Kissing bug disease linked to higher risk of cognitive impairment

People with Chagas disease appear to face a greater risk of cognitive difficulties, including memory and spatial problems, compared to those with other forms of heart failure. A new study published in PLOS Neglected Tropical Diseases suggests that these impairments are not just a byproduct of heart dysfunction, but may stem from direct or indirect effects of the disease on the brain.

Chagas disease is caused by a microscopic parasite called Trypanosoma cruzi, which is most often spread to humans by triatomine insects, sometimes called kissing bugs. The disease is widely recognized as endemic to 21 countries in Latin America, where millions of people are infected. However, recent updates from the Centers for Disease Control and Prevention and other public health researchers suggest that this geographic framing may be outdated.

Triatomine insects infected with T. cruzi have been found in 32 U.S. states, and multiple locally acquired human cases have been documented—particularly in Texas, where public health officials have reported dozens of autochthonous cases since 2013. The parasite has also been detected in wildlife, domestic animals, and zoo-housed mammals across the southern United States. This body of evidence has led researchers to argue that Chagas disease should be considered endemic, albeit hypoendemic, within the U.S., with stable sylvatic transmission cycles and occasional human infections.

Chagas disease can remain silent for years, but about one-third of infected individuals eventually develop chronic complications. Among the most severe outcomes is Chagas cardiomyopathy, a progressive form of heart disease that can result in heart failure and sudden death.

While the heart-related complications of Chagas disease are well-documented, much less is known about how the infection might affect the brain. Previous studies have hinted at cognitive difficulties among people with Chagas disease, but it has been unclear whether these problems stem directly from the infection or are secondary to cardiac dysfunction, which can impair brain perfusion and promote inflammation. The new study was designed to clarify this relationship by comparing cognitive function in people with heart failure caused by Chagas disease to those with heart failure from other causes.

The researchers recruited 518 patients with heart failure from four hospitals in Brazil. These individuals had heart failure from various causes, including Chagas disease, ischemic heart disease, hypertension, and alcoholism. Of the total group, 250 individuals had tested positive for Chagas disease. All participants were over 18 years of age and had no history of stroke, dementia, or other major neurological disorders. Those taking anticoagulants or unable to consent were excluded.

Each participant underwent a battery of neuropsychological tests that assessed various aspects of cognitive function, including memory, attention, executive function, and visuospatial abilities. The tests were standardized and adjusted for age using norms from Brazilian and U.S. populations. The researchers also collected demographic and clinical data, including left ventricular ejection fraction, a common measure of heart function.

To isolate the effect of Chagas disease on cognition, the researchers used statistical models that adjusted for confounding variables such as age, sex, educational level, and heart function. This allowed them to compare cognitive outcomes between patients with and without Chagas disease who had otherwise similar health profiles.

The study found that cognitive impairment was more common among individuals with Chagas disease compared to those with other types of heart failure. Specifically, 27.1% of the Chagas group met criteria for global cognitive impairment, compared to 13.1% in the non-Chagas group. The most pronounced deficits were in memory and visuospatial domains. People with Chagas disease performed worse on tests that required recalling visual patterns, drawing complex figures, or processing spatial information.

Importantly, the association between Chagas disease and cognitive impairment remained even after adjusting for potential confounders. Chagas disease was associated with nearly double the odds of global cognitive impairment and a 56% higher likelihood of problems in visuospatial tasks. Memory impairment also appeared more frequently in the Chagas group, although this association did not remain statistically significant in the fully adjusted analysis.

The pattern of impairment seen in this study differed from what is typically observed in other brain disorders. For example, Alzheimer’s disease usually begins with memory deficits, while vascular dementia tends to affect executive functioning more severely. In contrast, the Chagas-related cognitive issues appeared to impact memory and visuospatial abilities most consistently, suggesting a distinct underlying mechanism.

Participants with Chagas disease had better heart function overall than those with other cardiomyopathies, as measured by left ventricular ejection fraction. This further supports the idea that the observed cognitive deficits may not simply be a byproduct of poor cardiac output, but could reflect a more direct effect of the infection on the brain.

Although the study was not designed to determine the exact mechanisms behind the cognitive decline, the authors offer several plausible explanations for the cognitive effects. One possibility is that chronic inflammation linked to Chagas disease could affect the brain directly. Prior research has shown that inflammatory markers such as interferon-gamma and tumor necrosis factor are elevated in Chagas disease and may contribute to brain changes. Another possibility is that the parasite itself may invade brain tissue, as suggested by animal studies that have found behavioral changes associated with brain parasite load and altered serotonin signaling.

While the study excluded individuals with known strokes, the authors acknowledge that small, “silent” brain infarcts could still be present and contribute to cognitive problems. Brain atrophy, or shrinkage, has also been reported in people with Chagas disease and might reflect chronic damage. These factors are now being explored further in an ongoing neuroimaging component of the same research project.

As with any cross-sectional study, the research cannot definitively establish a cause-and-effect relationship between Chagas disease and cognitive impairment. It is possible that unmeasured factors, such as lifetime socioeconomic status or early-life educational opportunities, might contribute to the observed differences. The researchers did adjust for educational attainment, which is often used as a proxy for socioeconomic background, but some residual confounding may remain.

The study also did not include a healthy control group without heart disease, which would have provided additional context. However, the decision to focus on patients with heart failure was intentional, as it allowed the researchers to directly assess whether Chagas disease has an independent impact on cognition when heart function is already compromised.

The authors suggest that future studies should include brain imaging and longitudinal follow-up to better understand how cognitive decline progresses in Chagas disease and whether it can be slowed or reversed. Such research could help inform strategies for screening and intervention, especially in regions where the disease remains endemic.

This study adds to a growing body of research indicating that Chagas disease affects more than just the heart. Cognitive symptoms may go unrecognized in clinical settings, especially in low-resource areas where neuropsychological testing is not routinely available. If confirmed by further studies, these findings may call for the development of new guidelines for cognitive screening and support in patients with Chagas disease.

The study, “Cognitive impairment in Chagas disease patients in Brazil, 2007–2021: A cross-sectional study,” was authored by Carla J. Serrano, Maria E. Lisbôa-Marques, Thiago Cerqueira-Silva, Leila S. B. Santos, Murilo A. Oliveira, Iuri Ferreira Felix, Paulo R. S. P. de Sousa, Leonardo G. M. Cardoso, Pedro J. R. Muiños, Renata M. Maia, Marília B. Catto, Eric Aguiar Wittlich, Lucy Rodrigues-Ribeiro, Victor L. P. P. Botelho, Maria Carmo P. Nunes, Antonio Luiz P. Ribeiro, Lucas C. Barbosa e Silva, Roque Aras, Karen L. Furie, and Jamary Oliveira Filho.