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Chagas disease (also called American trypanosomiasis) is a Mammalian disease occurring only in the Americas. It is caused by the protozoan Trypanosoma cruzi, one of the kinetoplastid flagellates, transmitted to humans by triatomine insects known in the different countries as assassin bug, vinchuca, kissing bug, chipo, barbeiro, etc. Common triatomine vector species for trypanosomiasis belong to the genera Triatoma, Rhodinius, and Panstrongylus. The most common transmitting species are Triatoma protracta and Triatoma infestans. The disease causing agent is closely related to that of African sleeping sickness, although the assassin bug vector is not related to the tsetse fly, which carries African sleeping sickness.
Photomicrograph of Giemsa-stained Trypanosoma cruzi crithidia. Source: CDC History
The disease was named after the Brazilian physician Carlos Chagas, who first described it in 1910 but the disease was not seen as a major problem in humans until the 1960s. Chagas named the pathogen after Oswaldo Cruz, the noted Brazilian physician and epidemiologist who fought successfully epidemics of yellow fever, smallpox and bubonic plague in Rio de Janeiro and other cities in the beginning of the 20th century.
It has been hypothesized that Charles Darwin might have suffered from this disease as a result of a bite of the so-called Great Black Bug of the Pampas (vinchuca).
Epidemiology and geographical distribution
Chagas disease currently affects 16-18 million people, killing around 20,000 annually and with some 100 million at risk of acquiring the disease. Chronic Chagas disease is a major health problem in many Latin American countries. With increased population movements, the possibility of transmission by blood transfusion has become more substantial in the United States.
The disease is distributed in the Americas, ranging from the southern United States to southern Argentina, mostly in poor, rural areas of Central and South America.
Clinical manifestations
The human disease occurs in two stages: the acute stage shortly after the infection.
A local lesion (chagoma, palpebral edema) can appear at the site of inoculation. The acute phase is usually asymptomatic, but can present with manifestations that include fever, anorexia, lymphadenopathy, mild hepatosplenomegaly, and myocarditis. Most acute cases (10 to 20%) resolve over a period of 2 to 3 months into an asymptomatic chronic stage, which appears after several years.
The symptomatic chronic stage may not occur for years or even decades after initial infection. The disease affects the nervous system and heart. Chronic infections result in various neurological disorders, including dementia, damage to the heart muscle (cardiomyopathy, the most serious manifestation), and sometimes dilation of the digestive tract (megacolon and megaesophagus), as well as weight loss. Left untreated, Chagas disease can be fatal, in most cases due to the cardiomyopathy component.
Infection cycle
An infected triatomine insect vector takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound or through intact mucosal membranes, such as the conjunctiva. Inside the host, the trypomastigotes invade cells, where they differentiate into intracellular amastigotes. The amastigotes multiply by binary fission and differentiate into trypomastigotes, and then are released into the circulation as bloodstream trypomastigotes. Trypomastigotes infect cells from a variety of biological tissues and transform into intracellular amastigotes in new infection sites. Clinical manifestations can result from this infective cycle and cell death at the target tissues. For example, it has been shown in the 1950s at the Medical School of the University of São Paulo at Ribeirão Preto, Brazil (one of the excellence medical research centers on Chagas disease), that intracellular amastigotes destroy the intramural neurons of the autonomic nervous system in the intestine and heart, leading to megaintestine and heart aneurysms, respectively.
The bloodstream trypomastigotes do not replicate (different from the African trypanosomes). Replication resumes only when the parasites enter another cell or are ingested by another vector. The kissing bug becomes infected by feeding on human or animal blood that contains circulating parasites. The ingested trypomastigotes transform into epimastigotes in the vectors midgut . The parasites multiply and differentiate in the midgut and differentiate into infective metacyclic trypomastigotes in the hindgut .
Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents.
Laboratory Diagnosis
Demonstration of the causal agent is the diagnostic procedure in acute Chagas disease. It almost always yields positive results, and can be achieved by:
- Microscopic examination: a) of fresh anticoagulated blood, or its buffy coat, for motile parasites; and b) of thin and thick blood smears stained with Giemsa, for visualization of parasites.
- Isolation of the agent by: a) inoculation into mice; b) culture in specialized media (e.g. NNN, LIT); and c) xenodiagnosis, where uninfected reduviidae bugs are fed on the patient's blood, and their gut contents examined for parasites 4 weeks later.
Treatment
Medication for Chagas disease is usually effective when given during the acute stage of infection, only. The drugs of choice are benzonidazole or nifurtimox (under an Investigational New Drug protocol from the CDC Drug Service). In the chronic stage, treatment involves managing the clinical manifestations of the disease, e.g., drugs and heart pacemaker for chronic heart failure and heart arryhthmias; surgery for megaintestine, etc. The decision about whether to use antiparasitic therapy should be individualized in consultation with an expert.
Source
- American Trypanosomyasis (http://www.dpd.cdc.gov/dpdx/HTML/TrypanosomiasisAmerican.htm). CDC Disease Information (US Federal Government public domain).
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