Chagas Disease (cont.)
Charles Patrick Davis, MD, PhD
Charles Patrick Davis, MD, PhD
Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.
Melissa Conrad Stöppler, MD
Melissa Conrad Stöppler, MD
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
In this Article
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 7.7-15 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 subfamily 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. Image courtesy of the CDC. (Note that the human stages can occur in dogs, cats, and other mammals, while under experimental conditions, bedbugs can replace the triatomine bug stages and infect mice.)
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. Researchers have demonstrated (Nov. 2014) that in experimental conditions, bedbugs may become infected with T. cruzi from infected mice and then are able to reinfect mice, but human infection by bedbugs has not been documented to date.
Medically Reviewed by a Doctor on 12/10/2014
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