Amoebiasis is generally defined as infestation with Entamoeba histolytica with or without overt clinical symptoms. Dysentery has been recognized since the time of Moses and was discussed by Hippocrates, but the parasite was first identified in faecal specimens in 1869 by Lewis, and the clinical presentation of amoebic dysentery was first described in 1875 by Losch in St Petersburg, Russia. Although the disease is curable, it remains the third leading cause of death from parasitic infection in the world. Several factors have led to a failure to eradicate the disease.

First, the vast majority of human infestations with E. histolytica (at least 80 per cent) are completely asymptomatic. Luminal colonization by the parasite is usually detected by faecal examination for cysts or by serological screening of a population. In endemic countries there are innumerable carriers of the disease.

Second, human beings are not the only species affected by E. histolytica. Certain other animals (especially Macaque monkeys) are naturally infested with the parasite. Identical strains of amoeba affect Macaques and humans, and cross-infection has been reported.

Third, diagnostic techniques based on finding amoebae in the stools or specific antibodies in the serum have several inherent problems and are expensive. Epidemiological studies in an endemic area are difficult, if not impossible, to perform although the overall incidence of amoebiasis remains constant. In Thailand, at least, it has become much less important as a national health problem over the past 10 years. Morbidity and mortality rates have declined overall, and especially in patients with surgical complications of amoebiasis.

Nearly 500 million people worldwide (excluding China) excrete amoebae in the stool, and 8 to 10 per cent of these, predominantly those in Asia, Africa and Latin America, develop symptoms. The mortality rate is 0.2 per cent (75 000 deaths/year), and is highest among young children, who may be hypoimmune and can develop fulminating amoebiasis. In endemic areas infestation with E. histolytica increases steadily throughout life.

Amoebiasis presents in two distinct forms; intestinal and extraintestinal. The intestinal form affects the caecum, ascending colon, sigmoid colon, transverse colon, and rectum; the terminal ileum is rarely affected. Extraintestinal amoebiasis is found in the liver, lung, brain, and skin. The most common complication is liver abscess.

Intestinal amoebiasis is almost universal in the tropics, but the prevalence of infestation and the incidence of disease show geographical variation, probably because transmission and invasiveness vary with ecological and social conditions. The lack of published reports of amoebiasis from some areas of the world probably reflects a lack of medical enthusiasm rather than absence of the parasite. In Thailand, which has a population of 60 million, an epidemiological report from the Ministry of Health stated that there were 3000 to 5000 new cases of intestinal amoebiasis annually between 1985 and 1989, and 100 to 120 deaths each year. More information on stool and serological surveys is available from Mexico than from other developing countries in which this parasite is known to be endemic. In 1981 between 3 and 5 million of the 69 million Mexicans developed the antibody each year. There were 5 to 6 million clinical cases of amoebiasis and 10 000 to 30 000 deaths.

Human beings contract amoebiasis by consuming foods or drinks contaminated with the cysts of E. histolytica. After ingestation the quadrinucleate cysts reach the intestinal tract, where they develop into a metacystic stage and undergo an additional nuclear division; thus eight new uninucleate trophozoites emerge to complete the life-cycle. The trophozoites produce many proteolytic enzymes and cause tissue destruction by forming minute ulcers in the mucosa of the bowel in the ileocaecal and colorectal areas. These later expand and coalesce to form large, deep ulcers. The typical amoebic ulcer is flask-shaped. The latent period before the development of invasive amoebiasis varies: in an outbreak of the disease the usual incubation period is 1 to 4 weeks, but it can be as long as 1 year.

The onset of symptoms may be insidious, with lower abdominal pain. It can also be sudden, with high fever, bloody diarrhoea, foul-smelling stools, dysentery (most patients have tenesmus), and the pain of typhloappendicitis. The fulminant form is most common in youths, or those who are malnourished, pregnant, who have underlying systemic disease, or who are receiving corticosteroid therapy. The dysentery associated with amoebiasis is frequently confused with that of Shigella infection. Amoebiasis may also be confused with infection by Campylobacter jejuni, Yersinia enterocolitica, Escherichia coli, and Vibrio parahaemolyticus. The mild diarrhoeal syndrome of amoebiasis may be indistinguishable from salmonellosis, giardiasis, toxigenic E. coli diarrhoea, other infective diarrhoeas, and irritable bowel syndrome.

Definitive diagnosis of amoebic infection rests on finding amoebae in the stools or specific antibodies in the serum. It is important to remember that all methods of stool examination are tedious, time-consuming, expensive, and require a high degree of skill of the examiner.

