Chagas Disease: A Parasitic Infection with More than 100 Years of Discovery

Chagas ́disease (CD) is caused by the protozoan parasite Trypanosoma cruzi, and was discovered in 1909 by the Brazilian physician Chagas [1]. T. cruzi is transmitted when the infected feces of the triatomino vector are inoculated through a bite site or through an intact mucous membrane of the mammalian host. Vector transmission is the classical form of CD acquisition. This transmission route has the largest impact in Latin American countries and is also responsible for the maintenance of the disease [2]. T. cruzi can also be transmitted through blood transfusion, transplant organs, and congenitally [3]. In endemic countries, blood transfusion was considered the second most common way to acquire such parasitosis [4]. This infection has been recognized by WHO as one of the world ́s 13 most neglected tropical disease, because the people most affected are often poorest population, living in remote rural areas, urban slums or conflict zones. It is an important public health problem not only in Latin America where it is endemic in 21 countries but it is increasingly spreading in other areas such as Europe, North America, Japan and Australia, mainly due to migration [5,6]. Especially with respect to the quality control of serological screening for Chagas disease among blood donors, the occurrence of false positive results may lead to unnecessary disposal of blood units and consequently compromise the blood supply at blood centers [7]. Around 6 million people are affected worldwide and approximately 7000 deaths occur annually, making CD the major cause of death from a parasitic disease in Latin America and a significant contributor to the global burden of cardiovascular disease, with CD the main cause of infectious cardiomyopathy in the world [8]. The migratory trends of infected populations from rural areas to urban centres and/or to non-endemic regions along with changes in the ecogeographical distribution of vector populations have led to the gradual urbanization and globalization of Chagas disease, which is now recognized as an emerging worldwide threat to public health [9]. Latin America has made substantial progress toward the control of Chagas’ disease. The estimated global prevalence of T. cruzi infection declined from 18 million in 1991, when the first regional control initiative began, to 5.7 million in 2010 [10]. The Pan American Health Organization has certified the interruption of transmission by domestic vectors in several countries in South America and in Central America [11]. The initial phase of Chagas disease is known as Acute Phase starts when the parasite enters the body and extends for 40-60 days after initial infection. A local reaction known as a chagoma often develops at the point of entry, and a general malaise, with fever, lymphadenopathies, hepatomegaly and splenomegaly. There is sometimes a painless conjunctival reaction, with oedema of both eyelids on one side of the face (Romaña sign), and lymphadenitis of the pre-auricular ganglia. A few cases develop much more severe problems, of acute is occasionally myocarditis or meningo-encephalitis, are occasionally fatal [12]. Following an acute infection, all patients with Chagas disease will enter the chronic stage, for the most, part diagnosed by detecting IgG antibodies that react specifically with T. cruzi antigens. About 20% of patients with chronic Chagas disease develop chronic cardiomyopathy many years later. Clinically, Chagas cardiomyopathy manifests by sudden cardiac death (SCD), thromboembolism, precordial chest pain, arrhythmias and conduction defects, and chronic heart failure (CHF). Chagas disease is the most important cause of CHF in areas where the disease is endemic, mainly in patients with the advanced forms of the disease [13]. Diagnostic methods for T. cruzi can be included in three main groups: parasitological, serological and molecular. The parasitological diagnosis is to determine the presence of T. cruzi in the patient's blood, by smearing, or by culturing (Blood culture) or using non-infected, fed with the patient's blood to look for the parasite in the insect feces (xenodiagnosis). In the chronic phase of infection, the sensitivity of these methods is noticeably reduced due to the low parasitemia. The methods of serological diagnosis can determine the presence of antibodies against T. cruzi. The most employed are the enzyme-linked immunosorbent assay (ELISA), indirect immunofluorescence, haemagglutination indirect and Western blot. In all of them, the patient's serum is tested against T. cruzi (in solution or the intact parasite), considering that if the sample has anti-T. cruzi antibodies. The first ELISA evaluated were originally developed using total parasite homogenates or semi-purified antigenic fractions from T. cruzi epimastigote (the non-infective forms of the parasite). Diagnostic tests employing epimastigote antigenic extract have a limited specificity, associated to the fact of they do not possess highly reactive epitopes for IgG/IgM antibodies present in patients with acute or congenital Chagas disease [14]. Considerable variation in the reproducibility and reliability of these tests have been reported by different laboratories, mainly these fractions are complex mixtures of molecules that favors the appearance of crossEditorial