Introduction Disease biology Epidemiology Clinical Summary

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Amoebiasis

Professor dr. ali abid saadoon

Introduction Disease biology Epidemiology Clinical Summary

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Introduction
Amoebiasis is a parasitic protozoan disease that affects the
gut mucosa and liver, resulting in dysentery, colitis and liver
abscess. The causative agent, Entamoeba histolytica, is a
potent pathogen that is spread via ingestion of contaminated
food and water. Globally, amoebiasis is highly prevalent, and is
the second leading cause of death to parasitic disease.
This resource will outline the disease biology, epidemiology
and clinical principles of amoebiasis.

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Causative Organism
• The causitive orgainism is parasitic protazoan, called
Entamoeba histolytica.
Causative
Organism •What was once thought to be a single entity, is now
recognised as two morphologically identical but genetically
Life Cycle and distinct forms; E. histolytica (pathogen) and E. dispar
transmission 1 (commensal).
Life Cycle and •This has affected our understanding of amoeba distribution.
transmission 2 Many suspected cases of E. histolytica carrier, may simply have
been E. dispar colonisation
Pathogenesis 1 • The WHO recommendes that E. histolytica colonisation
should be treated,
Pathogenesis 2 however, treatment is
Self Assessment unnecessary for E. dispar
colonisation

E. Histolytica

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Life cycle and transmission 1

Causative • Entammoeba histolytica has a biphasic life cycle, existing in two

forms; as an infectious cyst and an amoeboid trophozoite
Organism

Life Cycle and Mouth - Cyst ingested

transmission 1
Passed in stool Excyst to trophozoite
Life Cycle and
transmission 2
Amoebic disease
Pathogenesis 1

Pathogenesis 2 Cyst Trophozoite

Self Assessment Invades gut mucosa – cyst formation

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 Life cycle

Life cycle

Epidemiology
Prevalence of amebic infection varies with level of 
sanitation and generally higher in tropics and subtropics
than in tempearate climates.

*Worldwide prevalence is about 10% to 50% 

*Cyst passers are important source of infection 

The true estimated prevalence of E. histolytica is close to 

1% worldwide.
Entamoeba histolytica is the second leading cause of 
mortality due to parasitic disease in humans. (The first
being malaria). Amebiasis is the cause of an estimated
50,000-100,000 deaths each year.

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Epidemiology

Epidemiology • Amoebiasis is found primarily in developing

tropical and subtropical countries where
Susceptibility
sanitation is poor, leading to a direct link
between faeces and ingestion (see Box-1).
Self Assessment Occasionally cases are reported in non-
endemic areas e.g. UK and USA. Usually due
to travel and immigration from endemic
areas.
• There are an estimated 40,000-100,000
Box-1. Amoebiasis rates/figures in endemic regions
deaths
-Egypt: due
accounts for 38% of topatients
amoebiasis worldwide
presenting with acute each
year.
diarrhoea in outpatient clinic.
-Mexico:1.3 million cases reported in 1996.
-Hue, Vietnam: 1500 of a 1million population over 5 years

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Susceptibility
•Generally considered to affect children and
Epidemiology
adults, of both sexes equally. However, some
data and anecdotal evidence suggests a male
Susceptibility
predominance.
Self assessment •Amoebic liver abscesses are most common in
males, 18-55.
•Susceptibility to liver abscess conferred by
HLA-DR3 and complotype SC01 in the
Mexican populations
•Other risk factors include oral and anal sex,
and contact with contaminated enema
apparatus.

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Transmission
1-driect contact of person to person( fecal-oral) 
 2- Veneral transmission among homosexual for
both gender ( oro-anal)
3- Food or drink contaminated with feces 
containing the E.his. cyst
4- Use of human feces (night soil) for soil fertilizer 
5- contamination of foodstuffs by flies, and 
possibly cockroaches

Pathogenesis
Effective factores: 
1- strain virulence: 
- classic strain

- non-classic strain; Laredo , Huff, ….

- pathogen zymodemes

2- susceptibility of the host; nutrition status, immune-sys. 

3- breakdown of immunologic barrier (tissue invasion) 

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Pathogenicity mechanisms
1- secreting proteolytic enzymes( histolysine ) and 
cytotoxic substances.

