What is Chagas disease?

Chagas disease, also known as American trypanosomiasis, is a tropical parasitic disease caused by the protozoan parasite Trypanosoma cruzi. It is primarily transmitted to humans and other mammals through the bite of infected blood-sucking insects, known as triatomine bugs or “kissing bugs.” In addition to vector transmission, Chagas disease can also be transmitted through blood transfusions, organ transplantation, congenital transmission from mother to child, and ingestion of contaminated food or drinks.


Once inside the body, the parasite infects various tissues, including cardiac muscle, gastrointestinal tract, and nervous system. The acute phase of Chagas disease may present with mild symptoms or be asymptomatic, making diagnosis challenging. However, if left untreated, the infection can progress to the chronic phase, which may lead to serious complications, including cardiomyopathy (heart disease) and megacolon or megaesophagus (enlargement of the colon or esophagus).


Chagas disease is endemic in parts of Latin America, where it poses a significant public health burden. While the disease primarily affects rural and impoverished populations, globalization and migration have led to cases being reported in non-endemic regions, including North America, Europe, and some Western Pacific countries.


What is the relationship between Chagas disease and oxidative stress?

Chagas disease is associated with oxidative stress, which plays a significant role in the pathogenesis of the disease. Oxidative stress occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body’s antioxidant defense mechanisms. In the context of Chagas disease, several factors contribute to oxidative stress:


  • Parasite-Induced Oxidative Stress: T. cruzi, the parasite responsible for Chagas disease, induces oxidative stress in host cells during infection. The parasite’s presence triggers the production of ROS by infected cells as part of the immune response, leading to oxidative damage to cellular components.


  • Inflammation and Immune Response: The inflammatory response mounted by the host’s immune system to combat T.  cruzi infection also generates ROS. Inflammatory cells, such as macrophages and neutrophils, produce ROS as part of their antimicrobial activity. However, excessive ROS production can cause tissue damage and contribute to the pathology of Chagas disease.


  • Tissue Damage: Chronic infection with T. cruzi can lead to tissue damage, particularly in organs such as the heart and gastrointestinal tract. Oxidative stress contributes to tissue injury by promoting lipid peroxidation, protein oxidation, and DNA damage, which can impair cellular function and exacerbate the progression of organ damage.


  • Mitochondrial Dysfunction: T. cruzi infection can disrupt mitochondrial function in host cells, leading to mitochondrial oxidative stress. Mitochondria are a major source of ROS production, and dysfunction in these organelles can further exacerbate oxidative stress and cellular damage.


  • Antioxidant Defense: The antioxidant defense mechanisms of the host play a critical role in mitigating oxidative stress and limiting tissue damage during Chagas disease. However, chronic infection and persistent oxidative stress may overwhelm these antioxidant defenses, leading to cumulative damage over time.


Overall, oxidative stress is intricately involved in the pathogenesis of Chagas disease and contributes to tissue injury, inflammation, and organ dysfunction.