Amoebiasis is a protozoan infection of the intestinal
tract that occurs due to ingestion of foods or water
contaminated with Entamoeba histolytica cysts.
Entamoeba histolytica was described by Lambl in1859
and Losch established its pathogenic nature.
Councilman and Laufler in 1981 described liver
Humans are the only host of E.histolytica and no
zoonotic reservoirs .
There are an estimated 50million cases of amebiasis
per year upto 10,0000 deaths
species of Entamoeba:
◦ Nonpathogenic: E. dispar, E. coli, E. hartmanni
◦ Pathogenic: E. histolytica , Dientamoeba fragilis,
which causes Dientamoebiasis
amoebiasis = A Parasitic infection caused by the
protozoan Entamoeba histolytica
◦ 2nd to Malaria as protozoan cause of death worldwide
10% of world’s population infected – Increased
prevalence in developing countries (up to 25%)
Amoebiasis is usually transmitted by the fecal-
indirectly through contact with dirty hands or
Infection is spread through ingestion of the cyst
form of the parasite, a semi-dormant and hardy
structure found in feces.
transmitted through contaminated food and water
Trophozoites living in the intestine undergo binary fission
Round and 10-20µ in size
Store glycogen granules and chromatoid bodies
Enters by forming a delicate cystwall around itself
Size is 12µ
Quadrinucleated cyst is the infective stage of the parasite
Ingested by human host pass along with food into the small
Wall of cyst dissolved by trypsin
Tetranucleate emerges out from cyst into lumen of large
intestine called excystment
Metacystic amoeba with four cystic nuclei from each
8 Small trophozoites from each metacystic amoeba
The Trophozoite Stage:
10-40 µm, fragile.
Reside, feed and multiply by binary fission in lumen
May invade – Lytic & physical mechanisms and
metastasize to liver and other extra-intestinal sites.
Galactose-containing molecules & receptors regulate cyst
The spherical structure (Trophozoites) has one
basophilic nuclei about the size of RBC’s. Note some
RBC's are phagocytosed by the Trophozoites
Trophozoites of E.histolytica interact with host through
a series of steps
1. Adhesion of target cell, phagocytosis and cytopathic
2. E.histolytica induces both Humoral and cell mediated
3. Virulence factors – In many circumstances lumen
dwelling Amoeba may be asymptomatic
4. Causes disease only when invade the Intestine
5. Virulence is associated with secretion of Cysteine
proteniase which assists the organism in digesting the
extracellular matrix and invading tissues
It is observed Cysteine proteinase produced by invasive
strains of E.histolytica inactivates the complement
factor C3 and are thus resistant to Complement
Trophozoites adhere to colonic mucosal glycoproteins via a
galactose and N-acetyl-D-galactosamine-specific lectin.
Adherence results in cell lysis (apoptosis) and PMN invasion.
PMN’s are then lysed releasing lytic enzymes, causing more
Small foci of necrosis in the intestinal wall coalesce to form
ulcers (Flask-shaped ulcers).
Parasites resist destruction by complement arm of immune
system via Gal/GalNac mediated inhibition of the membrane
Cell-mediated immunity is important in clearing infection
through generating γ-INF and TNF-α to activate macrophages
and Neutrophils to kill the trophozoite.
Area most commonly involved = Cecum, then Recto-
May invade blood vessels causing thrombosis,
infarction and dissemination via portal circulation to
liver and extra-intestinal sites eg. brain, pleura,
pericardium and genito-urinary system.
Most cases of amebiasis have very mild symptoms or
More severe infection may cause fever, profuse
diarrhea, abdominal pain, jaundice, anorexia, and
In severe cases, it can lead to development of abscesses
(pockets of amoebae and inflammatory cells) in the
liver or, more rarely, the brain.
Complications of Intestinal amoebiasis:
◦ Fulminant Amoebic Colitis with Perforation
May have a mortality rate of up to 50%
Children less than 2 yrs at increased risk of perforation
◦ Massive Haemorrhage
Due to vasculitis of large arteries or multiple ulcers leading
to small arterial leaks
A granulomatous thickening of the colon resulting from lytic
necrosis followed by secondary pyogenic inflammation,
leading to fibrosis and proliferative granulation tissue.
Lesions are firm, hard, may resemble a carcinoma.
◦ Amoebic Stricture
Resulting from fibrosis of intestinal wall. Can involve
rectum, anus or sigmoid.
Complications of Extra-Intestinal Amoebiasis:
Commonly found in Right Lobe of liver
Presents acutely with high fever, RUQ tenderness
Jaundice an unusual findings
◦ amoebic Peritonitis
As a complication of a ruptured hepatic abcess
◦ Pleuropulmonary amoebiasis
Caused by rupture of Rt. Lobe Liver abcess in 10% of patients
Has cough, pleuritic chest pain & dyspnoea
◦ amoebic Pericarditis
Rupture left lobeliverabscess
◦ Cerebral amoebiasis
Rare, has altered consciousness and focal neuro signs
o Genito-Urinary Involvement
Painful genital ulcers – Punched out appearance & profuse
Light Microscopy of Stool
◦ Identification of trophozoites / cysts in fresh stool
Not sensitive (miss up to two thirds of infections)
Cannot distinguish between E.histolytica and E. dispar
◦ Anti-amoebic antibodies (IgM) 70%
◦ Sensitive for amoebic colitis & 90%
◦ For liverabscess
Stool antigen-detection test
◦ Sensitive and Specific
A sample of freshly collected
Acts on the parasites in the lumen of the bow
Acts on the intestinal wall and liver
Drink only bottled or boiled (for 1 minute) water, or
carbonated (bubbly) drinks in cans or bottles.
Avoid fresh fruit or vegetables that were peeled by
Avoid milk, cheese, or dairy products that may not
have been pasteurized.
Avoid anything sold by street vendors.
Thoroughly cook all raw foods.
Thoroughly wash raw vegetables
and fruitchanging diapers, after
smoking or after using a tissue or
handkerchief. s before eating.
Reheat food until eaches at least
Wash your hands before preparing
food, before eating, after going to
the toilet or