The term amoebiasis is generally applied to infections with obligate parasitic species of amoeba, principally Entamoeba histolytica.Other parasitic species which occasionally cause human infections include E. polecki (primarily a parasite of pigs and reported mainly in Papua New Guinea) and Dientamoeba fragilis (often found in association with the helminth Enterobius vermicularis and now thought to be a trichomonad).
Transmission of E. histolytica is by the faeco-oral route and infection results from the ingestion of cysts, usually in contaminated food and drink. The cysts transform to trophozoites in the intestines and reproduction occurs by fission of the trophozoites. Further cysts develop and are excreted in the faeces.
Amoebiasis occurs throughout the world. It is more prevalent and severe in the tropics and subtropics, but is more closely related to sanitation and socio-economic status than to climate. Colonisation with E. histolytica can result in asymptomatic infection, but in other cases the trophozoites invade the wall of the large intestine causing ulceration and may migrate to other tissues, especially the liver, where they continue to divide and destroy tissue. Factors increasing susceptibility to tissue invasion include malnutrition, immunosuppression, and pregnancy.
Symptomatic amoebiasis may be classified as intestinal or extra-intestinal amoebiasis. Intestinal amoebiasis comprises two main states, amoebic dysentery and non-dysenteric amoebic colitis; amoeboma, a localised form of intestinal amoebiasis, and amoebic appendicitis may also occur. Hepatic amoebiasis, the most common form of extra-intestinal amoebic disease, may present as acute non-suppurative disease or as amoebic liver abscess. Amoebic infection is a less common cause of liver abscess than bacterial infection. Amoebiasis may also involve the skin, genito-urinary tract, or organs such as the lungs and brain.
Drugs used in the treatment of amoebiasis may be classified according to their site of action as follows:
luminal amoebicides acting principally in the bowel lumen.
Diloxanide furoate is widely used as the luminal amoebicide of choice, although clefamide, etofamide, and teclozan are also effective. Paromomycin and diiodohydroxyquinoline have also been used although most oral preparations of halogenated hydroxyquinolines have been withdrawn because of the association between clioquinol and subacute myelo-opticoneuropathy
tissue or systemic amoebicides acting principally in the intestinal wall and liver. These have included the alkaloid emetine, its synthetic derivative dehydroemetine, and the antimalarial chloroquine which acts principally in the liver
mixed amoebicides acting at all sites of infection, that is within the intestinal lumen and in the intestinal wall and other tissues. These have included metronidazole and other 5-nitroimidazole derivatives. However, because of their rapid absorption from the gastrointestinal tract, the nitroimidazoles are less effective against parasites in the lumen
In non-endemic areas, patients with asymptomatic intestinal amoebiasis (cyst passers) are generally treated with a luminal amoebicide. The choice of drug is influenced by availability; diloxanide furoate is generally used in the UK while diiodohydroxyquinoline or paromomycin are used in the USA.5 Standard treatment for invasive amoebiasis (amoebic dysentery; hepatic amoebiasis) is metronidazole, ornidazole, or tinidazole, followed by a luminal amoebicide to eradicate any surviving organisms from the lumen of the large intestine and prevent relapse.
The majority of patients with amoebic liver abscess defervesce after 3 to 4 days of treatment with metronidazole. Addition of chloroquine is an option in patients who do not respond;4 WHO recommends that hepatic abscesses should be lanced by needle aspiration. In severe cases of amoebic dysentery tetracycline given with a systemic amoebicide lessens the risk of superinfection, intestinal perforation, and peritonitis.
In acute diarrhoea of any aetiology the priority is to maintain hydration by prevention or treatment of fluid and electrolyte depletion, especially in infants and the elderly. Oral rehydration therapy is discussed under Diarrhoea on .
Drugs suggested for the treatment of Dientamoeba fragilis infections include diiodohydroxyquinoline, metronidazole, paromomycin, or tetracycline.Metronidazole has been suggested for E. polecki infections.
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