Entamoeba histolytica

Entamoeba histolytica: 
Morphology, Life Cycle, Pathogenic, Treatment and Controling messure.

Entamoeba histolytica (Gr., entos, within + amoeba, change +histos, tissue+lysis, dissolve), which is the causative organism of amoebic dysentery or amoebiasis in man.

 It harbours the upper part of the large intestine (colon) and very often becomes lodged in the liver, lungs, brain and testes.

Classification:

Group: Invertebrate
Phylum: Protozoa
Class: Rhizopoda
Family:Entamoebidae
Genus: Entamoeba
Species: E. histolytica

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History :

Entamoeba histolytica was first discovered by Friedrick Losch, a Russian zoologist in 1875. 

He discovered this protozoan in the faeces and intestinal ulcers of dysentery patient and succeeded in trans ferring it to puppies. 

Dobell, in his book 'Amoebac of Man', has given a very orderly account of Enta moeba histolytica and other species parasitizing man 

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Distribution and Incidence:

Entamoeba histolytica is cosmopolita (world-wide) in distribution, but its prevalen is greater in tropics and subtropics than in t temperate zones. 

It has been reported that incidence of infection is high in Mexico, Chir India and parts of South America. 

The incidence is considerably higher in rural a densely-populated urban areas.

 Infants und a year old are rarely infected with it, wh children and young adults are very suscepti to the parasite.

 It is estimiated that 10 world population is suffering from amoebias .

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Habit and Habitat :

Entamoeba histolytica is a microscopic endoparasite of man and is commonly found harbouring the lumen of the upper part of the large intestine, that is, the colon.

 Parasitologists believe that this parasite lives as a harmless commensal but, for reasons which are unknown, it invades the mucosa and sub-mucosa of the intestinal wall and causes amoebic dysentery or amoebiasis. 

 In a person suffering from this disease, the intestinal wall exhibits, in large numbers, minute ulcers which are formed as a result of the dissolution and destruction of the mucous lining of the intestine. 

 This is accomplished with the aid of a tissue-dissolving substance secreted by the parasite. Multiplying rapidly by binary fission and feeding vigorously on bacteria, red blood corpuscles and the tissue debris, the ent amoebae gather in large numbers in the ulcerated intestinal lining. 

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Morphology :

Entamoeba histolytica is a small micro scopic parasitic amoeba. It occurs in two distinct forms, the trophozoite or magna form and the precystic or minuta form.

1. Trophozoite form
2. Minuta form

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1. Trophozoite form: 

The trophozoite of E. histolytica is the most active, motile and feeding form which is pathogenic to man. 

It usually measures 20 to 30μ in diameter and, more or less, resembles the common amoeba in all structural details. 

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Plasmalemma:

The outermost body covering or plasmalemma is a thin, elastic and semi-permeable membrane. 

The cytoplasm is differentiated into the outer clear and non granular ectoplasm and the central more fluid and granular endoplasm. 

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Nucleus:

The endoplasm contains a nucleus which is seldom visible in a living organism. 

After being fixed and stained, it appears as a vesicular structure 4-6μ in size. 

It is bound by a thin and delicate muclear membrane, whose inner surface is encrusted with fine chromatin granules, arranged in a peripheral ring. 

In the centre of the nucleus is a small dot-like endosome or karyosome, often surrounded by a clear area or 'halo'. 

The fluid-filled space between the nuclear membrane and the endosome is marked by spoke-like striations of chromatin material.

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Food vacuoles:

Other inclusions of the endoplasm are food vacuoles that enclose the ingested red blood corpuscles (erythrocytes), white blood corpu scles (leucocytes), fragments of epithelial cells and bacteria. 

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Contractile vacuoles:

Contractile vacuoles are wanting in E. histolytica since it inhabits an isotonic environment. 

The osmotic concentration of its body protoplasm equals to that of the intestinal fluid of the host and hence no water enters the organism by osmosis. 

Thus, there is no need for osmoregulation.

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Pseudopodia:

When moving, E. histolytica produces anteriorly a large, broad and blunt pseudopodium. 

Hence the parasite is typically monopodial (Gr., monos, single +- podos, foot). 

It is only at this anterior end that the outer clear ectoplasm is sharply differentiated from the inner granular endoplasm. 

With a single pseudopodium the trophozoite moves with a forward-flowing movement.

