Medical expert of the article
New publications
American trypanosomiasis (Chagas disease)
Last reviewed: 05.07.2025
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
American trypanosomiasis (Chagas disease) is a transmissible natural focal protozoan disease, characterized by the presence of acute and chronic phases during the process.
In 1907, the Brazilian physician Chagas discovered the pathogen in triatomine (kissing) bugs, and in 1909 he isolated it from the blood of a patient and described the disease it caused, which was named Chagas disease in his honor.
[ Trypanosome development cycle
The development cycle of Tk cruzi occurs with a change of hosts: a) vertebrates (more than 100 species) and humans; b) a carrier of the pathogen (bugs of the subfamily Triatominae).
The development cycle in the vector takes place in the triatomine bug.
The invasive stage for the carrier, as well as for vertebrates and humans, are trypomastigotes. Since the piercing mouth apparatus, unlike the tsetse fly, is very weak in bedbugs and is not capable of piercing even human skin, they find abrasions or mucous membranes, conjunctiva, nasal membranes, lips (for which they received the name - kissing bug).
Bedbugs become infected when they feed on the blood of humans or animals containing trypomastigotes.
When entering the body of triatomine bugs (carriers of American trypanosomiasis), T. cruzi trypanosomes also reach the stomach of the insect, transform here into epimastigotes and multiply for several days. Then they pass into the hindgut and rectum, where they return to the trypomastigote form. From this moment on, the bugs become infectious. After or during the suction of blood, the bugs empty the rectum, and the pathogens get on the human skin or mucous membranes (conjunctiva, labial membranes, nose). In this regard, the causative agent of American trypanosomiasis belongs to stercorarial trypanosomiasis. The duration of the development cycle of parasites in the carrier is from 5 to 15 days, depending on the air temperature. A bug that has been infected once retains parasites for the rest of its life (about 2 years). Transovarial transmission is absent.
The invasive stage for the vertebrate host is the trypomastigote form. Transmission of the infection to humans and other warm-blooded animals occurs not directly through the bug bite, but through contamination of the bite wounds or mucous membranes with bug excrement containing trypanosomes. At the site of the bite, a "chagoma" is formed - the primary symptom of tryponasomiasis.
As a rule, bedbugs defecate directly during bloodsucking. Bedbug bites cause severe itching and inflammation, as a result of which parasites can be introduced into the wound during scratching. Cases of congenital trypanosomiasis have also been registered in humans.
After entering the body of a vertebrate animal (natural reservoir) or a human, trypomastigotes remain in the peripheral blood for some time, but do not multiply.
Then they penetrate muscle cells and endothelial cells of the lungs, liver, lymph nodes and other organs. However, parasites mainly accumulate in the cells of the heart muscle. Inside the cells, trypomastigotes are transformed into epimastigote and promastigote forms, and finally, at the end of the transformation, they turn into a rounded flagellate form - an amastigote, 2.5-6.5 μm in size, containing a round nucleus and a small oval-shaped kinetogiast. Inside the cell, amastigotes reproduce by binary fission.
A human or animal cell filled with amastigotes increases in size and turns into a pseudocyst, the membrane of which is the host cell wall. Before and immediately after the rupture of such a pseudocyst, the amastigote (bypassing the promastigote epimastigote stage) turns into a trypomastigote. The latter invade neighboring cells, multiply in the amastigote stage with the formation of new pseudocysts. Thus, amastigotes are purely intracellular parasites. Some of the trypomastigotes released from the pseudocyst and not entering neighboring cells enter the blood, where they circulate, and from there they can enter the carrier's body.
Epidemiology of American trypanosomiasis (Chagas disease)
The main carriers of the American tryponosomiasis pathogen are flying bugs: Triatoma megistis, Triatoma infestens, etc. These insects are distinguished by their bright coloring and relatively large size - 15-35 mm in length, they attack humans and animals at night. Transovarial transmission of trypanosomes from generation to generation does not occur in triatomine bugs.
The Chagas disease pathogen is transmitted by specific contamination. Trypanosomes excreted with bedbug feces during bloodsucking enter the human or animal body through damaged skin or mucous membranes of the eyes, nose, and mouth near the bite site. Trypanosomiasis can also be transmitted by food (including mother's milk) and blood transfusions.
