Chagas’ disease afflicts an estimated 8 million people worldwide, mostly in Latin America—though that figure is believed to be low, due to underdiagnosis. Caused by the parasite Trypanosoma cruzi, or T. cruzi, the infection is carried in animals and transmitted to humans by the triatomine bug, or kissing bug. While the disease is curable if treatment is started soon after infection, most cases are not caught in the early phases. Up to 30 percent of chronically infected individuals develop cardiac, digestive, or neurological complications, which can be lifelong. Harvard Public Health editor Madeline Drexler recently spoke with Barbara Burleigh, professor of immunology and infectious diseases, who has devoted her career to studying Chagas’ disease.
Q: What makes the Chagas’ disease parasite so formidable?
A: Unlike the malaria parasite—the main species of which infect humans, and lives only in red blood cells in the asexual stage—the Chagas’ disease parasite can infect almost any cell type with a nucleus. It can live in an opossum. It can live in a rat, in a dog. It can live within different cell types in the human body. It’s an amazingly adaptable and flexible organism. I think of it as the center fielder in a baseball game: ready for anything.
Q: Today, Chagas’ disease is spreading around the world—mostly because of migration. It’s been found in Canada, Japan, Australia, and many European countries. In the U.S., the Centers for Disease Control and Prevention estimates about 300,000 cases, across a band of at least 25 states, mainly in the lower half of the country—from California to Texas to Pennsylvania. Cats, raccoons, rodents, and other animals can carry the Chagas’ parasite. What is your fear about this spread?
A: Not all kissing bugs are equally good at spreading Chagas’ disease. I worry that climate change could expand the range of bugs that are better human vectors—those that leave the parasite on the skin after they bite people. These bugs could start
to creep north. Even now in certain areas in the southern United States, 50 percent of the bugs carry the T. cruzi parasite and a very high proportion of animals are infected with it.
Luckily, most people in the U.S. live in solidly constructed houses that prevent the bugs from coming in. But there are certain at-risk populations: homeless individuals, for example, in whom it is already happening at a low level. Blood can be screened for Chagas’ disease, but there are cases where it has spread through blood transfusion and organ transplantation, and from mother to child, though these instances are rare.
Q: Even in Latin America, where the disease is endemic, doesn’t Chagas’ disease often lurk unseen?
A: Yes, Chagas’ disease is often referred to as the “silent killer.” People can carry the parasite for years without knowing, and can therefore transmit it. Also, for someone to be diagnosed with the disease, they must test positive in at least two different tests. This can lead to delays and underdiagnosis.
Another reason for underdiagnosis is that there are different strains of the parasite circulating around. The current tests were developed to identify strains that circulate in the southern cone regions of South America. But in the Andean countries, as well as in Central America all the way through Mexico, a different strain predominates. The overwhelming bias in the field is that the Andean/Mexican strain is not virulent—but I disagree.
The problem is that diagnostic kits are less sensitive for the circulating strains in those areas. Someone who has Chagas’ disease and is dying from heart complications can actually test negative for the parasite. So there’s an effort now to make more region-specific or strain-specific diagnostic tests.
Q: What’s your big scientific question in regard to Chagas’ disease?
A: How does the Chagas’ disease parasite live inside human host cells and survive? We approach this from the outside in. Often, when scientists study intracellular pathogens, they look past the host cell to focus on the pathogen itself. Our lab looks at the parasite through the lens of the host cell. How does the host cell respond to infection? What does the host cell give to the parasite to help it survive? We use tools from mammalian cell biology, molecular biology, and molecular genetics to tackle this complex problem. Among other things, we have discovered that a balance between sugar and fat metabolism in a mammalian cell seems important for supporting the parasite’s growth.
Q: Could this research lead to better treatments?
A: Yes, I believe so. Our goals are, number one, to understand what the parasite needs to grow and survive in human cells and to use this information to identify possible drug targets in the parasite itself. At the same time, we want to understand whether the “parasite-feeding” pathways we are finding in the host could be targeted to control the parasite infection.
A key mystery to this infection is why it develops in one person and not someone else. Of the individuals infected with Chagas’, roughly 70 percent carry the parasite for life and never develop the disease. Could that figure be pushed to above 95 percent? If so, it forces you to rethink approaches to treatment. Do you need a vaccine or
a drug or a therapy that eliminates the parasite? Perhaps not. Maybe what you need is a way to keep the disease from progressing.
— Madeline Drexler is editor of Harvard Public Heath.