The causative agent of amoebiasis, Entamoeba histolytica, was discovered in 1875 by F. Loesch. In 1903, the organism was studied in detail by F. Schaudinn, who differentiated two amoeba species, Entamoeba histolytica and Entamoeba coli, which belong to the class Sarcodina, family Entamoebidae.

Entamoeba histolytica occurs in the human body in four forms:

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(1)vegetative large tissue form which feeds on the erythrocytes and does not become encysted — Entamoeba histolytica forma magna

(2)  vegetative small commensal encysted form which lives in the lumen of the large intestine — Entamoeba histolytica forma minuta

(3) precystic form is poorly motile and does not contain bacteria or other food inclusions

(4)  cysts which develop from the small forms

Non-pathogenic amoebas, E. coli, also live in the human intestine. They are somewhat larger than E. histolytica. Their cytoplasm is granular, and the vacuole contains bacteria, leucocytes, food particles, and glycogen but no erythrocytes. Pseudopodia seldom occur, and the cysts are larger than those of E. histolytica and possess eight nuclei.

Kittens and dogs infected through the rectum display typical dysentery lesions in the rectum and abscesses in the liver (extra enteric form of amoebiasis). The white rat is one of the best animals for experimental amoebiasis.

Infection is conveyed through cysts, which occur in water and food materials contaminated with faeces. Among the healthy population, 20 per cent, on average, were found to be cyst carriers. Amoebiasis prevails in eastern regions where water is supplied from aryk and the sanitary standards are low. The disease is widespread in the Middle East, India, Indo-China, North and Central Africa, Indonesia, South America, etc.

The disease becomes chronic and is accompanied by lesions in the large intestine, particularly in the caecum and ascending colon. The patient’s stool has the appearance of raspberry jelly and is uniformly impregnated with blood.

The parasite localises in the colon and rectum in which inflammatory oedema, ulcerations, necrosis of adjacent tissues, and gangrenous decomposition develop. The amoebas penetrate the mucous, submucous, and muscular coats, invade the intestinal vessels, and reach the liver along the branches of the portal vein.

Complications arise in the form of abscesses and necrosis of the liver and sometimes abscesses of the lungs and brain. Occasionally amoeba may enter the greater circulation, and in such cases, any of the organs may be involved.

Various species of bacteria play an essential role in the pathogenesis of amoebiasis, being responsible for the pathological process in combination with the entamoebas. Experimental studies of parasitocoenosis have shown that some species of streptococci (pneumococci) and E. coli in association with E. histolytica produce more severe forms of the disease and cause higher morbidity in laboratory animals.

The pathogenesis of amoebiasis is still not completely clear. It has been ascertained that if the intestinal mucosa and the body as a whole are normal, the E. histolytica may live in the intestinal lumen as a commensal causing no disease in man. A number of factors have been proven to facilitate penetration of the parasite into the tissues. Pseudopodia allow E. histolytica to enter the tissues, while the proteolytic properties of the parasite (the ability to produce a cytolytic enzyme) render it capable of destroying the intestinal epithelium. In addition, the parasite produces a toxic substance which possesses cytolytic and complement-fixing properties.

A relatively marked congenital insusceptibility to amoebiasis exists among people. It is assumed that insusceptibility is associated with a condition of non-sterile immunity. Of great importance are the resistance of the intestinal wall tissues and the ability of the body to neutralise the harmful effect of the co-members of the parasitocoenosis. Immunity in amoebiasis is unstable.

Fresh stools are examined under the microscope using a temperature-controlled microscope stage. E. histolytica can be demonstrated in the stools. For demonstrating cysts and glycogen granules under the microscope, a strong Lugol’s solution is added to the faeces (1 g iodine, 2 g potassium iodide, and 20 ml distilled water).

The presence of pathogenic amoebas may also be revealed by histological examination of tissues (stained with methylene blue, safranin, haematoxylin-eosin, and iron haematoxylin).

Laboratory amoebiasis may be reproduced by infecting kittens and white rats. The resulting condition is typical of the disease.

Emetine hydrochloride, metronidazole (trichopol), as well as chiniofon (yatren), delagil (resochin or chloroquine) have a highly effective therapeutic action. Antibacterial drugs — tetracycline, streptomycin, penicillin, and sulphonamides are given for the concomitant bacterial microflora, which aggravates amoebiasis.

All patients are transferred to a hospital and adequately treated. Preventive measures against amoebiasis also include fly control, and protection of food material and water from flies and contamination with faeces. The staff of catering establishments must be examined for cyst carriage. Health education of the population, aimed at raising the cultural level, and introducing hygienic habits must be carried out.

The author is an associate professor (retd.) and former head of the department of botany at Ananda Mohan College.