Chagas Disease (cont.)

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What is the history of Chagas disease?

Chagas disease was named after Carlos Chagas, who first described the parasite Trypanosoma cruzi in infected humans in 1909 while working for the Oswaldo Cruz Institute in Brazil. Chagas discovered that the parasites are transmitted to humans by entering breaks in the skin after they are deposited on the skin in insect feces. Chagas was the first scientist to discover all aspects of a new infectious disease; its pathogen (T. cruzi), main insect vector (triatominae or kissing bugs), hosts (humans, mammals), clinical manifestations, and epidemiology. The parasite species was named cruzi to honor his employer and scientific mentor, Oswaldo Cruz.

Chagas disease is also known as American trypanosomiasis because it mainly occurs in the Americas where the triatomine insects (kissing bugs) usually are found. These bugs and the mammals they infect range from states along the U.S. border with Mexico through Central America to the South American countries (for example, Argentina, Bolivia), where the disease is endemic. Almost all cases diagnosed in the U.S. are in immigrants from other countries in the Americas.

The disease is fairly common in Central and South America with an estimated 7.7 to 15 million infected people worldwide. Children have more acute-phase symptoms than adults. Fortunately, vector-control programs are working as prevalence rates are dropping in Brazil and other countries that have implemented these programs. However, because of warming climate trends, some researchers predict that Chagas disease will become more prevalent in the U.S. This is predicted because the vectors that carry the parasites are being found more often in the U.S., especially in the southern and middle states.

What causes Chagas disease?

Chagas disease is caused by a protozoan parasite named Trypanosoma cruzi. Infection of humans occurs when an insect vector (mainly Triatominae or kissing bugs, a member of the family Reduviidae and sometimes referred to as reduviid bugs) deposits feces that contains the parasites on human skin. The parasites then enter the mammalian (human) host through the bug bite, or breaks in the skin or conjunctiva. Occasionally, the parasites enter through mucosal cells of the mouth or airway when ingested or inhaled. The bugs often deposit feces near the eyes and lips; when the parasites enter the skin, swelling and redness (a chagoma) often develop. The term kissing bugs comes from the appearance of these symptoms that resemble skin changes that occur with prolonged kissing (hickies). In some individuals, the parasites eventually go into the bloodstream and lodge in various organs, especially the muscular structure of the organs. The parasites multiply and eventually cause chronic symptoms such as cardiac failure, arrhythmias, poor gastrointestinal motility, or death.

Humans who live in poor or primitive housing conditions that border or invade the habitats of Triatominae bugs cause a break in the normal life cycle of the insect vectors (bugs) and their usual hosts (over 100 types of animals), termed the sylvatic cycle. The bugs then enter the world of humans and their domesticated animals (cats, dogs) and transmit T. cruzi to them. When T. cruzi is transmitted from bugs to humans or human pets and back to the bugs, the life cycle is referred to as the domiciliary cycle. The life cycle of T. cruzi is complex; it has multiple developmental stages in both the insect vector (Triatominae bugs, also termed triatomine bugs) and mammalian (human and animal) hosts. The figure below from the CDC shows the developmental stages that occur in both the sylvatic and domiciliary cycles.

Life cycle of T. cruzi
Life cycle of T. cruzi. Image courtesy of the CDC.

T. cruzi has been reported to be transferred to humans from blood transfusions, organ transplantation, from mother to infant through the placenta, by ingestion, inhalation, and by laboratory accidents. Fortunately, these forms of transmission occur very infrequently.

Medically Reviewed by a Doctor on 7/29/2014

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