2 - contact-dependent cell killing 

3 – cytophagocytosis 

Amebic killing target cell: 

1- receptor-mediated adherence of amebae to target cell ( adherence lectin) 

2- amebic cytolysis of target cell 
3- amebic phagocytosis of killed target cell 

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Life cycle and transmission -details

Causative • Cysts (10-15μm) are ingested via contaminated food or water. A

Organism refractile wall containing chitin, allows the cyst to survive stomach
acid.
Life Cycle and • In the terminal ileum or colon, the parasite excysts and begins the
transmission 1 trophozoite stage.
• Trophozoites (10-50μm) are highly motile and pleomorphic. They
Life Cycle and are unable to survive outside the human gut.
transmission 2 • Energy is derived from the ingestion of bacteria and food particles.
No mitochondria are present in trophozoites. Respiration enzymes
Pathogenesis 1 are prokaryotic in origin and are anaerobic, converting:
glucose + pyruvate ethanol
•Trophozoites reproduce by binary fission and encyst in the colonic
Pathogenesis 2
wall. Cysts are passed in the stool where they become infectious.
• The signal for encystation is thought to be via epithelial
Self Assessment galactose/N-acetylgalactosamine specific lectin (gal-lectin) binding
protein.

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Pathogenesis 1
• Amoebic trophozoites invade the colon causing
Causative colitis. They may also invade the portal
Organism circulation and travel to the liver, causing liver
Life Cycle and
abscess.
transmission 1 Gastrointestinal Pathology
Life Cycle and • The spectrum of colitis in amoebiasis ranges from
transmission 2
mucosal thickening, to multiple cyst formation, to
Pathogenesis 1 diffuse Inflammation / oedema, to necrosis and
perforation of colonic wall.
Pathogenesis 2 •Binding of E. histolytica to epithelial cells via gal-
lectin. This molecule shows homologous to human
Self Assessment CD59, conferring resistance to complement . A
change in the epithelial permeability is induced,
probably via the inter-cellular tight junctions.
•.

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 Cell lysis and apoptosis of mucosa are thought to be mediated by •
amoebapores, peptides capable of forming pores in lipid bi-layers.
Trophozoites invade through to the submucosa causing flask shaped •
cysts .
Cysteine proteases released by trophozoites digest extracellular •
matrix in liver and colon, and induce interleukin-1 mediated
inflammation. Proteases also cleave IgA and IgG antibodies.
Neutrophils and macrophages are drawn to invasion sites. E. •
histolytica can lyse neutrophils leading to further tissue damage, and
contributing towards the induction of diarrhoea.
Inflammation is a significant cause of tissue damage, however, innate •
immunity may be the main combatant against the disease

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Pathogenesis 2
Hepatic Pathology
Causative • Trophozoites invading the colonic mucosa may enter the hepatic
Organism circulation and reach the liver
•Well circumscribed abscesses are
Life Cycle and formed in the liver containing
transmission 1 liquefied cells surrounded by
inflammatory cells and trophozoites
Life Cycle and •Adjacent parenchyma is usually
transmission 2 unaffected
Amoebic liver abscess
Pathogenesis 1

Pathogenesis 2

Self Assessment

Histological cross section of classical flask Amoebic colitis with multiple ulcer formation
shaped amoebic ulcer in colonic mucosa.

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 Clinical symptoms
Asymptomatic infection Symptomatic infection

Intestinal Amebiasis Extraintestinal Amebiasis

Dysenteric Non-Dysenteric colitis Hepatic Pulmonary The extra foci

Liver abscces Acut nonsupprative

Intestinal Amebiasis symptoms: Diarrhea or dysentery, abdominal pain, cramping ,

anorexia, weight loss, chronic fatigue

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Presentation
Some individuals carry E. histolytica asymptomatically. 4 -
10% will go on to develop the disease within a year.
Presentation Gastroenterological
Diagnosis • Gradual onset (weeks) of bloody diarrhoea, occasionally
with small volumes of mucoid stool. If blood is not visible,
Treatment and stool is usually ‘haem’ positive due to the breach of the
Management mucosa.
• Abdominal pain and tenderness.
Vaccine
• Leucocytes and pus may be present in stool. Fever
Development 1
present in <40% of patients.
• Weight loss and anorexia can be present.
Vaccine
Development 2
•In more severe cases fulminant amoebic colitis develops.
Liver involvement is more common in these cases, along
Vaccine with paralytic ileus, toxic megacolon and mucosal
Development 3 sloughing. Over 75% of patients with fulminant colitis
develop intestinal perforation.
Self Assessment

