Brief note on the life cycle and pathogenicity of Entamoeba

Entamoeba histolytica is cosmopolitan in distribution, commonly found in epidemic form in tropical and sub-tropical regions. The more epidemic condition of these protozoa is reported from India, China, Philippines, South America, Thailand and Mexico.

In India, its effect is on higher level in humid climate as compared to dry and cold climates. Allahabad, Agra, Kolkata, Mumbai, Chennai, Delhi, Kanpur and Gorakhpur are comparatively more infected than other places.

About 40% patients of mental hospital in Georgia are infected by this parasite. It is unicellular trophozoite of about 25, u which inhabits the lower portion of small and large intestine of man.

The protoplasm is not completely differentiated into ecto-and endoplasm and it contains food vacuoles. The spherical nucleus contains peripheral granules. E histolytica when observed is found to be very much active moving by single interiorly directed pseudo0poium but after some time, when kept outside the host body, become sluggish.

The faecal contamination of drinking water and raw vegetables or contaminations by infected and careless food handling are the mode of transmission of this parasite.

No intermediate host is involved in the life cycle of this parasite. The transmission of parasite from man to man takes place through tetranucleate cysts.

Prior to cyst formation the trophozoites become immobile smaller, discharge the food particles, round off and form the cyst wall. The nucleus is divided into two, then four and ultimately it is called as tetranucleate cyst.

These cysts when come out with faecal matter contaminate the food and water. When man drinks water or eats food, containing cysts, the parasite again reaches the host. The house flies help in rapid spread of this parasite. The pathology of this parasite has been studied in detail. As man takes food or water contaminated with tetranucleate cysts, the wall of ingested cyst dissolves in the intestine of man and amoebae come out in the lumen of the intestine.

The first site for the colonization of amoebae in the intestine is in the caecal area but if it does not occur, the primary colonization occurs in the lower level of the large intestine. As amoebae enter the intestinal wall, the lesion is formed due to lytic necrosis of the mucosa.

In due course of time, the number of amoeba in the colony increases and they proceed in a narrow channel, down to the base of the mucosa, and confined to the epithelial layer. Now amoebae gradually form a passage through the muscular mucosa into the sub mucosa where they were spread easily and produce primary lesion.

In the primary lesion, there is no complication and the tissue reaction does not occur in this stage. From the submucosa, the amoebae may proceed into the muscular coats and make a passage into the serosa and ultimately cause perforation there.

Further, they may be carried into the extra intestinal tissue like liver, lungs, brain and skin. Outside the intestinal tract any amoebic lesion, if develops, is without any exception secondary to one or more lesion, if develops, is without any exception secondary to one or more lesions in the large intestine.

The trophozoites of primary bottleneck lesions are squeezed out with faecal streams due to the peristaltic movements but few trophozoites come contact with mucosa produce necrotic ulceration at sigmoid rectal area.

Sometimes these trophozoites may be regurgitated into the distal region of the ileum and form colony, due to which majority of the lesions are formed. The primary lesions in large intestine may be maintained for sometime which later on is enlarged.

In case where these lesions become chronic, it is invaded by bacteria resulting in the discharge of blood and mucus into the lumen of the intestine, which passes out with the stool. In the liver, there is a tendency for these lesions to increase in number of which one or very few may become large and form the so-called amoebic liver abscess.

The number of cysts passed out daily by one man was found to be 30,000 to 45,000,000 in case of serious infection. The cysts of E, histolytica can survive for about seven days in water or in moist faces but are very susceptible to dry conditions or higher temperatures.

The dried cysts may be carried by air for a long distance and contaminated the vegetables, food and swimming pools. Major diseases caused by E. histolytica are intestinal amoebiasis, amoebic hepatitis, Amoebiasis of viscer and Amoebiasis cuties.

It is also found that sometimes-infected persons are not suffering from amoebic disease but function as carriers of this disease. In this condition the destruction and regeneration of the intestinal; tissues are taking place at the same rate hence the infected person does not suffer from dysentery, although stool contains the cysts of this parasite.

Prevention and Control:

Amoebiasis has to be accepted as a major health problem, only then serious efforts would be made by concerned and also no community basis must be detected and noted for official records of the local and national health departments. If it is in chronic stage, a careful survey must be made to know whether water, food material or possibly, which source is responsible for the spread of the disease an epidemic form and then only seriousness would be realized to make practical efforts to remove the causative factors.

Quick and proper disposal of human faeces should be made.

The green vegetable should be washed properly before cooking to ensure that vegetable is free from cysts.

The irrigation of green vegetable with probably contaminated water should be checked.

Chinifon is an anti-amoebic compound, which is administered orally and may be taken in aqueous solution for more effective action.

Diodoquin is used in killing the amoebic trophozoites in the lumen and wall of the intestine and is given orally. Its proprietary name is diodoquin.

Lodochlorhydroxyquine is similar to chinioforn in action and is given orally. The proprietary name of this impounds is vioform.

Carbarsone is proved to be the most satisfactory drug in case of intestinal amoebic infection and equally effective in extra-intestinal amoebiasis. It is administered orally.

Bismuth glycolylarsanilate is very effective for treating intestinal cases but ineffective in hepatic amoebiasis. It is taken orally and its proprietary name is milibis.

Chlorquine phosphate is the most effective in hepatic amoebiasis bust the least effective in intestinal amoebiasis.