Chagas Disease (American Trypanosomiasis)

Updated: Jul 06, 2023
Author: Louis V Kirchhoff, MD, MPH; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD 



Chagas disease, also known as American trypanosomiasis, is caused by infection with the protozoan parasite Trypanosoma cruzi. The organism T cruzi and infection in humans were first described in 1909 by the Brazilian physician Carlos RJ Chagas.[1]  T cruzi mostly is found in blood-sucking triatomine insects (kissing bugs) and small mammals in a sylvatic cycle that is enzootic from the southern and southwestern United States to central Argentina and Chile. T cruzi infection in humans occurs in a spotty distribution throughout the range of the sylvatic cycle.

New cases of vector-borne T cruzi infection usually occur in persons who live in primitive houses in areas where the sylvatic cycle is active. The living quarters are invaded by infected triatomines, which become domiciliary. Infected insects take blood meals from humans and their domestic animals and deposit parasite-laden feces. The parasites then are transmitted via contact with breaks in the skin, mucosal surfaces, or the conjunctivas. Transmission also can occur congenitally, via blood transfusion and organ transplantation, and by ingestion of food and drink contaminated with feces from infected bugs. A couple dozen cases of T cruzi transmission via laboratory accidents have been reported, but none recently.[2]

T cruzi infection is life-long. A minority of persons with long-standing T cruzi infection develop the serious cardiac and gastrointestinal problems that characterize chronic symptomatic Chagas disease.

The parasite

T cruzi is a member of the family Trypanosomatidae in the order Kinetoplastida and belongs to a special section called Stercoraria. The infective forms of T cruzi are contained in the feces of the insect vectors and gain entry into its mammalian hosts through contamination. This mechanism of transmission contrasts with that of the two subspecies of African trypanosomes that cause human disease, Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense, which are transmitted via the saliva of their vectors, and with the mechanism by which a nonpathogenic trypanosome found in the Americas, Trypanosoma rangeli, is transmitted to its mammalian hosts.

As with other parasites that infect both mammalian and insect hosts, the life cycle of T cruzi is complex (see image below).

Life cycle of triatomines. Courtesy of the CDC. Life cycle of triatomines. Courtesy of the CDC.

The T cruzi life cycle consists of 3 main developmental forms. Epimastigotes are an extracellular and noninfective form of the parasite found in the midgut of insect vectors, where they multiply by binary fission. As epimastigotes (depicted in the first image below) move to the hindgut, they differentiate into metacyclic trypomastigotes (depicted in the second image below), which are nondividing forms resistant to mammalian complement that have the capacity to infect mammalian cells. They enter local cells through breaks in the skin, mucous membranes, or the conjunctivas and transform into the third morphologic form, amastigotes. Amastigotes multiply intracellularly until the host cell is overwhelmed, at which point they transform into bloodstream trypomastigotes.

Chagas disease (American trypanosomiasis). The try Chagas disease (American trypanosomiasis). The trypomastigote is the infective flagellated form of the parasite found in the blood of the mammalian hosts (blood trypomastigote) and in the hindgut of vectors (metacyclic trypomastigote). Image courtesy of Peter Darben, MD.


Chagas disease (American trypanosomiasis). The epi Chagas disease (American trypanosomiasis). The epimastigote form of Trypanosoma cruzi is the multiplying stage of the parasite that grows in the gut of the insect vector and also in cell-free culture medium as shown here. Image courtesy of Peter Darben, MD.

As the host cells rupture, the trypomastigotes are released into the lymphatics and bloodstream, through which they spread to distant sites and invade new host cells. See image below.

Trypanosoma cruzi trypomastigotes in a mouse blood Trypanosoma cruzi trypomastigotes in a mouse blood smear (Giemsa, x625). Courtesy of Dr. Herbert B Tanowitz, New York, NY.

This process continues asynchronously for the life of the host. Small numbers of trypomastigotes may be ingested in blood meals taken by uninfected triatomines. The trypomastigotes then transform into epimastigotes in the midgut of these insects, thus completing the cycle.

T cruzi also can be transmitted when mammalian hosts ingest infected insects, and this mechanism of transmission may play a major role in maintaining the sylvatic cycle.

