen detection test with PCR assays showed comparable sensitivities
when performed directly on fresh stool specimens [35].
Serology — Serology is a useful diagnostic tool for amebiasis. E. histolytica

infection results in the development of antibodies; E. dispar infection does not.
Antibodies are detectable within five to seven days of acute infection and may
persist for years. Approximately 10 to 35 percent of uninfected individuals in
endemic areas have anti-amebic antibodies due to previous infection with E.
histolytica [3]. Therefore, negative serology is helpful for exclusion of disease, but
positive serology cannot distinguish between acute and previous infection.
Indirect hemagglutination (IHA) is the most sensitive serologic assay; it is positive in

approximately 90 percent of patients with symptomatic intestinal infection [3]. Agar
gel diffusion and counterimmunophoresis are less sensitive than IHA but usually
only remain positive for 6 to 12 months, which may make them more useful in
endemic areas [36]. A commercially available ELISA that has a sensitivity of 93
percent compared to IHA has also been developed [37].
Molecular methods — Detection of parasitic DNA or RNA in feces via probes can
also be used to diagnose amebic infection and to differentiate between the three
different strains, but these methods are primarily research tools [38,39].
Polymerase chain reaction (PCR) techniques can detect E. histolytica in stool

specimens [33,40-42]. One study showed that PCR was significantly more sensitive
than either microscopy or cultures, and that it was 100 percent specific for E.
histolytica [43]. PCR is about 100 times more sensitive than fecal antigen tests
[44].
A number of investigators have developed PCR methods for the diagnosis of

intestinal amebiasis and differentiation between pathogenic and nonpathogenic
amebae [45-47]. These methods are highly sensitive and specific research tools, but
are generally not yet commercially available for diagnostic clinical testing [44].
Visual inspection of the colon — Sigmoidoscopy and/or colonoscopy can be

performed either to make the diagnosis of amebiasis or to exclude other causes of
the patients' symptoms. However, colonoscopy is not recommended as a routine
diagnostic approach since intestinal amebic ulcerations increase the likelihood of
perforation during instillation of air to expand the colon.
Scrapings or biopsy specimens, best taken from the edge of ulcers, may be positive
for cysts or trophozoites on microscopy, and antigen testing for E. histolytica may
be positive. Colonic lesions in amebic dysentery range from nonspecific mucosal
thickening and inflammation to classic flask-shaped amebic ulcers (picture 2).
TREATMENT — All E. histolytica infections should be treated, even in the absence

of symptoms, given the potential risk of developing invasive disease and the risk of
spread to family members [1,3]. The goals of antibiotic therapy of intestinal
amebiasis are to eliminate the invading trophozoites and to eradicate intestinal
carriage of the organism.
E. dispar and E. moshkovskii infections do not require treatment. In countries where

amebic infections are endemic, asymptomatic patients incidentally found to have
stools positive for amebae are frequently presumed to have infection with E.
dispar/E. moshkovskii and are not further evaluated or treated. As antigen tests that
can differentiate between E. dispar/E. moshkovskii and E. histolytica become more

widely available in these countries, this practice may change.
Clinical approach — Invasive colitis is generally managed with metronidazole

(alternative therapies include tinidazole, ornidazole, and nitazoxanide), followed by a
luminal agent (such as paromomycin, diiodohydroxyquin or diloxanide furoate) to
eliminate intraluminal cysts [2]. A ten day course of metronidazole eliminates
intraluminal infection in many cases, but a second agent is still warranted [48].
Asymptomatic patients with E. histolytica (and not E. dispar/E. moshkovskii) should
be treated with an intraluminal agent alone.
Dosing for metronidazole is 500 to 750 mg PO three times daily for 7 to 10 days in
adults and 35 to 50 mg/kg per day in three divided doses for 7 to 10 days in
children. Shorter duration of metronidazole is generally not recommended [49,50].
Metronidazole is well absorbed from the gastrointestinal tract; intravenous therapy
offers no significant advantage as long as the patient can take oral medications and
has no major defect in small bowel absorption. Metronidazole resistance in E.
histolytica trophozoites has not been reported [51].
Alternatives to metronidazole include tinidazole, ornidazole, and nitazoxanide

[49,50,52]. Tinidazole (2 g PO daily for three days) has a cure rate of 90 to 93
percent [49,50,53]. One review showed that tinidazole resulted in greater resolution
of clinical symptoms compared with metronidazole, but there was inconclusive
evidence of its advantage in eradication of E. histolytica in the stools [20]. Tinidazole
is also better tolerated than metronidazole.
Intraluminal infection can be treated with one of the following regimens:

paromomycin (25-30 mg/kg per day orally in three divided doses for seven days),
diiodohydroxyquin (650 mg orally three times daily for 20 days for adults and 30-40
mg/kg per day in three divided doses for 20 days for children), or diloxanide furoate
(500 mg orally three times daily for 10 days for adults and 20 mg/kg per day in three
divided doses for 10 days for children).
Peritonitis — In patients who have suspected or proven peritonitis, broad spectrum

antibacterial therapy should be administered. Surgical intervention is required in the
setting of significant bowel perforation or abscesses that fail to respond to antibiotic
therapy. Toxic megacolon requires colectomy.
PREVENTION — Prevention of amebic infection in travelers to endemic areas

involves avoidance of untreated water in endemic areas and uncooked food, such as
fruit and vegetables that may have been washed in local water. Amebic cysts are
resistant to chlorine at the levels used in water supplies, but disinfection with iodine
may be effective. Avoiding sexual practices that may lead to fecal-oral contact is
also advisable. (See "Travel advice", section on 'Behavioral precautions'.)
Vaccine development — There is some evidence of partial acquired immunity to

the organism. Protection from invasive disease has been associated with mucosal
IgA antibodies to the amebic adherence lectin [14,15]. However, recurrent intestinal
infection and persistent colonization does occur despite detectable antiamebic
antibodies [54]. Thus, it seems probable that acquired, but incomplete, immunity
against infection occurs, and a vaccine that can reduce infection and/or invasive
disease may therefore be feasible.
The relative importance of systemic and mucosal, cellular and humoral immunity is
unclear. Several amebic proteins associated with virulence have been identified and
are being studied as potential vaccine components. Development of both parenteral
and oral vaccines for humans is in progress [55].
SUMMARY AND RECOMMENDATIONS
Intestinal amebiasis is caused by the protozoan Entamoeba histolytica.

