Amoebiasis

The right clinical information, right where it's needed

Last updated: May 29, 2018

 Table of Contents
Summary 3

Basics 4
Definition 4
Epidemiology 4
Aetiology 4
Pathophysiology 4
Classification 6

Prevention 7
Primary prevention 7
Screening 7
Secondary prevention 7

Diagnosis 8
Case history 8
Step-by-step diagnostic approach 8
Risk factors 9
History & examination factors 10
Diagnostic tests 11
Differential diagnosis 12

Treatment 14
Step-by-step treatment approach 14
Treatment details overview 14
Treatment options 15

Follow up 17
Recommendations 17
Complications 17
Prognosis 18

Guidelines 19
Diagnostic guidelines 19
Treatment guidelines 19

References 20

Images 23

Disclaimer 26
 Summary

◊ Amoebiasis is a common cause of diarrhoea in infants in low-income countries. Amoebiasis also

causes colitis that can present with diarrhoea and/or dysentery that can be acute or last more than 1
week. Abdominal tenderness and weight loss are common with amoebic colitis.

◊ Amoebic liver abscess presents with right upper quadrant pain. May not present with diarrhoea, but
will usually have a preceding history of diarrhoea.

◊ Rare cause of brain abscess.

◊ Most patients will have travelled to or resided in an endemic area in the 12 months preceding
presentation.

◊ Diagnosis is confirmed by detection of Entamoeba histolytica antigen or DNA in stool or antibodies

against the parasite in serum.

◊ Treatment is with nitroimidazoles (including metronidazole or tinidazole) followed by luminal agents

such as paromomycin or diloxanide furoate to prevent relapse.
 Amoebiasis Basics

Definition
Amoebiasis is caused by the parasite Entamoeba histolytica . It causes diarrhoea and colitis. Spread of
infection from the intestine can result in liver abscess (via haematogenous dissemination). Extension from
BASICS

liver abscess can lead to pleural and pericardial effusion. Rarely, brain abscess may occur.[1] [2] [3] [4] [5] [6]

Epidemiology
There is a higher incidence of amoebiasis in developing versus industrialised countries, although reliable
prevalence data are hard to find. Most amoebic infections occur in Central and South America, Africa, and
Asia.[2] Estimates on the prevalence of Entamoeba infection range from 1% to 40% in Central and South
America, Africa, and Asia, and from 0.2% to 10.8% in endemic areas of developed countries such as the
US.[8] [9] [10] [11] Entamoeba histolytica infection in the US is seen most commonly in immigrants and
travellers from endemic areas, with approximately 3000 cases seen annually.[4] In most cases, disease
presents within the first year of return to or arrival in the country.

Intestinal infection with E histolytica affects all ages and both sexes equally. However, 90% of amoebic liver
abscesses occur in men aged 20 to 40 years.[1] [2] [3] [4] [5] It is also seen in men who have sex with men
(although the non-pathogenic amoeba E dispar is more common in this setting than E histolytica ).[1] [2]
[12]

Outbreaks in institutions, particularly those for people with mental retardation, have occurred.[1] [2] Men
who have sex with men, faecal-oral contamination, lower educational achievement, and older age were
associated with increased risk for amoebiasis among people seeking voluntary counselling and testing for
HIV infection in Taiwan.[13]

Globally, E histolytica accounts for 2% to 4% of cases of diarrhoea presenting to a hospital or a clinic.[1] [2]
[3] [4] [5] [6] [7]

Aetiology
Amoebiasis is contracted by ingestion of the cyst of Entamoeba histolytica , which is found in faecally
contaminated food and water. Transmission can also occur indirectly through sexual intercourse or contact
with faecally contaminated objects. Cysts are environmentally stable, being resistant to chlorination and
desiccation.
[Fig-1]

Pathophysiology
The life-cycle of E histolytica begins with ingestion of faecally contaminated food or water. The infective cyst
form of the parasite survives passage through the stomach and small intestine. It excysts in the bowel lumen
to form motile and potentially invasive trophozoites.

In most infections, the trophozoites aggregate in the intestinal mucin layer and form new cysts, resulting in
a self-limiting and asymptomatic infection. However, galactose/N-acetyl-galactosamine (Gal/GalNAc) lectin-
mediated adherence to and lysis of the colonic epithelium can initiate trophozoite invasion into the colon in
some cases.