Patients with fulminating amoebic colitis have all the features of severe ulcerative proctocolitis. They pass several blood-stained, mucous stools per day, and have severe tenesmus, high fever, abdominal pain, a distended abdomen with tenderness, toxaemia, rapid pulse, low blood pressure, and even shock. Colonic perforation is accompanied by signs of peritonitis.

Mucus and blood are found on digital rectal examination. Palpation reveals oedema and ulceration of the rectal mucosa; this is confirmed at proctoscopy. Sigmoidoscopy should be performed with extreme care since insufflation of the colon (or administration of an enema) increases the incidence of perforation. If the disease is confined to the right colon, the rectosigmoid area may appear normal; a limited examination will therefore not exclude the diagnosis of amoebic colitis. Endoscopy shows ulcers all over the rectal mucosa, varying from pinhead size up to 2 cm in diameter (Fig. 1) 2642. Most ulcers are covered with a yellow exudate.

Cotton buds should not be used to collect ulcer exudate or mucous stool because amoebic trophozoites may adhere to the cotton and produce a false-negative result. A small spoon or even biopsy forceps yields better results. The specimen should be examined immediately. Microscopic examination of two or three stool specimens will yield amoebic trophozoites in up to 70 per cent of cases. Punch biopsy of the ulcer edge for histological examination can also be performed (Fig. 2) 2643. Serological tests for E. histolytica are positive in 85 per cent of patients with amoebic colitis.

Plain radiographs of the abdomen are important when acute fulminating amoebic colitis is suspected. At an early stage there is generalized gaseous distension of the bowel. Later, when colonic necrosis is imminent, there is marked dilatation of the large bowel from caecum to sigmoid colon (toxic megacolon).

Metronidazole is the most popular drug for the treatment of amoebiasis. It is effective, simple to use, and rarely causes side-effects. Emetine hydrochloride remains the drug of choice in severe infections, despite the fact that it is more toxic and more difficult to administer.

Metronidazole (400 mg orally) is administered three times a day after meals for 5 days for acute amoebic colitis and for 10 to 12 days for chronic cases. More than 90 per cent of patients respond to this regimen, and less than 10 per cent require a second course of treatment 2 weeks after the first. Emetine is not required for the treatment of intestinal amoebiasis.

Patients with hepatic amoebiasis (amoebic liver abscess) require 600 mg of metronidazole orally four times a day for 1 day only. Ninety-seven per cent of patients respond to this treatment. The parenteral administration of the drug should be reserved for those patients unable to tolerate anything by mouth. The 3 per cent of patients who do not respond to metronidazole require dihydroemetine or emetine hydrochloride (1 mg/kg.day for 3 to 5 days in the acute form and for 9 days in the chronic form) followed by oral diodoquine (10 grains three times a day after meals for 3 weeks). An excellent response is obtained in almost all patients.

Operation is indicated for toxic megacolon, peritonitis from colonic perforation, or severe bleeding. Before 1970 procedures included total colectomy, segmental colectomy, and colostomy with simple closure of the perforation. Overall mortality rates reached 70 to 100 per cent, the same as for non-operative treatment.

The optimal management for acute fulminating amoebic colitis remains controversial. Most authorities agree that operation is indicated only for patients who fail to respond after 48 h of intensive management, unless peritonitis develops in the interim.

It is best to avoid aggressive surgery and use minimal procedures to deal with the problem. If there is no obvious necrosis of the bowel, simple suture, faecal diversion, and drainage should suffice in severely ill patients. If necrosis is present, segmental resection of the affected segment of bowel is essential, followed by a double-barrelled colostomy.

Complications requiring surgical treatment arise in 1 to 4 per cent of patients with intestinal amoebiasis. The most common complication is colonic perforation and peritonitis. A few individuals develop an annular inflammatory mass or amoeboma in the colon, which is sometimes tender and may be indistinguishable radiographically from colonic carcinoma. Another rare but fatal complication is fulminating amoebic colitis with toxic megacolon. A few patients develop a chronic irritable bowel syndrome. Very rarely severe proctocolitis extends to the perineal skin.

Among 1477 patients undergoing surgery for peritonitis at Siriraj Hospital, Bangkok, between 1981 and 1988, there were seven cases (0.47 per cent) of colonic perforation due to amoebiasis with generalized peritonitis and five cases (0.34 per cent) of fulminating amoebic colitis and toxic megacolon. The incidence of these complications has been markedly reduced by the use of metronidazole.

