Infectious Disease Online
Pathology of Amebiasis (Entamoeba Histolytica Infection)
Amebiasis is caused by the protozoan parasite Entamoeba histolytica.
The annual number of Entamoeba histolytica infections throughout the world is believed to be approximately 50 million.
Visit: Amebic Meningoencephalitis
Intestinal diseases in Entamoeba Histolytica Infection:
1)Asymptomatic 2) Dysentery 3) Acute necrotizing colitis with perforation 4)Toxic megacolon 5) Ameboma 6) Perianal ulceration with fistula formation.
Intestinal amebiasis may involve any part of the bowel. It usually involves caecum and ascending colon followed by sigmoid colon, rectum, and appendix.
In severe cases the entire colon is involved.
There may be extension into the terminal ileum.
Diarrhea with blood in the stool- Infection due to Shigella, salmonella, campylobacter, enteroinvasive and enterohemorrhagic Escherichia coli.
Noninfectious conditions include inflammatory bowel disease, ischemic colitis, diverticulitis and arteriovenous malformation.
Amebic lesions begin as small foci of necrosis that progress to ulcers.
In the early stages the colonic ulcers have a narrow neck and thus appear as small nodules with a minute surface opening (5 mm in diameter).
As the ulcers enlarge they always retain their undermined base but the ulcerated area of the mucosa becomes larger.
(Muscle coat of the large intestine form a barrier to the penetrating trophozoites which fan out latarally producing a flask-shaped ulcer with narrow neck and broad base).
Large irregular geographic patterns are formed on the bowel mucosa.
The base of the ulcer is covered by grey - white exudate.
There is always undenuded mucosa between the ulcers.
Typical endoscopic appearance of amebic colitis- Small discrete areas of ulceration (red arrow) with normal intervening mucosa (black arrow).
Occasionally (5 -10% cases) the trophozoites penetrate the muscle and serous layers to produce intestinal perforation.
Ameboma- Napkin-like constrictive lesion of the colon.
This is an inflammatory thickening of the bowel wall in response to the parasites.
It resembles carcinoma of colon in location, symptoms, gross and radiographic appearance.
The ulcer is typically 'flask- shaped' and the broad base is composed of fibrin and cellular debris.
A sharp line divides the necrotic and viable mucosa (this feature demonstrates the lytic action of the trophozoites).
Trophozoites are found on the surface of the ulcers, in the exudate and in the crater.
They are frequently found in the submucosa, muscularis propria, serosa and small veins of the submucosa.
There is little inflammatory response in the early ulcers.
However, as the ulcer widens there is accumulation of neutrophils, lymphocytes, histiocytes, plasma cells and sometimes eosinophils.
Histologic sections of an ameboma reveal granulation tissue, fibrosis, chronic inflammatory cells and clusters of trophozoites usually concentrated in the submucosa near small points of ulceration.
Amebic trophozoites are spherical or oval-shaped (15 - 20 micrometer in diameter) with a thin cell membrane and single nucleus with prominent nuclear border and central karyosome.
The cytoplasm is vacuolated (may be confused with macrophages).
The PAS procedure stains the cytoplasm of the trophozoites (red) and makes them stand out in tissue section.
The organisms will appear black when stained by the Heidenhain's iron hematoxylin method.
Presence of trophozoites containing red blood cells is indicative of tissue invasion by virulent Escherichia histolytica parasites.
Organisms are also demonstrated by immunoperoxidase stains.
Life cycle of Entamoeba Histolytica:
Cysts do not invade tissue.
These are spherical thick- walled (5 - 25 micrometer) and have four nuclei.
Infection is initiated by ingestion of faecally contaminated water or food.
In humans the cyst wall is resistant to destruction by the acid content of the stomach.
There is excystation in the small intestine.
A quadrinucleated metacystic ameba divides to form four small trophozoites.
These develop into adult trophozoites and colonize the large intestine (particularly caecum).
In the colon -
1. Trophozoites form new cysts (self- limiting, asymptomatic infection-90%) which is excreted in stool.
2. Trophozoites invade the intestinal epithelium (10%) causing ulcerative lesion as seen in amebic colitis
3. Extraintestinal amebiasis (less than 1%) occurs by direct extension or hematogenous route.
- Amebic liver abscess - Parasites penetrate portal vessels and embolize to the liver. Patients may have single or multiple liver abscesses.
The abscess cavity is sometimes filled with chocolate coloured pasty material (anchovy sauce-like). The wall contains abundant fibrin and trophozoites are clustered in the fibrin at the junction of viable and necrotic tissue.
- Peritonitis and intra-abdominal abscesses - Caused by intestinal perforation or by rupture of liver abscess.
- Liver abscess penetrate the diaphragm to involve pleura and lung.
- Involvement of pericardium results in pericardial effusion, amebic pericarditis, cardiac tamponade and cardiac failure.
- Rarely liver abscess or a lesion in the colon may spread amebae to the brain by hematogenous route.
Cerebral lesions localize in any part of the brain.
Initially there are minute areas of softening which expand to larger necrotic lesions.
- Cutaneous amebiasis results from extension of rectal amebiasis ( to the anus , perianal skin and vulva) or extension of an amebic liver abscess (to the skin of the abdominal wall or flank).
Macroscopically there is marked epithelial hyperplasia (with a cauliflower-like surface resembling carcinoma) punctuated by small circumscribed ulcers.
Histologically, there is papillary acanthosis of the epithelium and chronic inflammatory response.
Trophozoites are concentrated over points of ulceration in adjacent epidermis and in the superficial layers of the ulcer.
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