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Amoebiasis Basics
Neutrophils responding to invasion contribute to cellular damage at the site of invasion. Once the intestinal
epithelium is invaded, extraintestinal spread into the peritoneum, liver, and other sites is possible.

Factors controlling invasion versus encystation include parasite quorum sensing signalled by the Gal/GalNAc

BASICS
lectin interactions of amoebae with the bacterial flora of the intestine, and host innate and acquired immune
responses.

Trophozoites are always present in the gut in patients with amoebic diarrhoea and dysentery (diarrhoea with
blood or mucus), and diagnosis should concentrate on identifying the parasite in stool by antigen detection
and the serum antibody response against the invasive parasite.[1] [2]

Invasion of the trophozoites through the intestinal epithelium leads to amoebic diarrhoea and colitis. Invasion
involves a unique nibbling process by the parasite on the intestinal lining, termed amoebic trogocytosis.[14]

Haematogenous dissemination via the portal venous system results in amoebic liver abscess and infection in
other sites such as the brain, although this is rare.[1] [2] [3] [4] [5]

Life-cycle of Entamoeba histolytica

Reproduced from New England Journal of Medicine (2003); used with permission

[Fig-3]

[Fig-4]

[Fig-5]

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 Amoebiasis Basics
[Fig-6]

Classification
BASICS

Taxonomy classification[6]
Infectious:

• Entamoeba histolytica
Commensal:

• Entamoeba dispar
• Entamoeba moshkovskii
• Entamoeba bangladeshi
• Escherichia coli
• Entamoeba hartmanni
• Entamoeba polecki
• Entamoeba gingivalis

Clinical manifestations[2]
1. Asymptomatic colonisation

• Presence of E histolytica in stool in the absence of colitis or extraintestinal manifestations

2. Intestinal amoebiasis

3. Extraintestinal amoebiasis

• Amoebic liver abscess

• Splenic abscess
• Empyema
• Pericarditis
• Brain abscess

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Amoebiasis Prevention

Primary prevention
Primary prevention is accomplished by taking precautionary measures against ingestion of faecally
contaminated food and water, particularly in endemic areas, such as not drinking tap water and not
consuming food that may have been washed in contaminated water.[1]

Screening
Family members in the household of an index case should be screened.[2]

Secondary prevention
There is evidence of household transmission of amoebiasis, so it is prudent for all household contacts of the
patient to be screened for amoebiasis with stool antigen detection tests and serum antibodies.[1] [5]

To reduce risk of spreading infection, patients should be advised to wash hands regularly and not to share
household towels.

PREVENTION

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 Amoebiasis Diagnosis

Case history
Case history #1
A 23-year-old woman complains of diarrhoea lasting several weeks. She has lost weight, has not had
fever, and has not noticed blood in the stool. The diarrhoea started while she was travelling in Mexico.

Case history #2
A 39-year-old man presents to the accident and emergency department with right shoulder pain that
he has been experiencing for 2 months. He reports that the pain has radiated to his back. He has been
having night sweats and chills and has lost 10 to 15 pounds in weight. He has also had abdominal pain
for 3 days and a non-productive cough. He was born in Iran and recently emigrated to the US. Physical
examination identifies hepatomegaly and decreased breath sounds over the lower two-thirds of the right
lung. Neurological examination is normal.

Other presentations
Amoebiasis is asymptomatic in 80% of cases. Diarrhoea is the most common illness caused by
Entamoeba histolytica , although intestinal disease may present as dysentery (diarrhoea with blood
or mucus) rather than diarrhoea alone. An amoeboma, which is a mass of granulation tissue in the
colon that can be similar in appearance to colonic carcinoma, may also be detected. Less common
extraintestinal manifestations are peritonitis from perforation of the intestine and pleural or pericardial
effusions from direct extension of a liver abscess and brain abscess (almost all patients with brain
abscess due to E histolytica also have a liver abscess).[1] [2] [3] [4] [5] [6] [7]

Step-by-step diagnostic approach

DIAGNOSIS

Diagnostic tests should be performed before starting therapy for those in whom amoebiasis is suspected.
Diagnosis is confirmed by detection of Entamoeba histolytica antigen in stool samples, by positive serology,
or by PCR. Because no single test approaches 100% sensitivity, it is prudent to use a combination of
serology with either PCR or antigen detection in stools for diagnosis.

