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Chagas disease 

Chagas disease

Chapter:
Chagas disease
Author(s):

M.A. Miles

DOI:
10.1093/med/9780199204854.003.070811_update_001

Update:

Epidemiology—prevalence in southern Texas.

Treatment—discussion of chemotherapy of chronic disease.

Prevention—experimental vaccines.

Updated on 31 May 2012. The previous version of this content can be found here.
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date: 23 April 2017

Trypanosoma cruzi, the protozoan parasite which causes Chagas disease, is a zoonosis with many mammal host and vector species. It is transmitted to humans by contamination of mucous membranes or abraded skin with infected faeces of bloodsucking triatomine bugs, also by blood transfusion, organ transplantation, transplacentally, and orally by food contaminated with infective forms. It multiplies intracellularly (pseudocysts) as amastigotes in mammalian cells, particularly heart and smooth muscle, from which flagellated trypomastigotes emerge to reinvade cells or circulate in blood. Around 10 million people are infected in Latin America; imported cases and congenital cases may occur elsewhere.

Clinical features

There are classically three phases. (1) Acute—may be asymptomatic, or with manifestations including fever, myalgia, headache, vomiting, diarrhoea, anorexia, facial or generalized oedema, rash, generalized lymphadenopathy, and hepatosplenomegaly; there may be a lesion at the portal of entry; fatal in less than 10%. (2) Meningoencephalitic—rare in adults, excepting those who are immunocompromised (most typically with HIV/AIDS); also seen in congenital cases. (3) Chronic—occurs in up to 30% of those recovering from the acute phase; most often with cardiac involvement (typically cardiomyopathy leading to congestive cardiac failure, with risk of arrhythmia and ECG abnormalities due to focal inflammatory lesions of the conducting system), also megaoesophagus and megacolon. Infection is opportunistic, relapsing in the immunocompromised.

Diagnosis

(1) Acute phase—parasitaemia is scanty, but circulating trypomastigotes may be detectable in the acute phase by microscopy of blood, enhanced by concentration methods. (2) Chronic phase—multiple blood cultures or feeding and subsequent dissection of laboratory-reared triatomines (xenodiagnosis) may reveal infection. (3) Serological testing—can demonstrate evidence of infection, but needs to be standardized with reference sera and by external quality control.

Treatment

(1) Acute phase—proven cases should be treated promptly with nifurtimox or benznidazole, but there is no guarantee that a full course of treatment will eliminate the infection. (2) Chronic phase—the value of drug treatment for adults is still debated; supportive care may include the following (a) for heart disease—conventional drug treatment for cardiac failure and arrhythmias; cardiac pacemaker; (b) for megaoesophagus—dilatation; segmentary removal of stomach muscle; replacement of the distal oesophagus; (c) megacolon—resection and anastomosis with the rectal stump.

Prevention

Proven methods of controlling domestic triatomine bugs include insecticide spraying (with pyrethroids), health education, community support, and house improvement. Serological surveillance of children detects residual endemic foci or congenital transmission and is vital for monitoring the success of control programmes. The Southern Cone programme against Triatoma infestans is considered a model for international cooperation in disease control. There is no vaccine.

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