Numerous biological, biochemical, and molecular studies have shown that the population of T cruzi is highly diverse.[3, 4, 5, 6, 7, 8, 9]  Although T cruzi is a diploid organism in which some genetic exchange may occur in insect vectors,[10] its genetic and phenotypic diversity is thought to result from the clonal multiplication of the epimastigote and amastigote forms. The consensus is that T cruzi can be divided into 6 discrete taxonomic units (DTUs; TcI through TcVI). The strains in each DTU show variability in geographic, epizootic, epidemiologic, and pathogenic characteristics.[11] Unfortunately, no clear associations have been found between the strain groups and pathogenicity or drug susceptibility. In general, the extensive genetic and, more recently, proteomics data generated so far, including the framework of the DTUs, have not yet led to new tools to reduce transmission, advances in the management of clinical disease, new drugs, or a vaccine. In the area of diagnosis, however, the results of molecular work on T cruzi have led to the development of highly accurate assays that are used widely to detect T cruzi infection. 

Vectors of T cruzi

Triatomines, which transmit T cruzi, belong to the family Reduviidae in the order Hemiptera. Reduviidae has 22 subfamilies, including the Triatominae.[12, 13] Although the vectors of T cruzi occasionally are referred to as reduviids, this term is not appropriate since the vast majority of the species in the family Reduviidae are phytophagous or insectivorous and do not transmit the parasite.

All triatomine species are able to transmit T cruzi to humans, but only a handful become domiciliary to any great extent and are important as T cruzi vectors. Many more triatomine species are involved in the widespread sylvatic cycles. Triatomines have 5 nymphal stages (instars), all of which can harbor and transmit T cruzi.

The three vector species most important in the transmission of T cruzi to humans include Triatoma infestans, Rhodnius prolixus (see image below), and Triatoma dimidiata. Historically, T infestans has been the most important by far, as it has been the primary vector in the sub-Amazonian endemic regions. Since the early 1990s, under the aegis of the Southern Cone Initiative (SCI), which is supported by the World Health Organization (WHO) and the Pan American Health Organization (PAHO), Chagas disease control programs in Argentina, Bolivia, Brazil, Chile, Paraguay, and Uruguay have focused on eliminating domiciliary T infestans. 

Rhodnius prolixus, a common vector of Trypanosoma Rhodnius prolixus, a common vector of Trypanosoma cruzi. Eggs, first- and second-stage nymphs, and adult.

These efforts have been widely successful, so much so that Uruguay (1997), Chile (1999), and Brazil (2006) have been declared free of vector‑borne transmission.[14, 15]

Major progress in vector control also has been achieved in Argentina, Paraguay, and Bolivia. Programs similar to the SCI have been implemented in the Andean nations and Central America, where R prolixus typically is found.[16, 17] The range of T dimidiata is similar but also extends far into Mexico. Other domiciliary species occupy more restricted areas and play less-important roles in the transmission of T cruzi to humans. The sylvatic species can colonize human dwellings and thus present a potential risk for transmission. 

Mammalian hosts of T cruzi

T cruzi infection has been found in more than 100 mammalian species throughout the range mentioned above, which includes the southern and southwestern United States. Mammals typically involved in sylvatic cycles of transmission include opossums, armadillos, raccoons, monkeys, wood rats, and coyotes, among many others.[18, 19, 20, 21, 22, 23, 24]

Pets such as dogs and cats can become infected in enzootic regions, likely as they eat parasitemic prey or ingest infected insects.[25, 26, 27] It is of interest that Carlos Chagas observed T cruzi in the blood of wild marmosets and a domestic cat before he discovered the parasite in the blood of his first infected patient, Berenice. In some situations, dogs have been shown to be an important link in the maintenance of the domiciliary cycle and consequent transmission to humans.[28]

Livestock occasionally have been found to be infected with T cruzi, but the parasite is not known to adversely affect their health. Birds, amphibians, and reptiles are naturally resistant to T cruzi infection. In some situations, however, birds may be important sources of blood meals for triatomines.

The modes of transmission of T cruzi to humans

Historically, most transmission of T cruzi to humans has resulted from the contamination of vulnerable surfaces (eg, breaks in the skin, mucosae, and the conjunctivas) with the feces of infected vectors. However, as noted, vector-borne transmission has been reduced markedly in many endemic countries. Transfusion transmission was a major public health problem in endemic countries for decades, but, as accurate serologic assays for T cruzi infection were developed and screening of blood donors became mandatory and were implemented throughout the endemic range, this problem essentially has been eliminated.[29]

Not surprisingly, T cruzi can be transmitted via transplantation of organs obtained from persons with chronic infection, and occasional reports of this in Latin America[30] and in the United States[31, 32, 33, 34] have appeared.