Clinical evaluation
Amoebiasis should be considered in any individual who presents with diarrhoea or liver abscess and who
has travelled or lived in an endemic area in the previous 12 months. Other populations at risk of infection
are institutionalised individuals and men who have sex with men.

Presentation is subacute in many cases. Key symptoms of infection are diarrhoea that has lasted for
several days or longer and abdominal pain. Entamoeba histolytica diarrhoea is usually lacking blood or
mucus, and is therefore indistinguishable from diarrhoea caused by a variety of other enteropathogens.
Patients may report blood in their stool. Weight loss is reported by about 50% of patients.[1] Right upper
(RU) abdominal pain in a man aged 20 to 40 years, with or without coincident diarrhoea, could indicate
an amoebic liver abscess.[1] [2] [3] [4] [5] Patients may report altered mental status if brain abscess is
present.

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Amoebiasis Diagnosis
Physical examination
Fever is rare with intestinal infection but common with hepatic infection. With hepatic infection, jaundice,
RU tenderness, and hepatomegaly may be present. Liver abscesses may extend into the pleural or
pericardial cavities (rare), resulting in signs of a pleural or pericardial effusion. Splenic abscess is a rare
manifestation of amoebiasis. Neurological abnormalities, such as limb weakness, may be present in
patients with a brain abscess.

Laboratory evaluation
If amoebiasis is clinically suspected, the definitive test is the TechLab E histolytica II antigen detection
test on a stool specimen. This is the only test specific for E histolytica ; all other detection kits detect the
E histolytica - E dispar - E moshkovskii species complex.[15]

If antigen testing is not available, stool PCR and real-time quantitative PCR (qPCR) testing are
alternatives and are highly sensitive and specific for the detection of E histolytica .[16] Real-time qPCR
is more sensitive than traditional PCR for stool samples.[16] Multiplex PCR of stool samples is available
through FDA-cleared gastrointestinal panels.[17] [18]Real-time PCR assay results of the urine and saliva
specimens are 97% and 89% sensitive for detection of E histolytica DNA in liver abscess and intestinal
infection, respectively.[19]

In patients with suspected amoebic disease, especially possible amoebic abscesses without coexisting
diarrhoea, serum antibody testing for E histolytica should be performed.[15]

Liver abscesses should be aspirated to determine aetiology. The pus should be analysed by PCR
or qPCR to identify whether the causal infection is amoebic and cultured to determine whether it is
pyogenic.[1] [2]

Microscopy is not specific for diagnosis of amoebiasis, as E histolytica cysts and trophozoites are
indistinguishable from those of E dispar and E moshkovskii . However, stool microscopy for ova,
cysts, and parasites is readily available and may demonstrate other infectious causes. The presence of
erythrophagocytic trophozoites is highly suggestive of E histolytica infection.

DIAGNOSIS
Colonoscopy
May be helpful if clinical suspicion is high and antigen detection tests are negative.[2] Endocytoscopy may
allow for real-time visualisation of amoebae in the lesion of colitis.[20]

Imaging
If liver involvement is suspected, a liver ultrasound should initially be performed. CXR and chest/
abdominal CT are indicated if an effusion due to abscess extension is suggested by clinical findings.

Patients with neurological symptoms should have a CT or MRI of the brain.[1] [5]

Risk factors
Strong

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 Amoebiasis Diagnosis
exposure in endemic areas
• Most patients with amoebiasis in the US will have visited or resided in an endemic area within the
previous 12 months.[1] [2] [3] [4] [5]

institutionalisation of mentally retarded people

• Outbreaks in institutions for people with mental retardation have been reported.[1] [2] [3] [4] [5]

men who have sex with men

• Commensal amoeba Entamoeba dispar is responsible for most infections, but Entamoeba histolytica
infections also occur in this population.[1] [2] [3] [4] [5] [12]
• Oral and anal sex are risk factors.[1] [2] [3] [12]

male sex
• Ninety percent of amoebic liver abscesses are found in men aged 20 to 40 years.[1] [2] [3] [4] [5]

History & examination factors

Key diagnostic factors
presence of risk factors (common)
• Key risk factors include exposure in endemic areas, institutionalisation, men who have sex with men,
and male sex.

diarrhoea (common)
• Patients may have had diarrhoea for 1 week or more at the time of presentation.[1] [15] Entamoeba
histolytica diarrhoea is usually lacking blood or mucus, and is therefore indistinguishable from
diarrhoea caused by a variety of other enteropathogens.
• Less than 50% of patients with a liver abscess will have diarrhoea at time of presentation, although a
past history of diarrhoea or dysentery is common.
DIAGNOSIS

Other diagnostic factors

generalised abdominal pain (common)
• Present in some patients with amoebiasis.

