Tropical diseases Chagas' disease: American trypanosomiasis
This infection, due to Trypanosoma cruzi, is confined to the Americas, from Texas to Argentina, and is particularly common in rural areas of Brazil, Argentina, Uruguay, Chile and Venezuela. Children and young adults are most often infected, because the trypanosome is transmitted by reduviid or triatomine bugs, which bite at night. These bugs commonly live in the mud or adobe walls of huts or stables, and in homes which have cracked walls through which they can enter. At least one hundred and fifty animal species carry the organisms, but particularly domestic dogs and cats, pigs, monkeys, opossums and armadillos. The clinical infection can be acute, subacute or chronic. It starts from the original bite as the trypanosomes spread through the lymphatics to the lymph nodes (7-14 days) and then into the blood stream 5 days later. T. cruzi multiplies within the host cell and the disease is extremely difficult to diagnose and treat: almost any part of the body may be affected, but particularly smooth and striated muscle, glial and nerve cells. The trypanosomes may be found in the blood for the first 6 weeks of the acute stage, but not thereafter. The characteristic lesion is a Chagoma, a fibrotic encapsulated focus which can develop at the site of inoculation or elsewhere. It is particularly important in the heart and central nervous system.
Apart from the acute and chronic phases, there is an uncommon subacute form affecting the heart, in which there are large numbers of the parasites in the peripheral blood and in the cardiac tissues. It is likely that there is also a latent phase, because millions of people in the endemic areas are known to have been infected yet do not show clinical signs of the disease. Careful electrocardiography and oesophageal motility studies suggest that although the disease is clinically silent, it is still active and capable of further progression.
The heart in Chaga's disease
T. cruzi infection results in a multi-focal myocarditis, causing cardiac enlargement and decreased cardiac pulsation. The findings on imaging are indistinguishable from any other myocarditis (Fig. 21). The acute stage usually resolves within a few weeks and goes on to a latent phase (which can occur without any previous clinical illness). Eventually, there may be progressive heart failure, but in some patients there is acute biventricular
failure, causing dramatic and sudden death in an apparently healthy individual.
The gastrointestinal tract in Chaga's disease
The oesophagus and colon are the other organs particularly affected in the chronic stage. In both the result is motor dysfunction and eventually denervation, causing decompensation and dilatation, and, eventually, stasis. After a phase in which there is abnormal contraction and in coordination, the oesophagus becomes enormously dilated and can be recognized on plain radiographs of the chest, or on contrast studies. There is often a large residual food content, because of the lack of propulsive peristalsis (Fig. 22).
The stomach and small intestine may be involved, resulting in megastomach or megaduodenum, but megacolon is more common. There will be chronic constipation, the bowel emptying incompletely and irregularly at intervals of days or even months. There is often impaction and obstruction due to desiccation of the bowel contents. As the bowel becomes more atonic and dilated, there may be sigmoid volvulus. Barium or other contrast enemas will show an enormously dilated large bowel with poor ability to empty (Fig. 23). The mucosa may be abnormal because of the retained contents. In a few cases there may be some parts of the colon where denervation is not complete and short segments remain comparatively normal.
In the later stages of Chaga's disease, the imaging diagnosis is not difficult. There are few diseases which cause such huge megacolon and
 a,b | Figure 22.
The changes in the oesophagus in Chaga 's disease. (Brazil)
a) An erect contrast barium swallow shows a normal oesophagus with normal peristalsis.
b) When supine, the same patient has tertiary oesophageal contractions.
c) In the intermediate stage, the oesophagus is dilated, the gastrooesophageal region is narrowed. This resembles achalasia.
d) In the advanced stage, the oesophagus is elongated and grossly dilated, with a fluid level and retained food. |
 c |
 d | |
mega-oesophagus. The retained liquid and food may obscure the development of oesophageal
carcinoma (Fig. 24), which may infiltrate the wall and allows rupture of the contents into the mediastinum, leading to abscess formation. Although the abnormalities on chest radiographs or
 | Figure 23.
Chaga's disease, (barium enema). Megacolon with dilatation and gross elongation. The sigmoid colon reaches into the upper abdomen. Obstruction due to volvulus is very likely to occur at this stage.
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 a | Figure 24.Chaga's disease
a) An air-contrast examination shows a small tumour
in the mid third of the oesophagus. It is essential to empty as much of the contents of a mega-oesophagus as possible, before doing the contrast examination.
b) The CT scan of the same patient confirms the thickening of the oesophageal wall and that the tumour has not spread into the mediastinum.
(All figures of Chaga 's disease - courtesy of Professor G. Cerri, Brazil). |
 b | |
mediastinal scanning may be obvious, clinically the leakage may be surprisingly silent. The
cardiac enlargement does not have specific characteristics. The problem with Chagas' disease, particularly for the patient, is that it remains silent for many years. Patients with asymptomatic megaoesophagus may present only cough and then a chest radiography is usually indicated. Widening of the upper mediastinum, especially on the right, may be seen, but only if the patient had a recent meal. The lateral view will show anterior displacement of the trachea as responsible for the "irritating" cough and very seldom the "
regurgitation" coughing.
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