Tropical diseases Amoebiasis
Infection with the pathogenic protozoan, Entamoeba histolytica, occurs worldwide and at all ages. Once known as amoebic dysentery, almost any part of the body can be infected, including the skin and the lungs. In some patients the colon and liver escape or show no clinical evidence of infection. A normal gastrointestinal tract certainly does not exclude amoebiasis. There are numerous strains of E. histolytica, which are non-pathogenic and others which are found as commensals. Amoebiasis may be non-invasive. Infection is acquired through contaminated food or drink, and is particularly prevalent where sanitation is poor. It is probable that flies and other insects also spread the disease.
There is a wide spectrum of clinical presentation. An amoebic infection may cause either severe, acute illness or chronic ill health. Many patients have a history of diarrhoea, but in contrast some patients are constipated. Acute amoebic dysentery presents with frequent loose, bloodstained stools, colic, tenesmus and in many cases, severe systemic illness. Chronic amoebic dysentery may cause ill health, yet the colonic symptoms may not be striking. Pain is usual in the right lower abdomen, and the liver may become enlarged and tender. Children may present with intussusception, adults with intestinal obstruction. Some patients will complain of cough and have symptoms of pneumonia with a pleural effusion, but no symptoms referable to the bowel.
Amoebiasis of the bowel
The most frequent sites of infection are the caecum, ascending and sigmoid colon. The amoebae burrow below the mucosa, and ulceration follows. Occasionally, the infection spreads outwards, through the muscle layer to the peritoneum. The earliest imaging abnormality is usually found in the caecum and right colon. There is local oedema and the bowel becomes less mobile: with a barium enema, the bowel mucosa appears hazy and spiculated, because of the oedema and ulceration. There may be areas of spasm and irritability, but as the oedema increases, the bowel wall is thickened and becomes rigid. The caecum becomes very distorted
a
|
b
|
c
|
d
|
Figure 1. Amoebic colitis
a) An amoebic infection distorting the caecum and causing mild ileocecal obstruction. There is a "skip" area of colitis at the splenic flexure and probably another in the descending colon. (Nigeria) b) Amoebiasis causing constriction in the proximal transverse colon and at the ileocoecal junction (Amoeboma). There are areas of ulcerating colitis just below the splenic flexure and just above the sigmoid colon. (Nigeria) c) Severe and extensive amoebic colitis, with spasm of the descending and sigmoid colon. There is shortening and ulceration of the caecum and ascending colon: the terminal ileum is dilated. (Nigeria) d) Late stage of amoebic colitis. The colon has become smooth, with decreased haustration, particularly the rectum and sigmoid. (Nigeria)
|
and there is usually reflux into the terminal ileum. There may be inflammatory pseudopolyps (Fig. 1 a).
Ultrasound will show the thickening of the wall of the right colon and as the diseases progresses, there will be a pericaecal mass. It is important to examine carefully the whole colon, because amoebic bowel infections often occur at several different sites, with intervening normal areas of bowel (Fig. 1 a). Only in Crohn's disease, tuberculosis and
lymphoma are similar multiple sites likely. When the infection is acute and severe (fulminating amoebic colitis), the colon may be very dilated, resembling the toxic megacolon which is seen in ulcerative colitis: perforation or
haemorrhage may occur. Fortunately, ulcerative colitis is rare in many parts of the world, which helps the differential diagnosis, but careful mucosal
biopsy is necessary if surgery is considered. In less severe cases, there can be coarse mucosal thickening throughout the length of the colon, with pericolic extension due to fistulae. Involvement of the small bowel, or extension to the bladder or skin, can occur but is uncommon. In the later stages the caecum becomes contracted, often with shortening of the ascending colon.
Fibrosis during healing can result in a smooth, narrow, rigid colon (Fig. 1 d).
Amoeboma
Amoebic infection can cause an amoeboma, which is a localised hyperplastic granulomatous reaction, usually in the colon, but sometimes in the ileum (Fig. 1b). This causes a large mass with central stenosis which closely resembles a carcinoma. Again, geography is important, because cancer of the colon is rare in many parts of the world and an amoeboma is often the more common cause of such a tumour. However, amoeboma are also geographically variable, being common in some regions and rare in others. Diagnostically, the demonstration of another area of colitis elsewhere in the bowel makes an amoebic infection more likely than a tumour. Unfortunately, neither ultrasound nor any other form of imaging can reliably distinguish between a carcinoma and an amoeboma; rectal biopsy followed by a short period of antiamoebic treatment may prevent unnecessary surgery (which can be dangerous with any severe amoebic infection).
Infants and children are not spared any of these varieties of amoebiasis, and, in addition, intussusception may be caused by the rigidity or swelling of a segment of amoebic bowel. Reduction by any form of internal pressure must be carried out with extreme caution.
Amoebiasis of the liver
Amoebic abscesses occur in any part of the liver. Patients do not always have a history of diarrhoea or other evidence of amoebiasis and there may be no amoebae in the stool or on rectal mucosal biopsy. Amoebic infection may not even be suspected clinically, because liver involvement may not present for many years after exposure, and the patient may never have been to the tropics. A recurrent fever, pain or local tenderness in the right upper quadrant of the abdomen, or an elevated diaphragm on a chest x-ray, sometimes with a pleural effusion, may be indications of an amoebic abscess (Fig. 3 a). However, a clinically normal liver does not exclude a hepatic abscess. The majority of liver abscesses are reliably demonstrated by ultrasound, CT or MRI (Fig. 2). Radionuclide scanning is less sensitive until the abscesses are large. Angiography may show a "blush" around the abscess, but is not a very helpful procedure: a tumour or another infection may be similar.