RU abdominal pain (common)

• May indicate an amoebic liver abscess.[1] [5]

weight loss (common)

• About half of patients may report weight loss due to the subacute nature of the disease.[1]

cough (common)
• Common in patients with liver abscess. Caused by phrenic nerve irritation and/or pleural effusion.[1]

fever (uncommon)
• Rare in intestinal infections but common in extraintestinal infections, such as liver and brain
abscesses.[1]

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Amoebiasis Diagnosis
altered mental status or limb weakness (uncommon)
• Present with amoebic brain abscess.[1] [3] [5]

dyspnoea (uncommon)
• Extension of liver abscess causing pleural or pericardial effusion.

guarding and rebound tenderness of the abdomen (uncommon)

• Present with acute necrotising colitis, toxic megacolon, or peritonitis due to amoebiasis.[1]

jaundice (uncommon)
• More common with pyogenic than amoebic liver abscess.[1] [5]

right lung decreased air entry and percussion note (uncommon)

• If pleural effusion present.

Diagnostic tests
1st test to order

Test Result
stool antigen detection positive for parasite
antigen
• Ordered before starting therapy in patients in whom amoebiasis is
suspected.
• Only the CellLab or TechLab Entamoeba histolytica II tests
specifically identify E histolytica ; other antigen detection tests detect
the E histolytica - E dispar - E moshkovskii species complex.[15]
PCR or qPCR of stool or liver abscess pus for E histolytica DNA amplification of amoebic
• If antigen testing is not available, stool PCR and real-time quantitative DNA

DIAGNOSIS
PCR (qPCR) testing are alternatives and are highly sensitive and
specific for the detection of E histolytica .[16]
• Real-time qPCR is more sensitive than traditional PCR for stool
samples.[16]
• Multiplex PCR of stool samples is available through FDA-cleared
gastrointestinal panels.[17] [18]
• PCR or qPCR on liver abscess pus is definitive for diagnosis of
amoebic liver abscess.
• Real-time PCR assay results of the urine and saliva specimens are
97% and 89% sensitive for detection of E histolytica DNA in liver
abscess and intestinal infection, respectively.[19]
serum antibody test positive for antiamoebic
antibodies
• Should be ordered before starting therapy in patients for whom
amoebiasis is suspected.[15]
• Less sensitive at time of presentation (60% to 70%) than at
convalescence.
• Patients remain positive for years after infection.[15]

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 Amoebiasis Diagnosis

Other tests to consider

Test Result
stool microscopy identification of
Entamoeba in stool
• Not as sensitive or specific as other tests but still used clinically to
confirm amoebic intestinal infection.[1] [2] [3] [4] [5]
colonoscopy granular, friable, and
diffusely ulcerated
• Biopsy specimens should be taken from the edge of the ulcer.
mucosa
Histology may show trophozoites.[2] Endocytoscopy may allow for
real-time visualisation of amoebae in the lesion of colitis.[20]
[Fig-4]
liver ultrasound homogeneous
hypoechoic round or oval
• Useful only in a patient with amoebic liver, not amoebic intestinal,
lesion
infection.[1]
• Unable to distinguish from a pyogenic abscess.[2]
CXR right hemidiaphragm
elevation or right-sided
• Performed if clinical findings suggestive of effusion and presence of
pleural effusion
liver abscess.
[Fig-5]
CT liver/chest/head rounded, well-defined,
low-at tenuation lesion;
• Unable to distinguish from a pyogenic abscess.[2]
wall commonly enhances
[Fig-6]
with contrast; pleural
effusion

MRI brain space-occupying lesion(s)

• Required if neurological symptoms.

Differential diagnosis
DIAGNOSIS

Condition Differentiating signs / Differentiating tests

symptoms
Infectious diarrhoea • Differential diagnosis is • Presence of specific
broad as various bacteria, infectious agent on stool or
parasites, and viruses cause serological testing.
diarrhoea.[21]

Ulcerative colitis • Absence of history of travel • Stool and antigen testing

to endemic areas. negative for infectious
• Bloody diarrhoea. agents.
• Typical colonoscopy and
biopsy appearance.