The rate of congenital (transplacental) transmission from mothers with chronic T cruzi infection to their newborns is about 5%, with a range of 2-10% in various studies.[35] To date, no measures have been defined to reduce or eliminate this form of transmission. As transmission by vectors and through transfusion of contaminated blood have been reduced, the proportion of new T cruzi infections that result from congenital transmission has increased. Nonetheless, the total number of instances of congenital transmission certainly has decreased as seroprevalence rates have fallen.[36, 37, 38, 39, 40]

In contrast to Toxoplasma gondii, vertical transmission of T cruzi is possible with successive pregnancies. Transmission of T cruzi via human milk appears to be extremely rare, and chronic T cruzi infection is not a contraindication to breastfeeding.[41] Several instances of transmission of T cruzi to groups of people via ingestion of food or drink presumably contaminated with the feces of infected vectors have been reported.[42, 43, 44] Finally, the facility of producing infective forms of T cruzi in the laboratory has resulted in occasional accidental transmissions in this context, but none have been reported in many years.[2, 45]  


An inflammatory lesion called a chagoma caused by T cruzi may appear at the site of entry in patients with acute Chagas disease. Histologic changes may include interstitial edema, lymphocytic infiltration, and reactive hyperplasia of adjacent lymph nodes due to intracellular parasitism of muscle and other subcutaneous tissues. When parasitized host cells rupture, trypomastigotes are released and often can be detected by microscopic examination of anticoagulated blood. As the infection spreads systemically, muscles, including the myocardium, and various other tissues become parasitized.[46]

Acute myocarditis, consisting of patchy areas of necrosis and infected cells, may develop (see image below).[47, 48] The pseudocysts occasionally seen in sections of infected tissues are intracellular aggregates of amastigotes. The patent parasitemias of the acute illness may be accompanied by lymphocytosis, and transaminase levels may be elevated. The cerebrospinal fluid may contain parasites.[49]  

Trypanosoma cruzi in heart muscle of a child who d Trypanosoma cruzi in heart muscle of a child who died of acute Chagas disease in Texas. (H&E, x900).

The heart is the most commonly affected organ in persons with chronic Chagas disease.[50, 51, 52, 53] Autopsy may reveal marked bilateral ventricular enlargement, often involving the right side more than the left, in the heart of patients who die of chagasic heart failure (see image below). The ventricular walls often are thin, and mural thrombi and apical aneurysms may be present. In addition, diffuse interstitial fibrosis, widespread lymphocytic infiltration, and atrophy of myocardial cells all may be present.

Chest radiograph of a Bolivian patient with chroni Chest radiograph of a Bolivian patient with chronic Trypanosoma cruzi infection, congestive heart failure, and rhythm disturbances. Pacemaker wires can be seen in the area of the left ventricle.

T cruzi parasites rarely are found during microscopic examination of stained sections of myocardial tissue; however, in numerous studies, T cruzi ‑specific polymerase chain reaction (PCR) assays have demonstrated parasites in areas of focal inflammation.[54, 55] Pathologic changes in the conduction systems of chronic chagasic hearts are common and often correlate with dysrhythmias.[56] Chronic inflammatory lesions and dense fibrosis frequently involve the right branch and the left anterior branch of the bundle of His, but lesions also may be found in other segments of the conduction system.

Salient features on gross examination of the colon or esophagus in patients with chronic chagasic gastrointestinal disease (megadisease) include dilatation and muscular hypertrophy of the affected organs (see images below).[57, 58, 59] Focal inflammatory lesions with lymphocytic infiltration are visible on microscopy. The number of neurons in the myenteric plexus often is markedly reduced, and periganglion and intraganglion fibrosis with accompanying Schwann cell proliferation, along with lymphocytosis, are present in most patients with megadisease. The functional effects of this parasympathetic denervation generally are limited to the esophagus or colon, although clinically manifest dysfunction of the ureters, biliary tree, and other hollow viscera has been reported.[60]

Barium swallow radiographic study of a Brazilian p Barium swallow radiographic study of a Brazilian patient with chronic Trypanosoma cruzi infection and megaesophagus. The markedly increased diameter of the esophagus and its failure to empty are typical findings in patients with megaesophagus caused by Chagas disease. Courtesy of Dr. Franklin A. Neva, Bethesda, MD.
Air-contrast barium enema of a Bolivian patient wi Air-contrast barium enema of a Bolivian patient with chronic Chagas disease and megacolon. The markedly increased diameters of the ascending, transverse, and sigmoid segments of the colon are readily apparent.