 This resembles the crawling of a garden slug (Limax spp.) and hence the movement is sometimes called 'limax-type movement'.

The nutrition in trophozoite is holozoic. 

It feeds by phagocytosis. The food particles are engulfed at the posterior end, where the plasmalemma is more sticky. 

Food particles adhere to it and the plasmalemma is invagi nated into the cytoplasm carrying the food particles along with it. 

The invaginated plasmalemma now separates off from the main plasmalemma to become the food vacuole.

Trophozoites develop from small minuta forms in the presence of definite environmental conditions.

 These penetrate into the mucosa and sub-mucosa of the intestinal wall, ingest erythrocytes, and may also spread to other tissues, chiefly the liver. 

Here they become larger and measure from 20 to 50μ in diameter.

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2. Minuta form:

The precystic or minuta form of E. histolytica is small, spherical, non-motile and non-feeding form and is non-pathogenic to man. 

It measures 12 to 15μ in diameter. In structural details it resembles the trophozoite except that it is smaller in size and the food vacuoles are absent.

The minuta forms do not feed. They live only in the lumen of the intestine, and are seldom found in the tissues. 

They undergo encystation and serve for the transmission of the parasite from one host to another.

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REPRODUCTION AND LIFE CYCLE OF ENTAMOEBA HISTOLYTICA 

Entamoeba histolytica is monogenetic (Gr., monos, one+ genos, race), i.e., only one host is required for its complete life cycle. 

It undergoes reproduc tion and life cycle only in man.

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Binary fission:

The tropho zoites multiply asexually by binary fission within the wall of the large intestine. 

The nucleus undergoes mitosis without the disappearance of the nuclear membrane. 

The mitosis is followed by cytokinesis or division of the cytoplasm. 

A a result, two daughter orga nisms are formed. They grow rapidly in size, feeding upon bacteria and host tissue elements and, in their turn, again multiply by binary fission. 

Some of them invade fresh host cells, while others become the precystic o minuta forms.

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Encystation:

The precystic o minuta forms encyst only in th lumen of the intestire and not in the tissues. 

They round up an secrete a thin, refractile, toug and flexible cyst wall aroun them. 

The cysts at this stage ar uninucleate. The single nucleus o the the cyst soon undergoes a mitotic division to form two nuclei, leading to the formation of binucleate cysts. 

A second mitotic division divides the two nuclei into four and thus tetranucleate cysts are formed. 

The whole process of encystation is completed within a few hours. 

The cysts of E. histolytica are spherical bodies which measure about 12μ in diameter. 

The young cysts contain one or two glycogen masses which gradually disappear as the cysts age. 

Besides, the cysts also contain one or more transparent, broad and rod-like bodies with blunt rounded ends.

 These are called chromatoid bodies or chromatoid bars. These stain deeply with haematoxylin, like chromatin, hence this name.

 According to Pitelka (1963) the chromatoid bodies are composed of ribonucleoprotein. 

They also disappear as the cysts mature, though less rapidly than the glycogen.

 Neal (1965) believes that their disappearance is due to the dispersion of their ribonucleoprotein throughout.

The tetranucleate cysts constitute the transmissive or infective stage. 

They do no develop further but pass out of the host in the faeces. 

They can remain alive for 10 days in moist stool. 

They are very suceptible for desiccation and die at a temperature of 50°C.

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Transmission and infection:

Infection depends upon intake of food or water conta minated with faecal matter containing cysts of E. histolytica. 

The food handlers, like cooks, sweetmeat sellers, hawkers, etc., who them selves are infected and are unhygienic by nature, act as cyst passers. 

The untreated human faeces voided by children and adults alike on the open grounds or crop and vege table fields (which is the usual practice in rural areas in India) is a common source of infection. 

The houseflies and cockroaches, which are coprophagous (feeding upon faecal matter), carry viable cysts on their legs or in their intestine and transfer them to the foodstuffs.

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Excystation:

 In the new host, the ingested cysts pass down the alimentary canal and reach the small intestine. 

The cyst wall protects them from the action of host's gastric juice during their passage through the stomach. 

After five or six hours, excystation takes place as the cyst wall is digested by trypsin in small intes tine releasing the tetranucleate amoeba (excystic amoeba or metacyst).