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Amoebiasis Diagnosis

Condition Differentiating signs / Differentiating tests

symptoms
Pyogenic liver abscess • Occurs predominantly in • Infective organism identified
females. in blood or pus culture.
• Jaundice is more common
with pyogenic liver abscess
than with amoebic liver
abscess.
• Associated with hepatobiliary
disease.

Necrotic hepatoma • Absence of history of • Aspirate of hepatoma

travel to endemic areas or negative for infectious cause.
diarrhoea.

Fascioliasis (liver flukes) • There are no physical • Key diagnostic test is

differentiating characteristics. positive serum antibody for
fascioliasis.
• Eosinophilia.

Echinococcal liver cyst • There may be no clinical • Positive serum antibody test
features of an echinococcal for echinococcus.
liver cyst (which is • Aspiration of cyst should
sometimes an incidental be avoided because of the
finding in a patient not possibility of anaphylaxis.
presenting with abdominal
complaints). It may present
with anaphylaxis caused by
spillage of cyst contents into
the peritoneum.

DIAGNOSIS

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 Amoebiasis Treatment

Step-by-step treatment approach

All Entamoeba histolytica infections should be treated.[1] [5] Treatment is given as soon as the diagnosis is
considered and following taking of samples for testing, as amoebiasis is a potentially fatal illness.

Symptomatic patients should initially be given a nitroimidazole (metronidazole or tinidazole). Nitroimidazoles

have excellent tissue penetration and are active for both luminal and invasive infection. There is no
recognised resistance to this class of antiamoebic medicine. This should be followed with a luminal agent
(such as paromycin or diloxanide) to eradicate gut colonisation and prevent relapse.[1] [5] [22] [23] [23]
Although they vary in their adverse effects, for most of these medicines adverse effects are generally minor,
whereas the infection is potentially fatal.

Asymptomatic patients also require treatment because of the risk for developing future invasive disease.[1]
[5] They should be treated with a luminal agent alone.[24]

Amoebic abscess
Percutaneous aspiration may be required for patients who do not respond to nitroimidazole treatment in 5
to 7 days, or with large (>5 cm diameter) or left lobe lesions.[1] [2] [5] [25] [26]

Treatment details overview

Consult your local pharmaceutical database for comprehensive drug information including contraindications,
drug interactions, and alternative dosing. ( see Disclaimer )

Acute ( summary )
symptomatic amoebiasis

1st nitroimida zole

plus luminal agent

abscess that does not adjunct aspiration

respond to nitroimida zole
after 5-7 days, large (>5
cm diameter) or left lobe
lesions

asymptomatic amoebiasis

1st luminal agents

TREATMENT

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Amoebiasis Treatment

Treatment options

Acute
symptomatic amoebiasis

1st nitroimida zole

Primary options

» metronidazole: children: 35-50 mg/kg/day

orally given in 3 divided doses for 7-10 days;
adults: 500-750 mg orally three times daily for
7-10 days

OR

» tinidazole: children: 50 mg/kg orally once

daily for 3 days (or 5 days if liver abscess),
maximum 2000 mg/day; adults: 2000 mg
orally once daily for 3 days (or 5 days if liver
abscess)

» Treatment is given as soon as the diagnosis

is considered and following taking of samples
for testing, as amoebiasis is a potentially fatal
illness.[1] [5]

» Nitroimidazoles have excellent tissue

penetration and are active for both luminal and
invasive infection.

» Treatment with nitroimidazole is followed

with a luminal agent to eliminate intestinal
colonisation.[22] [23]

» Although they vary in their adverse effects,

for most of these medicines adverse effects
are generally minor, whereas the infection is
potentially fatal.
plus luminal agent
Primary options

» paromomycin: children and adults: 25-35

mg/kg/day orally given in 3 divided doses for
5-10 days

OR

» diloxanide furoate: children: 20 mg/kg/day

orally given in 3 divided doses for 10 days;
TREATMENT

adults: 500 mg orally three times daily for 10

days

» Luminal agents are used after completion of

acute therapy with the nitroimidazole to eradicate

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 Amoebiasis Treatment

Acute
gut infection and thereby reduce the risk of a
relapse of infection.[23]
abscess that does not adjunct aspiration
respond to nitroimida zole
after 5-7 days, large (>5 » Aspiration of an amoebic abscess may be
cm diameter) or left lobe required for patients who do not respond to
lesions nitroimidazole treatment in 5 to 7 days, or those
at risk for rupture.[1] [2] [5] [25] [26]
asymptomatic amoebiasis