The pathogenesis of cardiac and gastrointestinal lesions of chronic Chagas disease was a focus of debate for decades. Beginning more than 20 years ago, however, convincing evidence has shown that low levels of parasites in chronically affected tissue, detectable with molecular methods, provoke a chronic inflammatory response that eventually leads to the pathologic changes observed microscopically and organ dysfunction.[54, 55, 61]  



United States

Despite the presence of the sylvatic cycle of T cruzi transmission in the southern and southwestern United States, only 23 cases of autochthonous transmission of the parasite have been reported.[47, 62]  Although some cases of T cruzi infection probably go unnoticed or unreported, autochthonous acute Chagas disease is rare in the United States. This concept is supported by the extreme rarity of T cruzi infection among US blood donors who were not born in or who have not traveled extensively in endemic countries.[63, 64, 65] The rarity of vector‑borne transmission of T cruzi to humans in the United States likely is due to the overall sparsity of vectors and the generally higher housing standards, which help prevent the vectors from becoming domiciliary. Despite this, triatomine insects have recently been reported as far north as Delaware[66] and the Carolinas.[67]

In contrast, the epidemiology of chronic T cruzi infection in the United States has changed markedly in the last few decades owing to the large number of people who have moved here from endemic countries. According to one recent estimate, 23 million persons from the endemic countries now live in the United States, 288,000 of whom have chronic T cruzi infection.[68, 69]  Approximately two thirds of these immigrants are from Mexico, where the overall prevalence of T cruzi infection is 0.5-1%.[70, 71]  Imported cases of acute Chagas disease are extremely rare.[72]

Five cases of transfusion-associated transmission of T cruzi were reported in the United States prior to the implementation of donor screening in 2007,[73] all of which occurred in immunocompromised patients.[74] Two additional such cases were found through trace-back studies after screening started.[75]

Two FDA‑approved tests are available for screening US blood donors for Chagas disease: the Ortho T cruzi ELISA Test System (Ortho Clinical Diagnostics, Rochester, NY)[76, 77] and the Abbott Prism/Alinity Chagas assay (Abbott Laboratories, Abbott Park, IL).[78] Donor samples positive in either of the two screening assays generally undergo confirmatory testing with the Abbott Enzyme Strip Assay (ESA) Chagas, which is the only FDA‑approved option for this purpose.[79, 80] The Chagas RIPA,[81, 82] which was used with FDA approval for confirmatory testing from 2007-2014, no longer is available for this purpose.

The data accumulated during the first 3 years of testing in the United States indicated that about 1 in every 13,000 US blood donors is infected with T cruzi (ie, repeat reactive in the Ortho or Abbott screening assays and positive in the Chagas RIPA or the Abbott ESA),[83] which is consistent with estimates made prior to the initiation of screening by groups familiar with the epidemiology of T cruzi in the United States. No instances of transfusion transmission of T cruzi in the United States are known to have occurred since donor screening was implemented.

Five recipients of organ transplants from 3 donors with T cruzi infection developed acute Chagas disease in the United States, one of whom died of the illness.[31, 32]  


T cruzi is endemic in Mexico and all the countries of Central America and South America. The Caribbean Islands are not endemic. In 2023, PAHO/WHO estimated that a total of 7 million people are infected with T cruzi and that about 12,000 deaths each year can be attributed to Chagas disease. The total number of new T cruzi infections per year was estimated to be 30,000, fully 9,000 of which result from congenital transmission.  Moreover, emigration of millions of people from endemic countries to nonendemic regions has resulted in several hundred thousand T cruzi–infected persons living in the latter areas, particularly in the United States and Europe.[84, 85, 86, 87, 88, 89, 90]  To give a country‑specific perspective on the relative prevalence rates, in 2007, PAHO published the following data regarding the countries most affected by Chagas disease: Bolivia (6.8% prevalence); Argentina (4.1%); El Salvador (3.4%); Honduras (3.1%); Paraguay (2.5%); Guatemala (2%); Ecuador (1.7%); French Guyana, Guyana, and Surinam (1.2%); Venezuela (1.2%); Nicaragua (1.1%); Brazil (1%); and Mexico (1%).[91]

