Introduction:
It is a common protozoan parasite found in the large intestine of human.
It is one of the leading parasitic causes of death in developing countries
It causes amoebic dysentery and liver abscess in human
Morphology:
The parasite occurs in 3 forms
Trophozoite
- It is the growing and feeding stage of parasite that is the only form which is present in tissues.
- Shape: It is irregular in shape
- Size: ranging from 12-60 µm; average being 20-30 µm (it is large and actively motile in freshly passed stool, while smaller in convalescent and carrier.)
- Cytoplasm: It is divided into two portions; a granular endoplasm and clear transparent ectoplasm. Nucleus, food vacuoles, erythrocytes, occasionally leukocytes tissue debris are present in endoplasm.
- Nucleus: It is single, spherical shape and size ranging from 4-6µ Nucleus contains central karyosome and fine peripheral chromatin anchored to the nuclear membrane giving a cartwheel appearance. The nucleus is not clearly seen in the living trophozoites, but can be clearly demonstrated in preparations stained with iron haematoxylin.
- Trophozoites possess pseudopodia which make them actively motile.
- Trophozoites are anaerobic parasite, (present in large intestine), the trophozoites divide by binary fission in every 8 hrs.
- The trophozoites survive up to 5 hrs at 370C and are killed by drying, heat and chemical sterilization. Trophozoites can’t cause disease.
Precyst
- It is the intermediate stage that exist between trophozoite and cyst
- It is smaller in size; 10-20µ
- It is slightly ovoid and round with blunt pseudopodium projecting from periphery
- No food material or RBC are found on its endoplasm.
- Trophozoites undergo encystment in the intestinal lumen. Encystment does not occur in the tissues nor in faeces outside the body.
- Before encystment. The trophozoites extrudes its food vacuoles and becomes round or oval.
- It contains two chromatid bars and a large glycogen vacuole.
- It then secretes a highly retractile cyst wall around it and becomes cyst.
Cyst
- It is the infective form of parasite.
- Shape: It is round or oval in shape
- Size: 10-20 µm in diameter
- It is surrounded by a highly retractile membrane which makes it highly resistant to gastric juice and unfavourable environment conditions.
- The early cyst contains a single nucleus and other structures: a mass of glycogen and chromatid bars which are cigar shaped refractile rods with rounded ends.
- The chromatid bodies are so called because they stain with haematoxylin like chromatin.
- As the cyst matures, the glycogen mass and chromatid bars disappear and the nucleus undergoes two successive mitotic divisions to form two and then four nuclei.
- The mature cyst is thus quadric nucleated.
- Mature cyst passed out in stool from infected patient and remained without further development in soil for few days.
Life Cycle:
Life cycle of histolytica is relatively simple which is consists of infective cyst and invasive trophozoites stage.
Life cycle completes in single host, i.e., human. In fact, human get infected with E. histolytica cyst from contaminated water and food. Infection can also acquire directly by ano-genital or oro-genital sexual contact. The mature Cyst is resistant to low pH of stomach and hence remain unaffected by the gastric juices. Eventually, the cyst wall is lysed by intestinal trypsin and when the cyst reaches the caecum or lower part of ilium excystation occurs.
Source: DOI: 10.13140/RG.2.2.31940.12169
Fig: Infection Cycle of Entamoeba histolytica
The neutral or alkaline environment as well as bile components favour excystation. Excystation of a cyst gives 8 trophozoites. Trophozoites are active and carried to large intestine by peristalsis of small intestine. Eventually, trophozoites then gain maturity and divide by binary fission. Trophozoites feeds on host ingesta and multiply by binary fission
The trophozoites adhere to mucus lining of intestine by lectin and secretes proteolytic enzymes which causes tissue destruction and necrosis. When parasites acquire access to blood, they move and cause extraintestinal illnesses. When the number of trophozoites rises, some of them stop reproducing and revert to cyst form via the process of encystation. The cyst is excreted along with faeces and contaminates food and water completing the life cycle.
Pathogenesis:
The human is commonest source of infection and the incubation period varies widely; generally, from 4-5 days. The large number of virulence factors such as lectin, lytic peptide, cysteine, proteinases and phospholipase are expressed by the parasite. Excystation of cyst in intestine releases 8 trophozoites which then colonizes the large intestine. Attachment of trophozoites with the colonic epithelium is dynamic process in pathogenesis. Following adhesion, trophozoites lyse the target cell with an ionophore-like protein, causing ion leaking from the cytoplasm.
Destruction of the tissues is resulted after the activity of the proteolytic enzymes secreted by the amoeba that result in giving flask shaped amoebic ulcer, which is a typical feature of intestinal amoebiasis. Trophozoites enter the columnar epithelium of the mucosa, producing lysis, and move deep within until they reach the submucosa layer, where they reproduce rapidly. Finally, amoeba damage a large region of the submucosa, resulting in the creation of an abscess, which then ruptures into an ulcer. The ulcer is flask shaped with broad base and narrow neck that may be localized in ileo-caecal region or generalized throughout the large intestine.
Parasites can spread from the colon to other critical organs such as the liver, heart, and brain via blood circulation. Amoebic abscesses are most common in the lungs and liver, with cerebral, cutaneous, and splenic abscesses occurring seldom.
Mode of infection:
- Faecal-oral route
- Ingestion of cyst contaminated foods and water
Clinical manifestation:
Intestinal infection
Asymptomatic
90% of E. histolytica infection is mild or asymptomatic
Symptomatic infection
Non dysenteric amoebic colitis (mild diarrhoea)
Acute amoebic dysentery: It is more common and characterized by fever, abdominal pain, and painfulness
Complications; toxic megacolon, fulminant (occurs suddenly and escalates quickly) amoebic colitis, ameboma, amoebic peritonitis, perianal ulceration.
Extra intestinal infection
- Hepatic infection:Â non suppurative hepatitis, liver abscesses, other complications
- Pulmonary infection: chest pain, dyspnoea (shortness of breath), non-productive cough
- Cerebral infection: It is rare and symptoms include fever, headache, fever, variations in mood, confusion, neck stiffness, weakness, and nausea.
- Genitourinary infection: involves kidney and genital organs
- Splenic infection
- Cutaneous amoebiasis
Laboratory Diagnosis:
Specimen; stool
Stool microscopy, Stool Ag detection, Stool culture, Serology, PCR
Specimen; Body aspirates
Microscopy, Ag detection, Serology, PCR, CT scan, MRI, Blood count
Treatment and prophylaxis:
- Antibiotics; Diloxanide furoate, diiodohydroxyquin, paramycin, metronidazole, imidazole
- 4-aminoquinoline; for extra intestinal infection
- Oral rehydration