Malaria parasites exist "cloaked" within red blood cells, where they divide into smaller cells called merozoites that are released into the bloodstream when the cell eventually bursts.

BIOGRAPHERS AND HISTORIANS generally believe that Charles Darwin caught Chagas disease during his voyage on The Beaglein the early 1830s, and that the disease may have been the root cause of the chronic illnesses that affected Darwin’s health until his death in 1882. Today, 123 years later, there is still no effective treatment for the chronic form of Chagas disease, which continues to kill tens of thousands of people annually. But after several decades of research, two scientists think they have found a possible cure.

The disease—caused by the parasite Trypanosoma cruzi, which is spread by biting insects known as “kissing bugs”—currently infects between 16 and 18 million people in Central and South America, with 120 million people at risk. Chagas disease occurs in an acute form mainly in children, but in adults there often are no acute symptoms. When the infection reveals itself a decade or two later, irreversible damage has been done to the heart, esophagus, and colon; the patient gets progressively sicker, usually dying of heart failure. The “kiss” of the parasite’s vector has aptly been called the kiss of death.

The drugs currently used to treat Chagas disease, mainly benznidazole, have serious drawbacks. They don’t work against the chronic form, which kills up to a third of those infected; they can have toxic side effects; and it is common for the parasite to have a natural resistance to them. So an alternative is badly needed. A team led by HHMI international research scholars Julio A. Urbina of the Venezuelan Institute of Scientific Research and Miguel A. Basombrio of the National University of Salta (Argentina) believes it has found that alternative in an experimental compound called TAK-187.

This compound, under investigation for a different therapeutic end as a possible systemic antifungal treatment, turns out to target the Achilles’ heel of T. cruzi, which Urbina, Basombrio, and colleagues have discovered from 25 years of studying the basic biology of the parasite. To complete its life cycle, T. cruzi needs to synthesize certain types of steroids, called sterols, that are present in nucleated cells. But the parasite cannot make use of the sterol that is most abundant in the tissue of its mammalian host—cholesterol. Instead, it prefers one called ergosterol.

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