Amebiasis is caused by infection with the intestinal protozoan Entamoeba histolytica. It is transmitted through ingestion of cysts from fecally contaminated food or water. Most infections are asymptomatic, but E. histolytica can cause intestinal disease ranging from dysentery to liver abscesses. Diagnosis involves examining stool samples for cysts or trophozoites. Treatment includes metronidazole plus a luminal amebicide for colitis or extraintestinal infections. Prevention focuses on safe water, sanitation, hygiene, and health education to reduce transmission.

1. Amebiasis
Dr. Nesar Ahmad Hamraz MD

2. Definition
Amebiasis is infection with the parasitic
intestinal protozoan Entamoeba histolytica
(the “tissue-lysing ameba”)
Most infections are probably asymptomatic
E. histolytica can cause disease ranging from
dysentery to extraintestinal infections,
including liver abscesses.

3. Causative agent:
Entamoeba histolytica

4. LIFE CYCLE AND TRANSMISSION
 E. histolytica exists in two stages
1) Cyst form
2) Trophozoite form
 Infection (of which humans are the natural hosts) is acquired by ingestion of cysts
contained in fecally contaminated food or water or, more rarely, through oral-anal
sexual contact
 Cysts survive stomach acidity and excyst within the small intestine
 form the 20- to 50-μm trophozoite stage
 Trophozoites can live within the large-bowel lumen without causing disease or can
invade the intestinal mucosa, causing amebic colitis
 In some cases, E. histolytica trophozoites invade through the mucosa and into the
bloodstream, traveling through the portal circulation
 reach the liver and causing amebic liver abscesses
 trophozoites may be excreted into the stool and killed by air
 Trophozoite cysts within the large bowel are excreted in the stool, continuing the
life cycle

5. Cyst form of E. Hystolytica

6. Trophozoite form of E. Histolytica

7. Life cycle
Life cycle

8. Epidemiology
 Most cases of amebiasis are due to Entameba dispare and
entameba moshkovskii which are non invassive parasites
 90% cases of amebiasis due to Entameba Histolytica are
asymptomatic
 10% of cases are symptomatic
 prevalence of Amebic liver abscess is 7 time is higher in men than
women
 The disease is more common in areas with poor sanitation and
crowding
 Mexico, India, tropical regions of africa, south and central of
America and Asia are endemic for disease
 Incidence of disease in this regions are 544 cases in100000
papulation
 Entamoeba histolytica is the fourth 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.

9. Trends of Amoebiasis

10. Pathogenesis
 Amoebic trophozoites invade the colon causing colitis. They may also invade the
portal circulation and travel to the liver, causing liver abscess.
 Gastrointestinal Pathology
 The spectrum of colitis in amoebiasis ranges from mucosal thickening, to multiple
cyst formation, to diffuse Inflammation / oedema, to necrosis and perforation of
colonic wall
 Binding of E. histolytica to epithelial cells via galactosamin-lectin. This molecule
shows homologous to human CD59, conferring resistance to complement . A
change in the epithelial permeability is induced, probably via the inter-cellular
tight junctions.
 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 proteinases released by trophozoites digest extracellular matrix in liver
and colon, and induce interleukin-1 mediated inflammation. Proteinases 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

11. Pathogenesis
 Hepatic Pathology
 Trophozoites invading the colonic mucosa may enter the hepatic
circulation and reach the liver
 Well circumscribed abscesses are formed in the liver containing liquefied
cells surrounded by inflammatory cells and trophozoites
 Adjacent parenchyma is usually unaffected

13. intestinal Extra intestinal
 Liver
 Lung
 Brain
 Skin
Asymptomatic
carriers
 Amoebic colitis
 Fulminant colitis
 Amoeboma
Clinical features

14. Incubation period:
Period of
communicability:
For duration of the
illness.
3 days in severe
infection; several
months in sub-acute
and chronic form. In
average case vary from
3-4 weeks.

15. Asymptomatic carriers (non invasive form)
- 90% without symptoms
- does not damage lumen
Invasive forms:
Amoebic colitis
- flask shaped ulcers superficial or deep
- abd pain, diarrhoea, blood, fever
- tenesmus, peri-anal ulcers
Fulminant colitis - <0.5%
- severely ill with high fever
- intestinal bleeding
- perforation
- paralytic ileus

16. Amoeboma
- 1% of cases
- inflammatory thickening of intestinal wall
- palpable mass with trophozoites
Symptoms of amoebic colitis
Symptoms Percentage
1. Diarrhea 100
2. Dysentery 99
3. Abdominal pain 85
4. Fever 68
5. Dehydration 5
6. Length of symptoms 2 to 4 weeks

17. Symptom Bacillary dysentery Amoebic dysentery
Onset Acute Gradual
General
Condition
Poor Normal
Fever High grade Little fever (adult)
Tenesmus Severe Moderate
Dehydration Frequent Little dehydration
(adult)
Faeces No trophozoites Trophozoites present
Culture Positive Negative

18. Extra-intestinal
Amoebic liver abcess
- via portal system
- 5% of invasive disease
- 10 times more common in men
Pleuropulmonary
- direct spread from liver abcess (10%)
- haematogenous spread
Brain
- abrupt onset & rapid progression
- death in 12-72 hrs

19. Amebic liver
abscess

20. Amebic pleuro-pericardial
abscess

21. Complications
• Amoeboma.
(localized granulomatous mass misdiagnosed
with carcinoma)
• Hemorrhage.
• Perforation of ulcer.
(secondary peritonitis --- rare but fatal)
• Stricture of colon.
(secondary to fibrosis)
• Appendicitis.
• Peritonitis
• Pleural Effusion

22. AMEBIASIS
Diagnosis
Fresh stool or colon mucus shows cysts or
trophozoites
Often 3 or more stool exams required
Serologic tests important to distinguish amebiasis
from ulcerative colitis
Sigmoidoscopy useful to inspect ulcers and obtain
stool or mucus for culture & stain
Abd. CT needed if liver abscess suspected
Abdominal Ultrasound

23. Differential Diagnosis
Bacterial Dysentery
Ulcerative colitis
Malaria
Typhoid Fever

24. Treatment of Amebiasis

25. Treatment of Specific Forms of Amebiasis
Asymptomatic Intestinal Infection
Asymptomatic carriers are treated with a luminal amebicide.
Standard luminal amebicides are:
Diloxanide furoate, Iodoquinol, and Paromomycin.
Therapy with a luminal amebicide is also required in the
treatment of all other forms of amebiasis.
Amebic Colitis
Metronidazole plus a luminal amebicide is the treatment of
choice for amebic colitis and dysentery.
Tetracyclines and erythromycin are alternative drugs for
moderate colitis but are not effective against
extraintestinal disease.
Dehydroemetine or emetine can also be used, but are best
avoided because of toxicity.

26. Metronidazole & Tinidazole
Metronidazole is the drug of choice in the treatment
of extraluminal amebiasis.
It kills trophozoites but not cysts of E histolytica and
effectively eradicates intestinal and extraintestinal
tissue infections.
Tinidazole, have similar activity and better toxicity
profile than metronidazole.

27. Prevention & Control
Primary prevention
- Safe excreta disposal
- Safe water supply
- Hygiene
- Health education
Secondary
- Early diagnosis
- Treatment

28. Primary prevention
Sanitation Water Food hygiene H edu.
-excreta -protect -protect food -long
-wash hands -sand filter -acetic acid term
-latrines -boiling -detergent
-food handlers
examine
treat
educate