Entamoeba Histolytica PDF

ENTAMOEBA HISTOLYTICA MORPHOLOGY: Entamoeba histolytica exists in three distinct forms: (i) trophozite or magna form, (ii) precystic or minuta form, and (iii) cystic form. i. Trophozoite or Magna form: Trophozoite of E.hystolytica is also known as the trophic or...

ENTAMOEBA HISTOLYTICA MORPHOLOGY: Entamoeba histolytica exists in three distinct forms: (i) trophozite or magna form, (ii) precystic or minuta form, and (iii) cystic form. i. Trophozoite or Magna form: Trophozoite of E.hystolytica is also known as the trophic or magna form. It is the most active form that is motile and feeds and is pathogenic to man. It usually measures 20 to 30μ in diameter and, more or less, resembles the common amoeba in all structural details. The outermost body covering or plasmalemma is a thin, elastic and semipermeable membrane. The cytoplasm is differentiated into the outer clear and non- granular ectoplasm and the central more fluid and granular endoplasm. ii.Precystic or minuta form: Precystic or minuta form of E.hystolytica is small, spherical, non- motile and non-feeding. 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. It lives in the lumen of the large intestine and is non-pathogenic to man but if the host's immunity is compromised, it changes into the magna form and invades the tissues of intestine. iii.Cysts: Under normal conditions, the minute form undergoes encystation. It becomes rounded and surrounded by a thin, highly resistant and refractive cyst wall. A mature cyst is a spherical body that measures 10 to 20μ in diameter. Its cytoplasm is clear and contains one or two glycogen masses (reserve food) and one or more characteristic, refractive, bar-like chromatoid bodies or chromidial bars with rounded ends. Both glycogen masses and chromidial bars gradually disappear. Chromidial bars are made of ribo-nucleoprotein which disperses throughout cytoplasm with their disappearance. Nucleus retains the characters of the trophozoite. To start with, the cyst is uninucleate but its nucleus divides to form a binucleate and finally a tetranucleate or quadrinucleate cyst. TRANSMISSION, EXCYSTATION, AND METACYSTIC DEVELOPMENT: Infection occurs due to ingestion of food or water that is contaminated with faecal matter containing tetranucleate cycsts of E.hystolytica. The food handlers like cooks, sweetmeat sellers, hawkers etc., who themselves are infected and are unhygienic by nature, act as cyst passers. Untreated human faeces voided by children and adults on open grounds or in crop and vegetable fields is a common source of infection. Houseflies and cockroaches, which are coprophagous (feed on faecal matter), carry viable cysts on their legs or in their intestine and transfer them to uncovered food. 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 the host’s gastric juices during their passage through the stomach. After 5 or 6 hours, excystation takes place as the cyst wall is digested by trypsin in the small intestine thereby releasing the tetranucleate amoeba, called the excystic amoeba or metacyst. Each metacyst immediately proceeds to divide by binary fission. Its nuclei divide in a specific pattern, accompanied by simultaneous cytoplasmic divisions, to produce 8 small uninucleate amoebulae or metacystic trophozoites. These metacystic trophozoites pass into the large intestine, undergo binary fission, and may (1) invade the host tissues, (2) live in the lumen of the large intestine without invasion, or (3) undergo encystations to pass out of the host in the faeces. CLINICAL FEATURES AND PATHOGENESIS: As mentioned earlier, E.hystolytica inhabits the lumen of large intestine of man as harmless minute forms. Whenever resistance of gut is lowered in infected people, these become pathogenic, change to magna forms and invade the intestinal wall. They make their way deep into 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 formation of abscesses in intestinal wall. Penetration into sub- mucosa by trophozoites is made possible by histolysis as well as cytolysis. The mechanism involves dissolution and necrosis of tissues and cells by a proteolytic enzyme of the nature of hystolysin secreted by trophozoites themselves. As sub-mucosa is eroded, the ulcers burst and blood capillaries rupture. The blood and the ulcer contents (mucus, cell debris, blood corpuscles, bacteria, and amoeba) pour into the lumen of the intestine and pass to outside with stool. This characterizes the amoebic dysentery or amoebiasis. The stool of a dysenteric person is usually acidic and consists of swarms of entamoebae as well. Person suffering from amoebic dysentery has repeated blood-mixed, slimy and foul-smelling motions and is confined to the lavatory. Sometimes, the trophozoites make their way, through blood circulation, into the brain, liver, spleen, lungs, and gonads. Here, they destroy the tissue and cause formation of abscesses (cavities containing pus). The affected liver becomes enlarged, congested and painful to touch. This pathological condition is referred to as amoebic hepatitis. Formation of abscesses in lung and brain usually prove fatal. LABORATORY DIAGNOSIS: Laboratory diagnosis of amoebiasis is based on the microscopic finding of cysts in ordinary stool, trophozoites in fresh warm stool or tissue or the demonstration of antibodies of Entomoeba histolytica in the blood using an enzyme-linked immunosorbant assay (ELISA). Presence of white, stone-shaped ‘Charcot-Leyden” crystals in the stool suggest the presence of E. histolytica. PREVENTION (PROPHYLAXIS) AND TREATMENT: 1. Preventive (Prophylactic) measures  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:  Washing hands with soap and water after handling dirty articles, before taking meals and after using the toilet.  Protection of foods and drinks from contamination by houseflies, cockroaches, etc. Cutting finger nails regularly.  Avoiding passing out of stool on open grounds, street sides, or vegetable fields. Avoiding use of unboiled water, improperly washed vegetables, and raw salads.  Municipal hygiene is the responsibility of the town areas, municipalities, or other local bodies. They must take the following preventive measures:  Periodical examination of food handlers to find out whether they are infected with E.hystolytica. On positive findings they should be treated properly.  Covering of the food articles by the traders.  Chemical treatment of human faeces to be used as fertilizer. Proper disposal of sewage.  Proper sanitation of roads, streets, lanes, and open drains. Purification of drinking water. 2. Treatment Treatment of amoebic dysentery is not very difficult but permanent cure is sometimes hard to achieve as relapses do occur. For temporary relief, an alkaloid Emetine is effective. A synthetic derivative of Emetine called Dehydroemetine, is equally effective. The antimalaria drug, Chloroquine is effective against amoebic abscesses in the liver but not elsewhere. Some of the latest iodine compounds, such as Vioform, Chuntofon, 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 the treatment of symptomatic amoebiasis has been the use of metronidazole (Flagyl) or iodoquinol (Yodoxin) as an amoebicide. It is very active against both intestinal and extra-intestinal amoebiasis. REFERENCES R.P Singh Immunology And Medical Microbiology 1st ed. (New Delhi,India), 2007 292-296