It has now been established that transplacental transmission of T. cruzi is also possible, but its level is relatively low: on average, 2-4% of infected children are born to sick mothers. The mechanism of the protective action of the placenta has not been fully studied.
Synanthropic and natural foci of Chagas disease are known. In foci of the first type, bugs live in adobe houses, barns, poultry houses, and burrows of house rodents. Especially many, up to several thousand bugs (with infection rates reaching 60% and higher), are found in adobe huts. In synanthropic foci, in addition to humans, reservoirs of the pathogen are dogs, cats, pigs, and other domestic animals. According to available data, the infection rate of dogs in synanthropic foci in certain areas of Brazil is 28.2%, in Chile - 9%, cats - 19.7% in Brazil, and 12% in Chile.
In natural foci, reservoirs of the pathogen are armadillos (they do not get sick themselves), opossums (the most important, since they have a high parasitemia index), anteaters, foxes, monkeys, etc. In Bolivia and some areas of Peru, guinea pigs, which the population keeps at home for food, have a certain significance as a reservoir of T. cruzi. Their natural infection rate reaches 25-60%.
People become infected when visiting such foci during the warm season, when the carriers are active. In natural foci, men are more often infected. In general, Chagas disease is recorded throughout the year in all age groups, but more often in children. Sporadic cases are more common, but epidemic outbreaks are possible with mass attacks of infected triatomine bugs on people.
Chagas disease is widespread and is found in virtually all countries of the American continent from 42° N to 43° S. Particularly active and persistent natural foci of the disease are located in Latin American countries south of Mexico, with the exception of the Caribbean islands, Belize, Guyana, and Suriname. Isolated cases of American trypanosomiasis have been described in the United States (Texas). The infection is most frequently recorded in Brazil, Argentina, and Venezuela; it is also found in Bolivia, Guatemala, Honduras, Colombia, Costa Rica, Panama, Paraguay, Peru, El Salvador, Uruguay, Chile, and Ecuador. The infection does not occur in other parts of the world. Chagas disease may be more widespread than is commonly believed. More than 35 million people live at risk of infection with T. cruzi. According to preliminary estimates, at least 7 million of them are infected.
What causes American trypanosomiasis (Chagas disease)?
American trypanosomiasis, or Chagas disease, is caused by Trypanosoma cruzi, which differs from the causative agents of African trypanosomiasis by its shorter body length (13-20 µm) and larger kinetoplast of trypomastigote forms. In fixed blood preparations, Tr. cruzi often has a curved shape, like the letters C or S (C- and S-forms).
The causative agent of American trypanosomiasis belongs to the class Stercoraria (Latin stercus - feces, oralis - oral), and the disease American trypanosomiasis (Chagas disease) - to stercoraria trypanosomiasis, thus the causative agent is transmitted through the feces of the bug - the carrier. In addition, Tr. cruzi is characterized by persistence (Latin persistere - to remain, to persist) - the ability of the parasite to remain in the host's body throughout life with the development of resistance (stability) to reinvasion (repeated infection). At the same time, trypanosomes continue to slowly multiply throughout the life of the host in the cells of some tissues.
Pathogenesis of American trypanosomiasis (Chagas disease)
T. cruzi parasitize and reproduce in the body of a human and vertebrate host, first in the macrophages of the skin and subcutaneous tissue, then in the regional lymph nodes, and then in all organs. Thus, when trypanosomes are introduced, a local tissue reaction develops in the form of cell destruction, infiltration and tissue edema, then the regional lymph nodes increase in size. The next stage of pathogenesis is parasitemia and hematogenous dissemination of trypanosomes with subsequent localization in the tissues of various organs, where the pathogens reproduce. The heart, skeletal and smooth muscles, and the nervous system are most often and severely affected. In the acute stage of the disease, parasitemia is quite massive in the early stages, but over time its intensity decreases, it is detected only periodically, and in the late stages of the chronic stage - in rare episodes. There is, however, an opinion that in the absence of treatment, parasitemia persists for life.