1st luminal agents

Primary options

» paromomycin: children and adults: 25-35

mg/kg/day orally given in 3 divided doses for
5-10 days

OR

» diloxanide furoate: children: 20 mg/kg/day

orally given in 3 divided doses for 10 days;
adults: 500 mg orally three times daily for 10
days

» Asymptomatic patients require treatment

because of the risk of developing future invasive
disease.[1] [5] They should be treated with a
luminal agent alone.[24]
TREATMENT

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Amoebiasis Follow up

Recommendations
Monitoring

FOLLOW UP
It is reasonable, but not a uniform recommendation, to carry out a follow-up stool antigen detection test on
completion of nitroimidazole and luminal therapy to confirm eradication of colonisation.

There is no need for follow-up imaging of an amoebic liver abscess after completion of therapy.

Patient instructions
Patients treated for amoebiasis should be warned of the side effects of the medications that they are
receiving, of the need to be adherent to the follow-up course of a luminal agent to eradicate colonisation
(and thereby prevent relapse), and of the symptoms and signs of complications of amoebiasis.

Complications

Complications Timeframe Likelihood

toxic megacolon short term low

Occurs in less than 1% of patients.

Occurrence may increase with corticosteroid use.

Requires surgery as unlikely to respond to antiamoebic medication.[1] [5]

acute necrotising colitis short term low

Occurs in less than 1% of patients.

Occurrence may increase with corticosteroid use.

Requires surgery as unlikely to respond to antiamoebic medication.[1] [5]

colonic perforation with peritonitis short term low

Occurs in less than 1% of patients.

Occurrence may increase with corticosteroid use.

Requires surgery as unlikely to respond to antiamoebic medication.[1] [5]

amoeboma variable low

Annular granulation tissue in the caecum or ascending colon, extending from the wall into the lumen. Can
be mistaken for colonic carcinoma.

Responds to medical therapy.[1]

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 Amoebiasis Follow up

Prognosis
FOLLOW UP

Amoebic colitis
Mortality rate is less than 2%.

Complications include toxic megacolon, colonic perforation with resultant peritonitis, and amoeboma
(granulation tissue in the intestinal lumen).[1] [2] [5]

Liver abscess
Mortality rate is less than 2%.

Complications include extension of the abscess into peritoneum, pleural cavity, or pericardium, and
haematogenous dissemination to the brain, lung, and skin.[1] [2] [3] [5]

Brain abscess
Rare complication and little is known about prognosis.

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Amoebiasis Guidelines

Diagnostic guidelines

Europe

Interim public health operational guidelines for amoebiasis (Entamoeba

histolytica)
Published by: Public Health England Last published: 2017

Treatment guidelines

Europe

Interim public health operational guidelines for amoebiasis (Entamoeba

histolytica)

GUIDELINES
Published by: Public Health England Last published: 2017

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of the topics can be found on bestpractice.bmj.com . Use of this content is
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 Amoebiasis References

Key articles
• Haque R, Huston CD, Hughes M, et al. Amebiasis. New Engl J Med. 2003;348:1565-1573. Abstract
REFERENCES

• Stanley SL Jr. Amoebiasis. Lancet. 2003;361:1025-1034. Abstract

• Chacin-Bonilla L, Bonillla E, Parra AM, et al. Prevalence of Entamoeba histolytica and other intestinal
parasites in a community from Maracaibo, Venezuela. Ann Trop Med Parasitol. 1992;86:373-380.
Abstract

• Haque R, Mollah NU, Ali IKM, et al. Diagnosis of amebic liver abscess and intestinal infection
with the TechLab Entamoeba histolytica II antigen detection and antibody tests. J Clin Microbiol.
2000;38:3235-3239. Full text

• Drugs for parasitic infections. Medical Letter. 2004;46:e1-12.