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 Local inflammatory masses, amoebomas, may cause obstructive •
symptoms.
Hepatic 
More common in men •
Liver abscess pan present in conjunction with bowel symptoms (10% •
of cases), or in isolation.
Sudden onset of upper abdominal pain with fever. Pain may radiate •
to right shoulder or be exacerbated by repiratory movements.
Hepatic tenderness may be present. Jaundice is unusual. •
Complicated liver abscess may develop if abscess ruptures into the •
peritoneal, pericardial or pleural cavity. Morbidity and mortality is
high.
Rarely, trophozoites may also invade the respiratory tract, brain and •
GU tract

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Pathology of Amebiasis

Flask-like Ulcer

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Extra-ntestinalAmebiasis

Pyogenic- Liver Abscess

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Liver abscess

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This is an amebic abscess of liver. Abscesses may arise in liver when there is seeding of
infection from the bowel, because the infectious agents are carried to the liver from the
portal venous circulation.

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Diagnosis

Paraclinical Diagnosis: 
Sigmoidoscopic examination: 
precence of a grossly normal mucosa between the ulcers serves to
differentiate amebic from bacillary dysentery,( the entire mucosa being
involvoed in bacillary dysentery).
Hepatomegally 
C.B.C. : leukocytosis in Amebic dys. rises above 12000 per microliter, 
but counts may reach 16000 to 20000 per microliter.

Laboratory Diagnosis
Entamoeba histolytica must be differentiated from other intestinal 
protozoa including: E. coli, E. hartmanni, E. dispare,……

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, and differentiation must
be based on isoenzymatic or immunologic analysis.

Molecular methods are also useful in distinguishing 

between E. histolytica and E. dispar and can also be used to
identify E. polecki.

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 Microscopy
Microscopic identification 
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).

Trophozoites of Entamoeba histolytica /E.

dispar ( trichrome stain )

Microscopy
B
A

In the absence of erythrophagocytosis, the pathogenic E. histolytica is

morphologically indistinguishable from the nonpathogenic E. dispar!

Each trophozoite has a single nucleus, which has a centrally placed karyosome
and uniformly distributed peripheral chromatin .

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Trophozoites of Entamoeba histolytica with ingested
erythrocytes (trichrome stain)

E F
The ingested erythrocytes appear as dark inclusions.
Erythrophagocytosis is the only morphologic characteristic that can
E. from the nonpathogenic E. histolytica be used to differentiate
.dispar

Cysts of Entamoeba histolytica

/E. dispar
GHI 

H I
Cysts of Entamoeba histolytica/E.
dispar ,permanent preparations stained
with trichrome.

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Immunodiagnosis
(Antibody Detection)
1- Antibody detection 

2- Antigen detection may be useful as an adjunct to 

microscopic diagnosis

The indirect hemagglutination (IHA) 

The EIA test detects antibody specific for E. histolytica in 

approximately 95% of patients with extraintestinal
amebiasis, 70% of patients with active intestinal infection,
and 10% of asymptomatic persons who are passing cysts of
E. histolytica.

Antigen Detection
Antigen detection may be useful as an adjunct to
microscopic diagnosis in detecting parasites and to
distinguish between pathogenic and nonpathogenic
infections.

Recent studies indicate improved sensitivity and specificity

of fecal antigen assays with the use of monoclonal
E. histolytica antibodies which can distinguish between
.infections E. dispar and

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Molecular diagnosis
In reference diagnosis laboratories, PCR is the method 
of choice for discriminating between the pathogenic
from the (nonpathogenic (E. histolytica) species
E. dispar.) species

Treatment
Intestinal Amebiasis: 
*Asymptomatic amebiasis(cyst passer): Diloxanide furoate ( 
furamide)
500 mg 3 times daily / 10 days

*Symptomatic amebiasis ( troph. & cyst): - Iodoquinol , 650 mg 

3 times daily/ 20 days or Metronidazole (Flagyl) , 750 mg 3 times daily/
10 days

*Amebic colitis: Chloroquine, 250 mg 2 times daily 

* Acute amebic dysentery: Emetine hydrochloride, 1mg/kg daily IM or 

SC

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 Treatment
Extraintestinal Amebiasis: 
*Amebic liver abscess, ameboma:
Metronidazole, as above plus dehydroemetine / 10 days or
Metronidazole or dehydroemetine as above plus
Chloroquine , 500 mg 2 times daily / 2 days,…..