As noted above, in recent years, the epidemiology of T cruzi infection has improved markedly in many endemic countries, as blood bank and vector-control programs have been implemented. Because of the success of programs directed at domiciliary vector programs, prevalence rates in younger age groups have been decreasing substantially in many areas.[14, 15, 92, 93, 94, 95] All endemic countries have adopted statutory or regulatory mandates for screening donated blood for T cruzi, the most recent of which was Mexico.[29, 96]

In the author’s view, the enormous progress made in controlling Chagas disease in recent decades clearly indicates that the obstacles hindering the complete interruption of T cruzi transmission to humans are primarily economic and political. In this context, no additional major advances, such as a more detailed understanding of the pathogenesis of Chagas disease,[97, 98] further genetic analyses,[99, 100, 101, 102, 103, 104]  novel diagnostic approaches, or breakthroughs in vaccine development,[105] appear to be necessary for its completion. 


Most of the estimated 12,000 deaths attributable to Chagas disease are due to chronic heart disease[51, 53, 106, 107] or, less frequently, megadisease or meningoencephalitis.[108] In persons with chronic chagasic heart disease, mortality primarily is due to the rhythm disturbances and congestive heart failure that result from the chronic inflammatory cardiomyopathy driven by the persistent presence of parasites in heart tissue. Embolization of intraventricular clots to the cerebrum and lungs can also contribute to mortality.

Persons with severe megaesophagus who do not receive medical attention can die of malnutrition and/or chronic aspiration pneumonitis. Megacolon (depicted in the image below) also can result in death, usually when volvulus develops and is not resolved surgically.

Chagas disease (American trypanosomiasis). Megacol Chagas disease (American trypanosomiasis). Megacolon.


T cruzi infection does not have a racial predilection.


T cruzi infection does not have a sexual predilection.


Morbidity during the acute phase of Chagas disease is more pronounced in children than in adults. The gastrointestinal and cardiac manifestations of chronic T cruzi infection become apparent many years or even decades after initial infection and thus occur almost exclusively in adults. However, the lifetime risk for the development of such symptoms in chronically infected persons is only 10-30%.[109, 110]




Incubation period

The incubation period of vector-borne acute Chagas disease is thought to be 7-14 days, but definitive data are not available because persons who live in areas of active transmission are generally continually at risk for exposure to the vectors. Although newly infected persons may be aware that their living quarters are infested by triatomine vectors, most blood meals are taken while people are asleep, so they are unlikely to recall being bitten.

The incubation period of acute T cruzi infection acquired through blood transfusion may be somewhat longer, but precise data are also lacking in this regard. 

Acute phase

In most instances of acute T cruzi infection, a specific diagnosis is not made because of the nonspecific nature of the signs and symptoms and because most cases occur in poor people who have limited access to medical care.

Acute Chagas disease carries a mortality rate of less than 5%. However, even this is likely a high estimate, since acute Chagas disease rarely is diagnosed specifically; thus, the denominator for the calculation of the fatality rate is not known. As noted above, death typically is caused by myocarditis[47, 111] and, less commonly, by meningoencephalitis.[112]

Some persons develop bothersome inflammatory lesions at the bite sites presumably caused by the injected salivary proteins, but their presence is not necessarily indicative of T cruzi infection.[113, 114, 115, 116, 117]  

In the vast majority of persons with acute Chagas disease, the manifestations resolve spontaneously within 4-8 weeks. This is followed by the chronic indeterminate (asymptomatic) phase of the disease (see image below).

Natural course of American trypanosomiasis. Courte Natural course of American trypanosomiasis. Courtesy of Dr. Patricia Paredes, Guadalajara, Jal., Mexico.

Indeterminate phase

By definition, the indeterminate phase of Chagas disease does not involve symptoms.

Most adults with T cruzi infection are unaware of their parasitosis, and a history consistent with acute Chagas disease from years prior rarely is given.

Persons who are diagnosed with indeterminate Chagas disease typically are identified through blood-donor screening or pre-employment serologic testing. 

