Entamoeba histolytica

Entamoeba histolytica is an anaerobic intestinal amoeba parasite that predominantly affects a man and causes amoebic dysentery and liver abscess.

History

Entamoeba histolytica was first discovered by Lösch in 1875 in Leningrad, Russia for causing disease in humans. Lösch discovered amoeba in ulcers of the colon at autopsy and induced it to a dog by rectal inoculation with human faeces.

Councilman and Lafleur showed that amoeba was the cause of the disease and Schaudinn distinguished Entamoeba histolytica from non-pathogenic commensals in Human Entamoeba coli in 1903.

Taxonomy for Entamoeba histolytica.

Kingdom:          Protista
SubKingdom:   Protozoa
Phylum:             Sarcomastigophora
Subphylum:      Sarconida
Class:                   Lobosea
Order:                 Amoebida
Family:               Endamoebidae
Genus:                Entameoba
Species:              Histolytica

 

Structure of Entamoeba histolytica

Entamoeba histolytica

There are 3 morphological stages of Entamoeba histolytica.
1. Trophozoite
2. Pre- cyst
3. Cyst

Trophozoite

Trophozoite of E.hystolytica

It is the growing or feeding or active stage.

  • Shape of a trophozoite is not fixed as it constantly changes its position.
  • Size: 18 to 40 μm
  • Motile and moves by pseudopodia.
The Cytoplasm
  • Ectoplasm: It is the outer zone of the cytoplasm. It is clear, less granular and sharply separated from the endoplasm.
  • Endoplasm: It is the inner zone of the cytoplasm and consists of abundant vesicles embedded in the cytoplasmic matrix. It has a ground glass appearance.
  • Cytoplasmic Vesicles: It contains ingested RBC, occasionaly leucocytes and tissure debris.
The Nucleus
  • Shape : Spherical
  • Size : 4-6μm
  • Structure :
    a) Karyosome: Small dot-like mass of chromatin, central in position, surrounded by a clear halo.
    b) Nuclear Membrane: Delicate inner surface is lined with a single layer of uniformly distributed granules.
    c) Space between the karyosome and nuclear membrane is transversed by a linin network having spoke like radical arrangements, giving a ‘cartwheel’ appearance

Pre-Cyst

  • Size: 10-20 μm.
  • Shape: Round or ovoid
  • Blunt pseudopodia present.
  • Movement is sluggish, no progression.
  • Endoplasm is free of RBC.
  • No ingested food particles present
  • Large nuclear structure

The Cyst

  • Shape: Spherical
  • Size: 9 to 15 μm in diameter
  • Surrounded by a highly refractile membrane
  • Chromatoid bars and glycogen are absent in a mature cyst.
  • The mature cyst contains 4 nuclei.
  • Not Destroyed by normal chlorination of water
  • Survives for weeks to months.

Reproduction

Excystation: Transformation of the cyst to trophozoite. Occurs only when the cyst enters into the alimentary canal of man.

Encystation: Transformation of a trophozoite to a cyst. Occurs inside lumen of the intestine of an infected individual.

Multiplication: Reproduction by binary fission. Occurs in the trophozoite stage

Transmission

Food, drink or hand contaminated with faeces containing the cysts to Entamoeba Histolytica.

By direct inoculation of trophozoites in the colon by anal sex or contaminated apparatus in colonic irrigation.

Life Cycle of Entamoeba histolytica

Life Cycle Of Entamoeba  Histolytica
Life Cycle Of Entamoeba Histolytica

Cysts and Trophozoites are passed in stool from an infected person. Cysts are generally found in formed stool whereas trophozoites are found in diarrhoeal stool. Infection by Entamoeba histolytica occurs when a person comes in contact with fecally contaminated food, drinks, hands consisting of a mature cyst.

After ingestion of a mature Quadri nucleated Cyst, excystation occurs in the small intestine. Trophozoites are released and migrate into the large intestine. In the large intestine, the trophozoite multiplies by binary fission and produce cyst.

Both trophozoites and cysts are passed with stool. Cysts have a protective covering and are able to survive days to weeks in the external environment whereas trophozoites are immediately and rapidly destroyed once outside the body. Trophozoites are not able to cause an infection even if they are ingested because they would not be able to pass the gastric acidic barrier.

Epidemiology

Infection by Entamoeba histolytica occurs worldwide but mostly occurs in tropical countries but especially in the area of poor sanitation.  Entamoeba histolytica infection is estimated to kill more than 55,000 people each year. Previously, it was thought that 10% of the world population was infected, but these figures predate the recognition that at least 90% of these infections were due to a second species, Entamoeba dispar. Infection of E. histolytica is also common in men who have sex with men.

Infections caused by Entamoeba Histolytica.

  1. Asymptomatic infections
  2. Symptomatic Infection

a). Intestinal amebiasis ( Primary Lesion)

  • Dysentry or bloody diarrhoea (acute and chronic)
  • Non-Dysentric colitis
  • Amoeboma of the colon

b). Extra-intestinal amebiasis ( Secondary or metastatic lesions):

  • Amoebic liver abscess (most common)
  • Pulmonary amebiasis
  • Other extra-intestinal foci (very rare) Pericardial amoebiasis, brain abscess

Pathogenesis of Intestinal Amoebiasis

The organism is acquired by ingestion of cysts that are transmitted by fecal-oral route in contaminated food and water. There is no animal reservoir. The ingested cysts differentiate into trophozoites in the ileum but tend to colonize caecum and colon.

Mature Quadri nucleated cysts are the infective for which enters into the body by ingestion of fecally contaminated water and food. Ecystation occurs within the lumen of the small intestine. During excystation nuclear division followed by cytoplasmic division gives rise to eight young trophozoites known as Amebula.

Active Trophozoites resides in the lumen of the caecum and large intestine where they adhere to the colonic mucus and epithelial layer by Galactose and N-acetyl D galactosamine specific amoebic lectin.

Trophozoites now release some proteolytic enzymes that degrade cellular attachment and matrix protein. They also release cysteine proteinase that degrades collagen, elastin disrupts the glycoprotein bond between mucosal epithelial cells, IgG, IgA, C3a, C5a. They also lyse neutrophils, monocytes, lymphocytes colonic cells by releasing phosphatidase A and amoebophore also capable of causing necrotic death of hosts cells.

All these actions cause the destruction of intestinal epithelium cells. Thus they produce abscess which breaks down and produce an ulcer. The earliest intestinal lesions are microulcerations of the mucosa of the cecum, sigmoid colon or rectum

These degenerations of connective tissue occur and amoeba enters submucosa. Submucosa extension of ulcerations causes the classic “flask-shaped”(small opening with broad base) ulcer containing trophozoites at the margins of dead and viable tissues.

Superficial ulcers do not extend beyond the muscular mucosae. Deep ulcers are limited to the submucous coat and may extend laterally to communicate with adjacent ulcers.

When the destruction is not limited to the submucosa but extends deeper into the muscular and even the serous layers, the following complications may arise.

Complications in Intestinal Amoebiasis

  • Local Peritonitis
  • Haemorrhage
  • Perforation
  • Generalized Peritonitis
  • Pericaceal or Pericolic abscess,
  • Sloughing
  • Gangrene in the large GUT

Clinical features

  1. Diarrhoea or dysentery – may be mild with only a few loose stools daily.
  2. Abdominal pain and cramping
  3. tenesmus or painful spasms of the anal sphincter.
  4. Flatulence
  5. Anorexia
  6. Weight loss
  7. Chronic fatigue