In this article we will discuss about Entamoeba Histolytica:- 1. Historical Background of Entamoeba Histolytica 2. Distribution of Entamoeba Histolytica 3. Habitat and Habitat 4. Structure 5. Nutrition 6. Life Cycle 7. Pathogenicity 8. Symptoms, Diagnosis and Treatment of Infection 9. Prevention (Prophylaxis) of Infection.
- Historical Background of Entamoeba Histolytica
- Distribution of Entamoeba Histolytica
- Habitat and Habitat of Entamoeba Histolytica
- Structure of Entamoeba Histolytica
- Nutrition in Entamoeba Histolytica
- Life Cycle of Entamoeba Histolytica
- Pathogenicity of Entamoeba Histolytica
- Symptoms, Diagnosis and Treatment of Infection Caused by Entamoeba Histolytica
- Prevention (Prophylaxis) of Infection Caused by Entamoeba Histolytica
1. Historical Background of Entamoeba Histolytica:
Entamoeba histolytica was first of all reported by a Russian Zoologist, Losch (1875), as Amoeba coli from the faeces of a patient suffering from dysentery. The genus Entamoeba was established by Cosagrandi and Barbagallo (1895); it should not, be confused with the genus Endamoeba which was established by Leidy (1879). Concilman and Loffteur (1901) worked out the pathogenecity of amoebiasis and amoebic ulcers.
The species Entamoeba histolytica was established by Schaudinn (1903) and he differentiated the pathogenic and non-pathogenic types. But, Walker and Sellards (1930) are credited for attributing pathogenic effects of this parasite. Craig (1962) has estimated that more than 10 per cent of world population is suffering from the infection of this parasite.
2. Distribution of Entamoeba Histolytica:
Entamoeba histolytica is world-wide (cosmopolitan) in distribution. But it is commonly found in epidemic form in tropical and sub-tropical regions than in the temperate region. The more epidemic condition of this parasite is reported from Mexico, China, India, Philippines, South America and Thailand.
Its incidence is relatively higher in rural and densely-populated urban areas particularly in those areas where the sanitary conditions are poor. In India, its effect is on higher level in humid climates as compared to dry and cold climates. The children and adults are more frequently infected; surprisingly, the males are more commonly infected than the females.
3. Habit and Habitat of Entamoeba Histolytica:
Entamoeba histolytica is microscopic and lives as an endo-parasite in the upper part of the large intestine, i.e., colon of man. It inhabits the mucous and sub-mucous layers of the large intestine. It feeds mainly on the tissues of the intestinal wall and often produces severe ulcers and abscesses.
In chronic cases, it may enter the blood circulation to reach the liver, lungs, brain and other organs. It causes a serious and often fatal disease known as amoebic dysentery or amoebiasis.
Entamoeba histolytica has also been reported from a variety of mammals, e.g., Gorilla, Orangutan, Chimpanzee, Gibbon, Baboon, Monkey, Dog, Cat, Pig and Rat, etc.
4. Structure of Entamoeba Histolytica:
Entamoeba histolytica exists in two distinct forms the magna or trophozoite form and the minuta or precystic form.
The mature parasite or active and motile adult is known as trophozoite. The trophozoites of E. histolytica are large, hence, called magna, usually 20-30 Entamoeba histolytica trophozoite, microns in diameter. It is feeding form which is pathogenic to man.
It resembles Amoeba in all structural details. The cytoplasm of trophozoite is differentiated into two distinct portions, the outer ectoplasm and inner endoplasm. The ectoplasm is clear, non-granular and hyaline, while the endoplasm is granular and fluid-like.
The pseudopodia may be short, broad and rounded, long and finger-like, mainly composed of ectoplasm. During locomotion, the rapidly advancing end of the body consists of a single clear pseudopodium, i.e., monopodial. With this single pseudopodium, it moves in a crawling fashion like garden slug, hence, the movement is also sometimes called limax-type movement.
The endoplasm contains the nucleus and food vacuoles containing the tissue fragments, erythrocytes, leucocytes and ingested bacteria, etc.
The nucleus is rounded, 4-6 microns in diameter and vesicular. The nucleus is composed of a delicate membrane, small peripheral chromatin granules and a centrally located small dot-like nucleolus or endosome or karyosome and chromatin granules arranged in spoke-like striations.
The nucleolus is surrounded by an indefinite clear area called halo. The presence of red blood corpuscles (R.B.Cs) in food vacuoles is an important characteristic feature of this parasite, as the capacity of ingesting R.B.Cs. is not seen in other intestinal amoebae of man.