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Metacystic development:

Each metacyst immediately proceeds to divide by binary fission. 

Its nuclei divide in a specific pattern, accompanied by simultaneous cytoplasmic divisions, to produce eight small, uninucleate amoebulae or metacystic trophozoites.

 These metacystic trophozoites pass into the large intestine and grow into mature trophozoites.

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PATHOGENESIS:

As already noted, E. histolytica lives in the lumen of the large intestine as harmless minuta forms.

 Whenever the resistance of the gut is lowered in infected people, these become pathogenic, change to magna forms and invade the intestinal wall by secreting the histolytic enzymes. 

The trophozoites make their way deep into the sub-mucosa by eating through mucosa of the intestinal wall. 

Here they multiply by binary fission and spread radially outward to form flask-shaped ulcers containing cellular debris, lymphocytes, blood corpuscles and bacteria. 

This causes the formation of abscesses in the intestinal wall. 

The penetra tion into the sub-mucosa by the trophozoites is made possible by histolysis as well as cytolysis. 

The mechanism involves the disso lution and necrosis of tissues and cells by a proteolytic enzyme of the nature of histolysin secreted by the trophozoites themselves. 

As the sub-mucosa is eroded by the trophozoites the ulcers burst and the blood capillaries rupture. 

The blood and the ulcer contents pour into the lumen of the intestine and pass to out side with stool. 

This characterizes the amoebic dysentery or amoebiasis. 

The stool of a dysen teric person is usually acidic and consists of swarms of entamoebae as well.

Sometimes, the trophozoites make their way through the blood circulation, into the brain, liver, spleen, lungs and gonads. 

Here also they destroy the tissues and cause formation of abscesses. Within the liver, the trophozoites cause severe lesion affecting the metabolic activities. 

Formation of abscesses in brain usually proves fatal.

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Mode of Transmission:

 It mainly occurs by ingestion of cysts in food or drinks. The contamination of food or drinks occurs by: 

(i) unhygienic habits of food handlers who by habit scratch the anus and then put the fingers in the food which they serve.

(ii) habit of defecating in open fields causing contamination of vegetables and then washing the bottom in ponds causing the contamination of water.

(iii) transmission of cysts from stools to food and drinks by flies and cockroaches.

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DIAGNOSIS:

Diagnosis, in a simple way, consists in the microscopical detection of trophozoites or cysts in faecal smears. 

The presence of white, stone shaped 'Charcot-Leyden' crystals in facces suggests the E. histolytica infection,

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THERAPY:

Treatment of amoebic dysentery is not very difficult but the permanent cure is sometimes hard to achieve as relapses do occur. 

For temporary relief, an alkaloid Emetine is effec tive. 

A synthetic derivative of Emetine, called Dehydroemetine, is equally effective. 

The anti malaria drug, Chloroquine is effective against amoebic abscesses in the liver but not elsewhere.

 Some of the latest iodine compounds, such as Vioform, Chiniofon, Diodoquin, etc., have shown more lasting results. 

Certain antibiotics, such as Fumagillin, Terramycin, Erythromycin and Aureomycin have proved to be effective in the eradication of the parasite. 

Perhaps the most significant advance in in the treatment of amoebiasis has been the use of metronidazole as an amebicide. 

It is very active against both intestinal and extra intestinal amoebiasis.

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PREVENTION (PROPHYLAXIS):

Prevention of infection is entirely a matter of hygiene, both personal as well as municipal.

 For personal hygiene it is suggested to adopt the following habits

1. Washing hands with soap and water after handling dirty articles, before taking meals and after using toilet. 

2. Cutting finger nails regularly.

3. Avoiding the use of unboiled water and improperly washed vegetables and raw salads.

4. Protection of foods and drinks from con tamination by houseflies, cockroaches, etc.

5. Avoiding the passing out of stool on open grounds, street sides or vegetable fields.

The municipal hygiene is the responsibility of the town areas, municipalities or other local bodies. 

They must take the following preventive measures:

1. Proper sanitation of roads, streets, lanes and open drains.

2. Purification of drinking water.

3. Proper disposal of sewage.

4. Covering of the food articles by the traders. 5. Chemical treatment of human faeces to be used as fertilizer.

6. Periodical examination of food handlers to find out whether they are infected with E. histolytica. On positive findings they should be treated properly. 

                Life cycle

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