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Joseli Lannes-Vieira
Laboratory of Interactions Biology, Oswaldo Cruz Institute/Fiocruz
American tripanosomiasis, later called Chagas disease after Brazilian researcher Carlos Chagas, who discovered it, is a relevant disease caused by infection by hemoflagellate parasitic protozoan Trypanosoma cruzi. The parasite is transmitted by triatomine bugs, which serve as vectors. The most significant modes of transmission of Chagas disease are still vectorial, whether through the lesion that results from the bite or through the ocular or oral mucosa. However, transfusional and congenital transmission are also epidemiologically relevant.
In the 1980’s, several authors estimated that the disease would be affecting about 18-20 million individuals in endemic areas in Latin America. Recent data from the World Health Organization, released after a meeting of specialists in Argentina in 2005, indicated the existence of 16-18 million people infected by T. cruzi. However, in a recent publication Dias Scielo estimates this number to range from 12 to 14 million people in Latin America alone; contaminated individuals have also been found in European and in North American countries, most of the times a result of migration as these infected individuals moved from their countries in search of better life conditions. These figures show the inexistence of a recent epidemiological survey and indicaate, as pointed out by the WHO, the still current need to know the prevalence and the incidence of the disease. In any case, figures illustrate the social importance of Chagas diasease 100 years after it was discovered.
In Brazil, acute cases of Chagas disease must be reported, according to Decree 5 of 21 February 2006 of the Secretary’s Office of Health Surveillance of the Ministry of Health. Due to the recent ourbreaks of acute infection by T. cruzi, especially through oral contamination, after a meeting of specialists and scientists in 2005 the Secretary’s Office of Health Surveillance of the Ministry of Health launched the I Brazilian Consensus on Chagas disease. It was reviewed and updated in 2015 as II Brazilian Consensus on Chagas disease. In 2011, the Brazilian Cardiology Society launched the I Latin American Guideline for the Diagnosis and Treatment of Chagas Cardiopathy. Official information provided by the Brazilian Ministry of Health regarding different aspects of Chagas disease can be consulted on the Portal of Health of the Ministry of Health.
Although initiatives by the WHO and by Latin American governments have led to the control of the vectorial transmission of the disease in different endemic areas by its main vector, Triatoma infestans, the inexistence of a vaccine and of an effective treatment, especially for patients with the chronic form of the disease, is still a challenge that needs to be faced. One of the current challenges in the treatment of patients infectd by T. cruzi is the identification of clinical and laboratory markers that indicate risk or prognosis for the development of arrhythmias, cardiac failure and death for a person with Chagas.
The diagnosis of acute, chronic or congenital infection uses parasitological, serological and molecular methods. After infection, most individuals go through an asymptomatic acute phase. Years or even decades after the acute phase of the infection, about 40% of patients develop symptomatic forms of the chronic phase of the disease.
The pathology is mainly characterized by its cardiac form, with dilated cardiomyopathy associated to myocarditis, fibrosis and cardiac dysfunction. About 10% of infected individuals develop the gastrointestinal form, which may result in megacolon and/or megaesophagus, frequently associated to the cardiac form, consisting the mixed chronic form, as recently revised by Moncayo and Higuchi and collaborators.
The reactivation of Chagas disease in subjects with HIV, people who have been the recipients of a transplant, or individuals with cancer has been described, including the presence of the nervous form. In these cases, the specific anti-parasite treatment is effective in controlling parasitemia and in the clinical improvement.
Experimental models, although restricted to the reproduction of some focal aspects of Chagas disease, make it possible to study the pathology and the physiopathogeny of the acute and chronic phases of the infection by T. cruzi.
Some hypothesis attempt to explain the pathogeny of the tissue damage that leads to organ dysfunction. It has been proposed that these damages are induced directly by the parasite and/or indirectly through the deregulation of specific immune response to the parasite, although the physiopathogenic factors that control the final result of the infection have not been elucidated, as revised by Higuchi and collaborators, Dos Reis, Cunha-Neto and collaborators, and Kierszenbaum. There is evidence that parasite persistence in the tissues associated to poorly adapted homeostatic mechanisms, such as the oxidative/antioxidative processes and pro-inflammatory/anti-inflammatory processes, are critical for the pathogenesis and the progression of Chagas disease, as revised by Higuchi and collaborators and by Lannes-Vieira. The progression of an infection, just like the resulting clinical status, depends on a complex parasite-host relation that involves environmental and genetic factors from both the host and the parasite. In this context, more recent studies also point to the possibility of a genetic predisposition of patients to develop the clinical forms of the chronic phase of Chagas disease.