• Gonzales ML, Dans LF, Martinez EG. Antiamoebic drugs for treating amoebic colitis. Cochrane
Database Syst Rev. 2009;(2):CD006085. Full text Abstract

• Chavez-Tapia NC, Hernandez-Calleros J, Tellez-Avila FI, et al. Image-guided percutaneous procedure

plus metronidazole versus metronidazole alone for uncomplicated amoebic liver abscess. Cochrane
Database Syst Rev. 2009;(1):CD004886. Abstract

References
1. Haque R, Huston CD, Hughes M, et al. Amebiasis. New Engl J Med. 2003;348:1565-1573. Abstract

2. Petri WA Jr, Singh U. Diagnosis and management of amebiasis. Clin Infect Dis. 1999;29:1117-1125.
Abstract

3. Solaymani-Mohammadi S, Lam M, Zunt JR. Entamoeba histolytica encephalitis diagnosed by

polymerase chain reaction of cerebrospinal fluid. Trans R Soc Trop Med Hyg. 2007;101:311-313.
Abstract

4. Snider C, Petri WA Jr. Travel Medicine. In: Rakel RE, ed. Conn's current therapy 2008. 61st ed. New
York, NY: W.B. Saunders; 2007.

5. Stanley SL Jr. Amoebiasis. Lancet. 2003;361:1025-1034. Abstract

6. Diamond LS, Clark CG. A redescription of Entamoeba histolytica Schaudinn, 1903 (amended Walker,
1911) separating it from Entamoeba dispar Brumpt, 1925. J Eukaryot Microbiol. 1993;40:340-344.
Abstract

7. Ali IKM, Hossain MB, Roy S, et al. Entamoeba moshkovskii infections in children in Bangladesh.
Emerg Infect Dis. 2003;9:580-584. Full text Abstract

20 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: May 29, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
Amoebiasis References
8. Rivera WI, Tachibana H, Kanbara H. Field study on the distribution of Entamoeba histolytica and
Entamoeba dispar in the northern Philippines as detected by the polymerase chain reaction. Am J
Trop Med Hyg. 1998;59:916-921. Full text Abstract

REFERENCES
9. Haque R, Faruque AS, Hahn P, et al. Entamoeba histolytica and Entamoeba dispar infection in
children in Bangladesh. J Infect Dis. 1997;175:734-736. Abstract

10. Chacin-Bonilla L, Bonillla E, Parra AM, et al. Prevalence of Entamoeba histolytica and other intestinal
parasites in a community from Maracaibo, Venezuela. Ann Trop Med Parasitol. 1992;86:373-380.
Abstract

11. Braga LL, Mendonca Y, Paiva CA, et al. Seropositivity for and intestinal colonization with
Entamoeba histolytica and Entamoeba dispar in individuals in northeastern Brazil. J Clin Microbiol.
1998;36:3044-3045. Full text Abstract

12. Watanabe K, Gatanaga H, Escueta-de Cadiz A, et al. Amebiasis in HIV-1-infected Japanese men:
clinical features and response to therapy. PLoS Negl Trop Dis. 2011;5:e1318. Abstract

13. Hung CC, Wu PY, Chang SY, et al. Amebiasis among persons who sought voluntary counseling
and testing for human immunodeficiency virus infection: a case-control study. Am J Trop Med Hyg.
2011;84:65-69. Abstract

14. Ralston KS, Solga MD, Mackey-Lawrence NM, et al. Trogocytosis by Entamoeba histolytica
contributes to cell killing and tissue invasion. Nature. 2014;508:526-530. Full text Abstract

15. Haque R, Mollah NU, Ali IKM, et al. Diagnosis of amebic liver abscess and intestinal infection
with the TechLab Entamoeba histolytica II antigen detection and antibody tests. J Clin Microbiol.
2000;38:3235-3239. Full text

16. Roy S, Kabir M, Mondal D, et al. Real-time PCR assay for the diagnosis of Entamoeba histolytica
Infection. J Clin Microbiol. 2005;43:2168-2172. Abstract

17. Buss SN, Leber A, Chapin K, et al. Multicenter evaluation of the BioFire FilmArray gastrointestinal
panel for etiologic diagnosis of infectious gastroenteritis. J Clin Microbiol. 2015 Mar;53(3):915-25. Full
text Abstract

18. Binnicker MJ. Multiplex molecular panels for diagnosis of gastrointestinal infection: performance, result
interpretation, and cost-effectiveness. J Clin Microbiol. 2015 Dec;53(12):3723-8. Full text Abstract

19. Haque R, Kabir M, Noor Z, et al. Diagnosis of amebic liver abscess and amebic colitis by detection
of Entamoeba histolytica DNA in blood, urine, and saliva by a real-time PCR assay. J Clin Microbiol.
2010;48:2798-2801. Full text Abstract

20. Hosoe N, Kobayashi T, Kanai T, et al. In vivo visualization of trophozoites in patients with amoebic
colitis by using a newly developed endocytoscope. Gastrointest Endosc. 2010;72:643-646. Abstract

21. Pfeiffer ML, DuPont HL, Ochoa TJ. The patient presenting with acute dysentery - a systematic review.
J Infect. 2012;64:374-386. Abstract

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: May 29, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
21
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 Amoebiasis References
22. Drugs for parasitic infections. Medical Letter. 2004;46:e1-12.