Contractile vacuole is entirely absent because E. histolytica lives in an environment which is isotonic. Since, the osmotic concentration of its body remains equal to its surroundings and, hence, no water enters in its body by osmosis. Therefore, there is no need of contractile vacuole.
The magna or trophozoic form of E. histolytica develops from small minuta form; it enters into the mucosa and sub-mucosa layers of the intestinal wall by dissolving its tissues. Thus, it makes small wounds in the intestinal lining which later develop into ulcers. After reaching into the intestinal tissues, ingests R.B.Cs and grows up to 60 microns in size.
It is the pre-cystic form which is smaller, spherical, non-feeding, non-motile and non-pathogenic. It measures to about 7-10 microns in diameter and resembles the trophozoite form in its structure except that it is smaller in size having no pseudopodium and contractile vacuole.
It lives only in the lumen of intestine and rarely found in the tissues. It undergoes encystation and helps in the transmission of the parasite from one host to another.
5. Nutrition of Entamoeba Histolytica:
In Entamoeba histolytica, the nutrition is holozoic. It feeds mainly upon the blood corpuscles, other host elements, bacteria and yeasts. It also absorbs substances saprozoically from the surrounding medium.
The trophozoite of Entamoeba histolytica reproduces normally by a process of simple binary fission in the intestinal wall and by a modified form of mitosis. The exact nature of the division of the nucleus is controversial but it is believed by many authors that it is probably a modified type of mitosis. Kofoid and Swezy observed six chromosomes in it. Entamoeba histolytica also has the capacity to encyst.
In fact, the nucleus divides by mitosis but without the disappearance of the nuclear membrane. It is, then, followed by the division of the cytoplasm (cytokinesis) resulting into two daughter entamoebae. These start feeding upon bacteria and host tissues, grow in size and again multiply by binary fission. Some of these forms may invade fresh intestinal tissues, while some of them become precystic or minuta form.
6. Life Cycle of Entamoeba Histolytica:
Entamoeba histolytica is monogenetic (Gr., mono = single; genos = race), i.e., its life cycle is completed in one host only; the host being the man.
Its life cycle is completed as follows:
The pre-cystic forms, under certain circumstances which are not well understood, remain small (7-10 microns in diameter) and live only in the intestinal lumen.
They undergo encystment but before encystment, the parasites round up, eliminate food vacuoles and accumulate considerable amount of food materials in the form of glycogen and black rod-like chromatoid granules. Soon each parasite secretes a thin, rounded, resistant, colourless and transparent cyst wall around it.
The cysts of Entamoeba histolytica vary in size from 10-20 microns (average 12 microns) in diameter. Its cytoplasm is clear and each cyst is mononucleate at this stage. Presence of chromatoid bodies is the characteristic of the cysts of Entamoeba histolytica. They occur either singly or in the multiples of two or more.
There is a controversy about the exact nature of these bodies. Some authorities consider them as nutrient material of the cysts, while others believe them as excess of chromatin thrown off during nuclear division. The chromatoid bodies are found in the early stages of the cysts but they disappear in the mature tetranucleate cysts.
Pitelka (1963) has suggested that the chromatoid bodies are made of ribonucleoprotein and Neal (1966) believes that the disappearance of chromatid granules occurs because of the dispersion of their nucleoprotein in the substance of mature tetranucleate cystic form.
The nucleus of the cysts divides twice so that each cyst now becomes tetranucleate. At this stage, the cyst is infective to a new host. Encysted forms pass out with the faecal matter of the host.
Transfer to new host:
The infective cysts remain viable for a considerable length of time outside the human intestine, if environmental conditions are favourable. Infection of fresh human host takes place by swallowing the infective cysts with contaminated food and drinks. Contamination of food and drinks is brought about by houseflies, cockroaches and food-handlers.
Houseflies generally carry the cysts from the faeces to the foods. Cockroaches have also been found to transport cysts from faeces to food. Food-handlers are also sometimes responsible for the contamination of food through touch by dirty fingers carrying the cysts under the nails. Through contaminated food or drinks, the infective cysts pass into the lower portion of the small intestine of the new host.
The excystment of cysts and metacystic development (Fig. 15.4) have been observed and studied specially by Dobell (1924) and Cleveland and Sanders (1930) in cultures. According to Dobell, in the process of excystation, a single tetranucleate amoeba (metacystic form) emerges from a cyst through a minute pore in the cyst wall.
