Antiamoebic Drugs

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Chapter: Essential pharmacology : Antiamoebic And Other Antiprotozoal Drugs

These are drugs useful in infection caused by the protozoa Entamoeba histolytica.



These are drugs useful in infection caused by the protozoa Entamoeba histolytica.


Amoebiasis has a worldwide distribution (over 40 million people are infected), but it is endemic in most parts of India and other developing countries. Poor environmental sanitation and low socioeconomic status are important factors in the spread of the disease, which occurs by faecal contamination of food and water. Amoebic cysts reaching the intestine transform into trophozoites which either live on the surface of colonic mucosa as commensals— form cysts that pass into the stools (luminal cycle) and serve to propagate the disease, or invade the mucosa—form amoebic ulcers (Fig. 60.1) and cause acute dysentery (with blood and mucus in stools) or chronic intestinal amoebiasis (with vague abdominal symptoms, amoeboma).



Occasionally the trophozoites pass into the blood stream, reach the liver via portal vein and cause amoebic liver abscess. Other organs like lung, spleen, kidney and brain are rarely involved in extraintestinal amoebiasis. In the tissues, only trophozoites are present; cyst formation does not occur. Tissue phase is always secondary to intestinal amoebiasis, which may be asymptomatic. In fact, most chronic cyst passers are asymptomatic. In the colonic lumen, the Entamoebae live in symbiotic relationship with bacteria, and a reduction in colonic bacteria reduces the amoebic population.


The ‘Brazil root’ or Cephaelis ipecacuanha was used for the treatment of dysentery in the 17th century. The pure alkaloid emetine obtained from it was found to be a potent antiamoebic in 1912 and remained the most efficacious and commonly used drug till 1960. Many 8hydroxyquinolines (quiniodochlor, etc.) became very popular drugs for diarrhoeas and amoebic dysentery, but have come under a cloud since they were held responsible for causing epidemics of SMON in Japan in 1970. Soon after its triumph as an antimalarial in 1948, chloroquine was found to be an effective and safe drug for hepatic amoebiasis. Diloxanide furoate was a useful addition in 1960, covering mainly chronic intestinal form of the disease. However, the most remarkable development was the demonstration of antiamoebic property of metronidazole in the early 1960s. This drug had been introduced a few years back as a well tolerated, orally effective agent for trichomonas vaginitis. Of the many congeners of metronidazole that were tested, tinidazole has emerged in the 1970s as a good alternative, and others have been added subsequently.




1. Tissue Amoebicides

a) For both intestinal and extraintestinal amoebiasis:


Nitroimidazoles: Metronidazole, Tinidazole, Secnidazole, Ornidazole, Satranidazole

Alkaloids: Emetine, Dehydroemetine


b) For  extraintestinal  amoebiasis  only: Chloroquine


2. Luminal Amoebicides


a)  Amide : Diloxanide furoate, Nitazoxanide

b) 8-Hydroxyquinolines: Quiniodochlor (Iodochlorohydroxyquin, Clioquinol), Diiodohydroxyquin (Iodoquinol)

c) Antibiotics: Tetracyclines


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