23. Gonzales ML, Dans LF, Martinez EG. Antiamoebic drugs for treating amoebic colitis. Cochrane
REFERENCES

Database Syst Rev. 2009;(2):CD006085. Full text Abstract

24. Blessmann J, Tannich E. Treatment of asymptomatic intestinal Entamoeba histolytica infection. N Engl
J Med. 2002;347:1384. Abstract

25. Chavez-Tapia NC, Hernandez-Calleros J, Tellez-Avila FI, et al. Image-guided percutaneous procedure
plus metronidazole versus metronidazole alone for uncomplicated amoebic liver abscess. Cochrane
Database Syst Rev. 2009;(1):CD004886. Abstract

26. Bammigatti C, Ramasubramanian NS, Kadhiravan T, et al. Percutaneous needle aspiration in

uncomplicated amebic liver abscess: a randomized trial. Trop Doct. 2013;43:19-22. Abstract

22 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: May 29, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
Amoebiasis Images

Images

Figure 1: Cyst of Entamoeba histolytica : iodine stain of stool sample

Reproduced from Current Concepts (2003); used with permission

IMAGES

Figure 2: Life-cycle of Entamoeba histolytica

Reproduced from New England Journal of Medicine (2003); used with permission

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: May 29, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
23
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 Amoebiasis Images
Figure 3: Trophozoites of Entamoeba histolytica : trichrome stain of stool sample
Reproduced from Clinical Infectious Diseases (1999); used with permission

Figure 4: Amoebic ulcerations of the colon: colonic ulcers averaging 1 mm to 2 mm in diameter on gross
pathology
Reproduced from New England Journal of Medicine (2003); used with permission
IMAGES

Figure 5: Posterior-anterior and lateral CXR of a patient with amoebic liver abscess: CXR findings include
elevated right hemidiaphragm and evidence of atelectasis
Reproduced from New England Journal of Medicine (2003); used with permission

Figure 6: Entamoeba histolytica brain abscess

24 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: May 29, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
Amoebiasis Images
Reproduced from Transactions of the Royal Society of Tropical Medicine and Hygiene (2007); used with
permission

IMAGES

This PDF of the BMJ Best Practice topic is based on the web version that was last updated: May 29, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
25
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
 Amoebiasis Disclaimer

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26 This PDF of the BMJ Best Practice topic is based on the web version that was last updated: May 29, 2018.
BMJ Best Practice topics are regularly updated and the most recent version
of the topics can be found on bestpractice.bmj.com . Use of this content is
subject to our disclaimer. © BMJ Publishing Group Ltd 2018. All rights reserved.
Contributors:

// Authors:

William A. Petri, Jr, MD, PhD, FACP

Wade Hampton Frost Professor of Epidemiology
Professor of Medicine, Microbiology, and Pathology, Chief, Division of Infectious Diseases and International
Health, University of Virginia, Charlottesville, VA
DISCLOSURES: WAP receives income from the University of Virginia for licensing fees for amebiasis
diagnostics produced by TechLab, Inc. These are donated in their entirety to the American Society of
Tropical Medicine and Hygiene by Dr Petri. WAP is also the author of a number of references cited in this
monograph.

Koji Watanabe, MD, PhD

Visiting Professor
Department of Infectious Diseases and International Health, University of Virginia, Charlottesville, VA
DISCLOSURES: KW declares that he has no competing interests.

// Peer Reviewers:

Ran Nir-Pa z, MD
Senior Lecturer in Microbiology and Medicine
Department of Clinical Microbiology and Infectious Diseases, Hadassah-Hebrew University Medical Center,
Jerusalem, Israel
DISCLOSURES: RNP declares that he has no competing interests.

Christopher Huston, MD
Assistant Professor of Medicine
Division of Infectious Diseases, University of Vermont College of Medicine, Burlington, VT
DISCLOSURES: CH declares that he has no competing interests.