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Diagnosis

Presentation • Clinical history is important. In low resource

settings this may be the means of diagnosis. A
Diagnosis
good travel history is important as disease may
Treatment and develop years after a visit to an endemic area.
Management
•Demonstration of E. histolytica in stool by
Vaccine
Development 1 microscopy (old), or ELISA assay for antigen
detection. Trophozoites only survive for short
Vaccine periods of time, therefore, fresh stool samples
Development 2 should be used
Vaccine
•Colonoscopy to confirm colitis and tissue biopsy
Development 3
for amoeba
Self Assessment
•Liver abscess; space occupying lesion on
CT/USS with positive amoebic serology

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Introduction Disease biology Epidemiology Clinical Summary
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Summary
•Amoebiasis is a major global cause of mortality and morbidity,
Summary due to dysentery. The causative organism, E. histolytica.
•E. histolytica has a biphasic life cycle and exists as an infective
References cyst and pathological trophozoite.
•The disease is spread via contaminated food and water, usually
due to poor sanitation.
•The disease is found in tropical and sub-tropical parts of the
world.

Every year, 40,000-100,000 people die from amoebiasis •

Certain genetic traits pre-dispose to certain pathologies. •
Patients usually present with abdominal pain, bloody stools and fever. Hepatic symptoms are •
more acute with upper abdominal pain and radiation to the right shoulder.
Treatment is with Nitroimidazole (e.g.metronidazole) and a luminal agent. Spread can be •
prevented by boiling water.
A potential gal-lectin vaccine is currently in development. Good results have been yielded •
with native gal-lectin vaccines, and moderate results with a DNA based vaccine. Immunity
appears to be mainly via a Th1 cell medicated response and secretory IgA

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Treatment and Management

Presentation • Amoebiasis, in particular with liver involvement, can be fatal if not

treated. Chemotherapy can effectively cure ameobiasis.
Diagnosis
• Nitroimidazole (e.g.metronidazole) is used to treat the invasive
Treatment and pathogens – 800mg t.d.s for 10 days.
Management
• This is followed by a luminal agent (e.g.diloxanide furoate) to
Vaccine eliminate colonisation – 500mg t.d.s for 10 days. This is also suitable
Development 1 for asymptomatic individuals.

Vaccine •Complicated liver abscesses should be drained surgically.

Development 2
Prevention
Vaccine
Development 3 •Boiling water for at least ten minutes kills amoebic cysts
effectively. Chlorine and iodine tablets are not thought to be 100%
Self Assessment effective.

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Questions
1) What are the symptoms of gastrointestinal amoebiasis?
Presentation 2) What are the symptoms of hepatic amoebiasis?
Diagnosis 3) Why is a good travel history important in diagnosis of
amoebiasis?
Treatment and 4) What investigations can be performed to confirm a diagnosis?
Management 5) Name two drugs and dosage regimes that can be used to treat
Vaccine amoebiasis.
Development 1 6) Is the following statement true or false?
“chlorine and iodine can be used to decontaminate water of
Vaccine E.histolytica with 100% effectiveness”
Development 2
7) Does Gal-lectin induce a Th1 or Th2 cell mediated immune
response?
Vaccine
Development 3 Reveal
Answer
Self Assessment

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Answers
1) What are the symptoms of gastrointestinal amoebiasis?
Gradual onset (weeks) of bloody diarrhoea, abdominal pain and tenderness, fever present in
<40% of patients, weight loss and anorexia, amoebomas, may cause obstructive symptoms.
Presentation 2) What are the symptoms of hepatic amoebiasis?
Sudden onset of upper abdominal pain with fever. Pain may radiate to right shoulder or be
exacerbated by repiratory movements.
Diagnosis Hepatic tenderness may be present. Jaundice is unusual
3) Why is a good travel history important in diagnosis of amoebiasis?
Treatment and A good travel history is vital to ascertain whether a patient has visited an endemic area. The
disease may develop over a year after travel.
Management
4) What investigations can be performed to confirm a diagnosis?
Vaccine Demonstration of E. histolytica in stool by microscopy (old), or ELISA assay for antigen detection.
Development 1 Colonoscopy may be performed to check for colitis and biopsy. Check for liver abscess
with USS or CT.
5) Name two drugs and dosage regimes that can be used to treat amoebiasis.
Vaccine Nitroimidazole (e.g.metronidazole)– 800mg t.d.s for 10 days. This is followed by a luminal agent
(e.g.diloxanide furoate) 500mg t.d.s for 10 days.
Development 2
6) Is the following statement true or false?
“chlorine and iodine can be used to decontaminate water of E.histolytica with 100%
Vaccine effectiveness”
Development 3 Boiling is the most effective methos for water decontamination
7) Does Gal-lectin induce a Th1 or Th2 cell mediated immune response?
Self Assessment Th1 cell mediated response

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