The liver is the organ most commonly affected by the extension of intestinal amoebiasis. Liver abscess can develop within days of an attack of amoebic dysentery or may follow after months or even years. Up to 50 per cent of patients have no previous symptoms suggestive of intestinal amoebiasis.

In 138 patients with amoebic liver abscess, the age distribution was 8 to 82 years (mean 45 years). Males were affected more often than females, with a ratio of 4.5 to 1. Amoebic liver abscess is rare in children.

The onset is usually gradual, with abdominal pain (79 per cent), fever (53 per cent), malaise, weight loss, and occasionally jaundice. The pain is often a vague discomfort in the right upper quadrant, and there is point tenderness between the ribs on palpation. Occasionally the symptoms are acute with fever, pain, and chills. Some 37 per cent of patients complain of painful and tender abdominal mass. Pain may be referred to the right shoulder and aggravated by deep inspiration. Hiccough reflects diaphragmatic irritation by a so-called ‘dome abscess’. The presentation may be with symptoms and signs of a complication: cardiac tamponade, shock, dyspnoea, or cough result from a complicated liver abscess rupturing into the pericardial sac, pleural cavity, lung, or bronchus. Ascites is another potential feature in chronic amoebic peritonitis following rupture of an abscess into the peritoneal cavity. Patients may be toxic, malnourished, and anaemic.

Rupture of an amoebic liver abscess into adjacent viscera is uncommon, but subdiaphragmatic abscess, empyema thoracis with or without bronchopleural fistula, lung abscess, amoebic pericardium, and hepatogastric, hepatoduodenal, or hepatocolic fistulae may develop. Occasionally the abscess ruptures into the subcutaneous tissues or the rectus sheath, and it can even burst through the skin. Other rare complications include haemobilia, amoebic brain abscess, and rupture into the portal vein or inferior vena cava. Common laboratory findings are anaemia, leucocytosis, and elevation in ESR and serum alkaline phosphatase.

The clinical manifestations of liver abscess are seldom pathognomonic. Serological tests are positive in about 90 per cent of cases.

Over the past 10 years the first author has undertaken ultrasound examination of the abdomen in over 10 000 patients. In about 70 per cent of cases the hepatobiliary system was examined. Liver abscess ranked as the third most common disease of the liver, exceeded only by diffuse parenchymal diseases and carcinoma. There were 364 cases of amoebic liver abscess diagnosed by ultrasonography: 53 of these patients had a firm clinical diagnosis made before ultrasound examination, 258 cases were suspected, and in 53 cases the clinician did not suspect liver abscess.

Ninety-eight per cent of amoebic liver abscesses are hypoechoic on the ultrasonogram, in contrast to the hyperechoic appearance of hepatoma. In the other 2 per cent of cases appearances are mixed, and clinical evaluation, serological tests, and ultrasound-guided tissue biopsy for histology are helpful. The ultrasonographic pattern is not particulary helpful in differentiating amoebic from pyogenic liver abscess. In approximately 90 per cent of cases of amoebic liver abscess, the abscess cavity is solitary, contains homogeneous contents, and is situated in the posterosuperior part of the right lobe of liver. Ultrasonography can demonstrate maturation of the lesion from its early formation to rupture of the abscess.

In the authors' experience ultrasonography can diagnose liver abscess with a sensitivity of 98 per cent, a specificity of 99 per cent and an accuracy of 99 per cent: for both diagnosing and locating the lesion it is as good as a CT scan. The important principle is that general surgeons should learn to use ultrasound just as effectively as physicians can use their stethoscope.

Operation is now seldom required for treatment of an amoebic liver abscess: even some ruptured abscesses can be treated conservatively. Patients with ruptured abscess with generalized peritonitis, or with liver abscess associated with an intestinal problem such as toxic megacolon, colonic perforation, or fulminating colitis still require operation. Many cases settle with appropriate amoebicidal therapy. Percutaneous needle aspiration is only required if the abscess cavity is larger than 5 cm in diameter and does not respond to amoebicidal therapy within 24 to 48 h.

Most of the deaths in amoebic liver abscess occur when the diagnosis is missed or overlooked. There was no death among the 364 cases of amoebic liver abscess treated at our hospital after ultrasonographic examination of the abdomen.

Abioye AA. Fatal amoebic colitis in pregnancy and puerperium: a new clinico-pathological entity. J Trop Med Hyg 1973; 76: 97 - 100.

Adams EB, MacLeod IN. Invasive amoebic dysentery and its complications. Medicine 1977; 56: 315 - 23.