Gradually, the next most important stage of the pathogenesis of American trypanosomiasis comes to the fore - allergic and autoimmune processes, as well as the formation of immune complexes. As a result of the pathogenic action of trypanosomes and their decay products, specific sensitization and autoallergy, inflammatory, infiltrative and degenerative changes in the cells of internal organs, the central and peripheral nervous systems occur.
The most affected organ in Chagas disease is the heart. In the acute stage of infection, a widespread interstitial inflammatory process develops in the myocardium with edema and destruction of myofibrils and infiltration by neutrophilic leukocytes, monocytes and lymphoid cells. Muscle cells adjacent to the infiltrate may undergo degenerative degeneration. In the chronic stage of Chagas disease, steady myocytolysis and fibrosis occur in the heart muscle, and cellular infiltration persists or increases.
In some patients infected with T. cruzi (more often in younger children), acute specific meningoencephalitis develops in the brain with mononuclear infiltration of the pia mater, perivascular inflammatory reactions, sometimes simultaneously with hemorrhage and glial proliferation.
The structures of the ganglia of the autonomic nervous system are seriously affected, which leads to disorders of the innervation of internal organs. Damage to the peripheral elements of the autonomic nervous system aggravates the disturbance of cardiac activity and is the cause of the occurrence of mega-organs in the gastrointestinal tract (megaesophagus, megagastrium, megacolon), urinary system, etc.
Symptoms of American Trypanosomiasis (Chagas Disease)
The incubation period of American trypanosomiasis (Chagas disease) is considered to be between 1 and 2 weeks. At the site of parasite inoculation, an inflammatory reaction occurs - "chagoma". In case of parasite penetration through the skin, the primary local inflammation resembles a non-suppurating furuncle. When penetrating through the mucous membrane of the eye, edema, conjunctivitis, and puffiness of the face - Romagna's symptom - occur. Local lymphangitis and lymphadenitis develop later.
General symptoms of American trypanosomiasis (Chagas disease): fever of a constant or remittent type with an increase in temperature to 39-40 °C, general adenopathy, hepatosplenomegaly, edema, sometimes macular rash. These clinical symptoms occur against the background of acute myocarditis and irritation of the meningeal membrane. Such symptoms of American trypanosomiasis (Chagas disease) are usually observed in endemic areas in children. Moreover, the severity of the course is more pronounced, the younger the patient. About 10% of cases end fatally as a result of progressive meningoencephalitis or severe myocarditis with heart failure.
After the acute period, the disease American trypanosomiasis (Chagas disease) passes into the chronic stage. The symptoms of this stage are vague. Often, the disease is asymptomatic for many years. Depending on the severity of the damage to the autonomic system and heart, symptoms of heart failure come to the fore, as well as the development of megaesophagus, megaduodenum, megacolon or megasigmoid with corresponding symptoms.
Diagnosis of American trypanosomiasis (Chagas disease)
In the acute stage, parasites are easily detected by microscopy of peripheral blood preparations. Along with stained fixed preparations, a crushed drop of blood can be examined, with mobile parasites clearly visible under a microscope. In the chronic stage, microscopy is ineffective.
Diagnosis of American trypanosomiasis (Chagas disease) uses serological reactions, most often - RSC with an antigen from the heart affected by trypanosomes. Xenodiagnostics has become widespread in endemic areas - feeding uninfected triatomine bugs on a patient with subsequent examination of the insect excrement in order to detect parasites. Isodiagnostic testing - inoculation of the patient's blood with laboratory animals, and an intradermal test with "crucin" (inactivated culture of T cruzi) are also used.
Who to contact?
Treatment of American trypanosomiasis (Chagas disease)
Specific treatment for American trypanosomiasis (Chagas disease) is not well developed. Nitrofuran derivatives are somewhat effective in the acute stage, especially during the "chagoma" period. Sometimes, in cases of megacolon, surgical treatment is indicated.
How to prevent American trypanosomiasis (Chagas disease)?
American trypanosomiasis (Chagas disease) can be prevented by using persistent contact insecticides to kill the bugs that carry it. Home improvement. Due to the presence of asymptomatic carriers in endemic areas, serological and xenodiagnostic testing of donors is mandatory.