Chronic Chagas disease: from basics to laboratory medicine

Abstract

Chagas disease, caused by Trypanosoma cruzi infection, is ranked as the most serious parasitic disease in Latin America and has huge potential to become a worldwide problem, due to increasing migration, and international tourism, as well as infectant transfer by blood contact and transfusion, intrauterine transfer, and organ transplantation. Nearly 30% of chronically-infected patients become symptomatic, often with a latency of 10–30 years, developing life-threatening complications. Of those, nearly 90% develop Chagas heart disease, while the others manifest gastrointestinal disease and neuronal disorders. Besides interrupting the infection cycle and chemotherapeutic infectant elimination, starting therapy early in symptomatic patients is important for counteracting the disease. This would be essentially supported by optimized patient management, involving risk assessment, early diagnosis and monitoring of the disease and its treatment. From economic and logistic viewpoints, the tools of laboratory medicine should be especially able to guarantee this. After summarizing the basics of chronic Chagas disease, such as the epidemiological data, the pathogenetic mechanisms thought to drive symptomatic Chagas disease and also treatment options, we present tools of laboratory medicine that address patient diagnosis, risk assessment for becoming symptomatic and guidance, focusing on autoantibody estimation for risk assessment and heart marker measurement for patient guidance. In addition, increases in levels of inflammation and oxidative stress markers in chronic Chagas disease are discussed.

Endogenous Allosteric Modulators of G Protein–Coupled Receptors

“…In patients with allergic asthma, autoantibodies showing antagonist-like activity at the b 2 -AR have been isolated (Turki and Liggett, 1995). Finally, in Chagas disease, digestive manifestations Endogenous GPCR Allosteric Modulators sometimes occur, leading to a syndrome called megaviscera (Haberland et al, 2013). Autoantibodies isolated from Chagasic patients with megacolon are able to bind and activate the M 2 mAChR, increasing the basal tone of the colon as well as inhibiting intracellular cAMP signaling (Sterin-Borda et al, 2001).…”

Cysteine mutagenesis improves the production without abrogating antigenicity of a recombinant protein vaccine candidate for human chagas disease

“…The parasites which cause Chagas disease are transmitted to humans and other mammals by blood-sucking "kissing bugs" of the subfamily Triatominae, but can also be spread via blood transfusion, organ transplantation, and congenital transmission. 1 In 2013, the number of people estimated to be infected with T. cruzi was approximately 9.4 million, mostly in Latin America. 2 Additional projections suggest that overall 60-100 million people are at risk of infection in the Western Hemisphere.…”

Lycopodium clavatum and Lycopodium complanatum subsp. chamaecyparissus ekstrelerinin antiprotozoal aktivitesi ve sitotoksisitesi

“…Malaria caused by the protozoa Plasmodium falciparum, P. ovale, P. vivax, and P. malariae is the most important of these diseases [5], followed by African trypanosomiasis (sleeping sickness caused by Trypanosoma brucei) [6], Chagas' disease caused by T. cruzi [7], and leishmaniasis caused by Leishmania species [8], all of which can be fatal if untreated. Conventional therapy against leishmaniasis consists of pentavalent antimonials and recently liposomal amphotericin B [9].…”