There are three species of intestinal amebae with identical morphologic
characteristics: E. histolytica, E. dispar, and E. moshkovskii. E. dispar and
E. moshkovskii are non-pathogenic and do not cause clinical disease; all
symptomatic disease is caused by E. histolytica. (See 'Introduction' above.)
Amebiasis occurs worldwide; the prevalence is disproportionately increased

in developing countries because of poor socioeconomic conditions and
sanitation levels. Areas with high rates of amebic infection include India,
Africa, Mexico and parts of Central and South America. In developed
countries, amebiasis is generally seen in migrants from and travelers to
endemic areas. (See 'Epidemiology' above.)
Clinical amebiasis generally has a subacute onset, usually over one to three
weeks. Symptoms range from mild diarrhea to severe dysentery producing
abdominal pain, diarrhea and bloody stools. Fulminant colitis with bowel
necrosis leading to perforation and peritonitis can occur, as can toxic
megacolon. Amebic colitis has been recognized in asymptomatic patients as
well. (See 'Clinical manifestations' above.)
Diagnosis is best accomplished by the combination of serology or antigen

testing together with identification of the parasite in stool or extraintestinal
sites (such as liver abscess pus). (See 'Diagnosis' above.)
All E. histolytica infections should be treated, even in the absence of

symptoms, given the potential risk of developing invasive disease and the risk
of spread to family members. The goals of antibiotic therapy of intestinal
amebiasis are to eliminate the invading trophozoites and to eradicate
intestinal carriage of the organism. We suggest treatment of invasive colitis
with metronidazole or tinidazole (Grade 2B). We suggest subsequent
treatment with paromomycin to eliminate intraluminal cysts (Grade 2C).
Dosing is outlined above. (See 'Treatment' above.)
Prevention of amebic infection in travelers to endemic areas involves

avoidance of untreated water in endemic areas and uncooked food, such as
fruit and vegetables, that may have been washed in local water. Amebic
cysts are resistant to chlorine at the levels used in water supplies, but
disinfection with iodine may be effective. (See 'Prevention' above.)
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? Intestinal Entamoeba histolytica amebiasis

There are three species of intestinal amebae with identical morphologic

EPIDEMIOLOGY — Amebiasis occurs worldwide; the prevalence is

In developed countries, amebiasis is generally seen in migrants from and travelers to

Invasive, extraintestinal amebiasis (eg, hepatic abscesses) are more frequent in

PATHOGENESIS — The host-parasite interaction is complex, and the virulence of

Secretion of proteinases by the trophozoites

The pathogenicity of amebic trophozoites is facilitated by adherence to colonic

CLINICAL MANIFESTATIONS — The majority of entamoeba infections are

blood and mucus in stools and the presence of hematophagous trophozoites

Amebic colitis has been recognized in asymptomatic patients. Among 5193

Rarely, intestinal amebiasis may present as a chronic syndrome of diarrhea, weight

Uncommonly, localized colonic infection resulting in a mass of granulation tissue

DIAGNOSIS — Diagnostic techniques include microscopy, antigen detection,

Diagnosis is best accomplished by the combination of serology or antigen testing

Stool microscopy — The demonstration of cysts or trophozoites in the stool

Organism excretion can vary; a minimum of three specimens on separate days

Antigen testing — Antigen detection is sensitive, specific, rapid, easy to perform,

Serology — Serology is a useful diagnostic tool for amebiasis. E. histolytica

Indirect hemagglutination (IHA) is the most sensitive serologic assay; it is positive in

Polymerase chain reaction (PCR) techniques can detect E. histolytica in stool

A number of investigators have developed PCR methods for the diagnosis of

Visual inspection of the colon — Sigmoidoscopy and/or colonoscopy can be

TREATMENT — All E. histolytica infections should be treated, even in the absence

E. dispar and E. moshkovskii infections do not require treatment. In countries where

can differentiate between E. dispar/E. moshkovskii and E. histolytica become more

Clinical approach — Invasive colitis is generally managed with metronidazole

Alternatives to metronidazole include tinidazole, ornidazole, and nitazoxanide

Intraluminal infection can be treated with one of the following regimens:

Peritonitis — In patients who have suspected or proven peritonitis, broad spectrum

PREVENTION — Prevention of amebic infection in travelers to endemic areas

Vaccine development — There is some evidence of partial acquired immunity to

SUMMARY AND RECOMMENDATIONS

Intestinal amebiasis is caused by the protozoan Entamoeba histolytica.

Amebiasis occurs worldwide; the prevalence is disproportionately increased

Diagnosis is best accomplished by the combination of serology or antigen

All E. histolytica infections should be treated, even in the absence of

Prevention of amebic infection in travelers to endemic areas involves

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1. Haque R, Huston CD, Hughes M, et al. Amebiasis. N Engl J Med 2003;

Microbiol 1993; 31:2845.

Hyg 2010; 83:909.

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