The tetranucleate metacystic form produces a new generation of trophozoites by a diverse series of nuclear and cytoplasmic divisions which result in the production of eight uninucleate amoebulae.
These are called metacystic trophozoites. No sexual phenomena have been observed during these changes. The metacystic trophozoites feed on the contents of the intestine and grow in size to form the trophozoites of the next generation. The trophozoites stay in the lumen of the intestine for a particular period when they may attack the wall of the intestine and start the life cycle again.
7. Pathogenicity (Pathogenic Effects) of Entamoeba Histolytica:
Entamoeba histolytica causes amoebic dysentery, abscesses in liver, lungs and brain and non-dysenteric infections.
1. Amoebic Dysentery:
Entamoeba histolytica secretes a tissue dissolving enzyme (probably of histolysin nature) that destroys the epithelial lining of the colon and causes its necrosis and forms the abscesses (small wounds) which later become flask- shaped bleeding ulcers. The cavity of these ulcers is generally filled with mucus, bacteria, amoeba and cell debris. The abscesses pour their contents into the lumen of the intestine.
The ulcers vary greatly in number and size; in severe cases almost the entire colon is undermined. The ulceration of colon may produce severe dysentery. In amoebic dysentery, the stools are acidic and contain pure blood and mucus, in which swarms of amoeba and blood corpuscles, are usually present. The patient feels discomforted due to the rectal straining and intense gripping pains with the passage of blood and mucus stools every few minutes.
2. Abscesses in Liver, Lungs and Brain:
Sometimes Entamoeba histolytica may be drawn into the portal circulation and carried to the liver. In liver the parasites settle, attack the liver tissue and form abscesses. The patient has pain in liver region, fever and high leucocyte number, a condition referred to as amoebic hepatitis.
Lung abscesses are fairly frequent; these are usually caused by direct extension from a liver abscess through the diaphragm. The lung abscesses usually rupture into a bronchial tube and discharge a brown mucoid material which is coughed out with the sputum. Sometimes the parasite also forms abscesses in the brain. Abscesses elsewhere are rare.
3. Non-Dysenteric Infections:
Although amoebiasis is usually thought of as the cause of dysentery with blood and mucus containing stools or of liver abscesses, these conditions are actually the exception rather than rule and some workers have reported that as many as 90% of dysentery cases in temperate climates are apparently symptomless. Even in tropics, dysentery is exceptional.
Although about 10% of the general population is infected with Entamoeba histolytica, yet most of them are carriers or passers. The symptoms commonly associated with chronic amoebiasis are abdominal pain, nausea, and bowel irregularity, with headaches, fatigability and nervousness in minority of cases.
8. Symptoms, Diagnosis and Treatment of Infection Caused by Entamoeba Histolytica:
As referred, the infection of Entamoeba histolytica causes amoebiasis. The common symptoms are the passing out of stool with blood and mucus, abdominal pain, nausea, flatulence and bowel irregularity with headache and fatigability, etc.
Diagnosis of Entamoeba Histolytica:
The microscopic examination of the stool of an infected man shows the presence of trophozoites and cysts in it. The presence of stone-shaped, white coloured crystals of Charcot- Leyden suggests the infection of Entamoeba histolytica.
Treatment (Therapy) of Entamoeba Histolytica:
For prompt relief of acute or sub-acute dysentery the injections of Emetin are given. But certain antibiotics, such as Fumagillin, Terramycin, Erythromycin and Aureomycin are more effective and may be given orally.
For eradication of intestinal infections or in chronic cases, certain arsenic compounds (Carbarsone, Thiocarbarsone and Vioform) and a number of iodine compounds (Yatren, Diodoquin and Vioform) are effective. For amoebiasis of liver or lungs, Chloroquine is quite effective. The most significant advancement in the treatment of amoebiasis is the use of Metronidazole and Tinidazole as both luminal and tissue amoebicide.
9. Prevention (Prophylaxis) of Infection Caused by Entamoeba Histolytica:
Following measures are essential in the prevention of the disease:
1. Sanitary disposal of faecal matter.
2. Perfect sanitation and protection of water and vegetables from pollution.
3. Washing of hands with antiseptic soap and water before touching the food.
4. Cleanliness in preparing the food.
5. Protection of foods and drinks from houseflies, cockroaches, etc.
6. Raw and improperly washed and cooked vegetables should be avoided.