The ultrasound appearance of amoebic hepatitis varies with the stage of the infection. At first, before there is abscess formation, there will be hypo- or anechoic areas, most often in the right lobe of the liver. The borders are vague and ill-defined, but the general shape is round or oval, varying from 1-20 cm in size. Some have marked back-wall enhancement. While similar areas may be found in any infection, a subcapsular les ion is more likely to be amoebic than pyogenic, and if amoebic, most patients will have more than one hepatic lesion.
In the later stages, as liquefaction develops centrally, thick-walled, roughly circular abscesses can be recognized with ultrasound (Fig. 2 b). Many have internal debris, and most are surrounded by hypoechoic oedema or hyperechoic compressed liver parenchyma. High dose contrast infusion or contrast angiography will show these changes as a non-specific halo "blush" around the abscesses (Fig. 2a).
In the early stages of an amoebic infection, the lesions may be isoechoic and not demonstrated with ultrasound. Repeat scanning is essential, because the abscesses change quite quickly and will become obvious as the infection progresses. The images shown by CT and MRI will follow a similar sequence of changes (Fig. 2 c, d, e), but have no imaging advantage over ultrasound, except in the transitory phase when the lesions are isoechoic. Even then, a few hours is all that is required before
a | Figure 2.Amoebic liver abscess. a) If ultrasound or other scanning is not available, a liver abscess can be demonstrated by intravenous high dose contrast infusion, with tomography. This large amoebic abscess shows a well marked peripheral, hypervascular inflammatory rim. (Kenya) b) A liver abscess shown by ultrasound. (Kenya) c) A CT scan of an amoebic abscess at an early stage, with poor edge definition (arrowheads). (Pakistan) d) The abscess becomes more clearly shown (arrows). (Pakistan) e) Amoebic abscesses in both lobes of the liver. (Pakistan) |
b |
c | |
d | |
e | |
| |
a | Figure 3.Amoebiasis in the chest. a) An amoebic hepatic abscess causing a raised right diaphragm with pleural effusion and right lower lobe oedema and infection. (Kenya) b) An amoebic hepatic abscess causing a subphrenic abscess, elevation of the right diaphragm, right pleural effusion and lower lobe oedema. (Egypt) c) A large right amoebic empyema with raised right diaphragm and right lower lobe consolidation, all due to an amoebic abscess in the liver. (Nigeria) |
b |
c | |
there will be positive results with
ultrasound. After treatment the abscess may heal completely over a period of months, or may leave a scar which may calcify eventually. If untreated or unresponsive (or subject to
trauma) the abscess may rupture into the biliary tract or peritoneum,
pericardium or chest. It is extremely difficult to distinguish between amoebic and pyogenic abscesses in the liver with any form of imaging. The early lesions may suggest hepatoma or even
hepatitis or
haematoma. Aspiration may be necessary, or the result of specific treatmen assessed before a pyogenic abscess or infected hepatic
cyst can be excluded.
Amoebiasis of the chest
An amoebic liver abscess may be associated with a pleural effusion or empyema on either side of the chest, and there may be lower lobe pneumonia. Amoebic abscesses may rupture into the pericardium, particularly from the left lobe of the liver, or may also rupture into the pleura or lung (Fig. 3). The contents may then be coughed up, a dramatic and rather unpleasant event, which produces thick, pink, stained sputum instead of ordinary sputum. A "collar-stud" abscess penetrating through the diaphragm may result in a true amoebic pneumonia, but more often the lung reaction is a result of static pulmonary oedema because of the immobile diaphragm, with secondary pyogenic infection.
It is also important to remember that an amoebic lung abscess can occur even without evidence of liver or bowel infection. If communicating with the bronchus, there can be a fluid level in the abscess. Such lung abscesses are usually thick-walled, but cannot be distinguished radiologically from a pyogenic abscess or even some cases of tuberculosis. When pulmonary amoebiasis is suspected, careful ultrasound of the liver may show a clinically unexpected hepatic abscess. Even if the liver is normal, the possibility of an amoebic infection must be considered whenever the re is a lung abscess which fails to respond to standard treatment.
Amoebiasis of other sites
Amoebic infections can occur in the brain and skin. Cutaneous amoebiasis can be a primary infection, but is usually an extension of an intestinal or hepatic source. Skin involvement around the anus is particularly common: ultrasound should be used to exclude a perirectal abscess. Except around the terminal ileum, where involvement may occur when there is a caecal infection, amoebiasis seldom affects the small bowel. This is helpful when trying to differentiate between amoebiasis, tuberculosis and Crohn's disease.
Wherever it may occur, a high level of suspicion is essential for the diagnosis of an amoebic infection. A chest radiograph which shows an elevated diaphragm on one side, with or without a pleural effusion, a large, tender liver with abnormal ultrasonography, bowel obstruction from a "tumour" with areas of colitis elsewhere, intussusception in small children, or a perianal fistula can all be the presenting evidence of amoebiasis. But of course, patients of any age may still appear with classical amoebic dysentery and ultrasound may show a normal liver. Amoebiasis can be very confusing!
Philip E.S. Palmer, with Stanley P. Bohrer, Carlos Bruguera, Xing-Rong Chen, Mahmoud R. EImeligi, Hassen A. Gharbi, S.B. Lagundoye, M. W. Wachira