Archampong EQ. Peritonitis from amoebic liver abscess. Br J Surg 1972; 59: 179 - 81.

Barker DC, Swales LS. Characteristics of ribosomes during differentiation from trophozoite to cyst in axenic Entamoeba sp. Cell Differ 1972; 1: 297 - 306.

Bray RS, Harris WG. The epidemiology of infection with Entamoeba histolytica in The Gambia, West Africa. Trans R Soc Trop Med Hyg 1977; 71: 401 - 7.

Board of Health of the City of Chicago, Department of Public Works of the City of Chicago, U.D. Public Health Service. Public Health Service. Epidemic amoebic dysentery: the Chicago outbreak of 1933. National Institute of Health Bulletin No.166. Washington DC: U.S. Government Printing Office, 1936.

Buri R, Viranuvatti V, Harinasuta C. Three cases of pericardial effusion due to rupture of amoebic liver abscess. Am J Gastroenterol 1955; 23: 45 - 54.

Dobell C. Researches on the intestinal protozoa of monkeys and man. IV. An experimental study of the histolytica like species of Entamoeba living naturally in Macaques. Parasitology 1931; 23: 1 - 72.

Dupont HL, Pickering LK. Infections of the gastrointestinal tract: microbiology, pathophysiology, and clinical features. New York: Plenum, 1980.

Dysentery epidemic in Central America. Lancet 1970; ii: 969 - 70.

Elsdon-Dew R. The epidemiology of amoebiasis. Arch Parasitol 1968; 6: 1 - 62.

Gill GV, Bell DR. Persisting tropical diseases amongst former prisoners of war of the Japanese. Practitioner 1980; 224: 804 - 13.

Greaney GC, Reynolds TB, Donovan AJ. Ruptured amoebic liver abscess. Arch Surg 1985; 120: 55 - 61.

Greenstein AJ, Barth J, Dicker A, Bottone EJ, Aufses AH. Amoebic liver abscess: a study of 11 cases compared with a series of 38 patients with pyogenic liver abscess. Am J Gastroenterol 1985; 80: 472 - 8.

Guerrant RL. Amoebiasis: introduction, current status and research questions. Rev Infect Dis 1986; 8: 218 - 27.

Healy GR. Immunologic tools in the diagnosis of amoebiasis: epidemiology in the United States. Rev Infect Dis 1986; 8: 261 - 72.

Hoare CA. Reservoir hosts and natural foci of human protozoal infection. Acta Trop 1962; 19: 281 - 317.

Johnston JG, Stewart JB, Roberts DM. Intestinal amoebiasis for 36 years. Postgrad Med J 1980; 56: 802 - 3.

Kanani SR, Knight R. Relapsing amoebic colitis of 12 years standing exacerbated by corticosteroids. Br Med J 1969; 2: 613 - 4.

Lewis EA, Antia AU. Amoebic colitis: review of 295 cases. Trans R Soc Trop Med Hyg 1969; 63: 633 - 8.

Meerovitch E, Healy GR, Ambroise-Thomas P. Amoebiasis survey in Calcutta (India), Bangkok (Thailand), Medellin (Colombia), and San Jose (Costa Rica). Can J Public Health 1978; 69: 286 - 8.

Nanda R, Baveja U, Anand BS. Entamoeba histolytica cyst passers: clinical features and outcome in untreated subjects. Lancet 1984; ii: 301 - 3.

Oyerinde JPO, Ogunbi O, Alonge AA. Age and sex distribution of infections with Entamoeba histolytica and Giardia intestinalis in the Lagos population. Int J Epidemiol 1977; 6: 231 - 4.

Powel SJ, Wilmot AJ, Elsdon-Dew R. Further trials of metronidazole in amoebic dysentery and amoebic liver abscess. Ann Trop Med Parasitol 1967; 51: 511 - 20.

Rally PW, et al. Sonographic findings in hepatic amoebic abscess. Radiology 1982; 145: 123 - 6.

Thompson JE, Forlenza S, Verna R. Amoebic liver abscess: a therapeutic approach. Rev Infect Dis 1985; 7: 171 - 9.

Viranuvatti V, Harinasuta T, Plengvanit U, Choungchareon P, Viranuvatti V. Liver function tests in hepatic amoebiasis based on 274 clinical cases. Am J Gastroenterol 1963; 4: 345 - 61.

Wagner VP, Smale LE. Lischke JH. Amoebic abscess of the liver and spleen in pregnancy and the puerperium. Obstet Gynecol 1975; 45: 562 - 5.