Chronic symptomatic Chagas disease

Ten to 30% of persons with chronic indeterminate Chagas disease develop clinical manifestations due to the infection. The most common and serious problems are cardiac, which are caused by an inflammatory cardiomyopathy that results from the persistent presence of the parasites in the heart.

Cardiac symptoms

A wide variety of atrial and ventricular rhythm disturbances, including right bundle branch block, left anterior hemiblock, and third-degree atrioventricular block can result in palpitations, dizziness, syncope, and even sudden death.[118, 119]

Cardiomyopathy and consequent congestive heart failure can result in shortness of breath, decreased exercise tolerance, easy fatigability, lower-extremity edema, and nocturia, as well as other signs and symptoms.

Thromboembolism can result in stroke, as well as pulmonary and arterial embolization to areas other than the brain.[120, 121, 122]

Gastrointestinal symptoms

The gastrointestinal symptoms associated with chronic T cruzi infection typically result from denervation of hollow viscera and consequent dysfunction.

Megaesophagus is the most common anatomic finding and typically results in symptoms similar to those of achalasia, such as dysphagia, odynophagia, substernal discomfort, and a sensation that ingested food and liquids do not move forward properly.

Megacolon usually results in constipation and pain, and some affected patients can go for long periods between bowel movements. In advanced cases, bowel obstruction and/or volvulus can occur, requiring surgical treatment.

Gastric dilatation in patients with Chagas disease has been described, as has megaureter, but these manifestations are relatively rare. 


Acute phase

Symptoms of acute Chagas disease may include malaise, anorexia, myalgia, and headache, but many recently infected persons are asymptomatic.

Intermittent fevers occur, but they do not follow a specific pattern.

Some patients have lesions at the portal of entry of the parasites. Romaña sign (unilateral painless periorbital and palpebral edema) occurs when the parasites have contaminated the conjunctivae. Romaña sign is viewed as a classic sign of acute Chagas disease but develops in few newly infected persons. A chagoma, which is an indurated inflammatory skin lesion, may develop when parasites enter through a break in the skin. Romaña sign and chagomas may persist for several weeks. The lymph nodes that drain either of these lesions may be enlarged.

Hepatomegaly and splenomegaly may occur in children with acute Chagas disease, often accompanied by generalized lymphadenopathy.

Varying degrees of generalized edema may occur in acutely infected persons, particularly children.

Some patients with acute T cruzi infection develop a nonpruritic morbilliform rash called schizotrypanides.

Persistent tachycardia may be present.

Signs of acute myocarditis and resulting heart failure may develop in a small minority of patients with acute Chagas disease.[46, 47, 48]

Neurologic dysfunction may develop in acutely infected children with meningoencephalitis.[123]  

Chronic phase

Any of the physical findings of acute T cruzi infection can occur in chronically infected persons in whom the infection is reactivating due to natural (HIV infection) or iatrogenic immunosuppression.[124, 125, 126, 127, 128, 129, 130, 131, 132]  In such patients reactivation of the indolent T cruzi infection can occur in a manner and with a severity not seen in immunocompetent persons.[133, 134]

Chronic chagasic cardiomyopathy may manifest as the following:

  • Signs of congestion due to isolated left-sided heart failure may be present in the early stages of chronic chagasic cardiomyopathy. Biventricular failure with peripheral edema, hepatomegaly, ascites, and pulmonary congestion are more common in the later stages.
  • Signs of thromboembolism may appear, mostly with embolization to the brain, lungs, and extremities.

Chronic chagasic megaesophagus may manifest as the following:

  • Weight loss and, in severe cases, cachexia
  • Hypertrophy of the salivary glands
  • Pneumonitis related to regurgitation and aspiration of the food retained in the esophagus or stomach (particularly during sleep)
  • Erosive esophagitis, with increased risk for esophageal cancer

Chronic chagasic megacolon may manifest as the following:

  • Abdominal distention
  • Fecaloma
  • Signs of intestinal occlusion, sigmoid volvulus


It is not known which parasite characteristics or host factors cause some persons with chronic T cruzi infection to develop clinically apparent cardiac and gastrointestinal lesions (10‑30%), while others remain infected for life but do not develop symptoms related to the infection. This pattern of variable clinical penetrance is not particularly surprising, however, since it is similar to that observed in most other infectious diseases. Parasite strain, host immunogenetics, nutrition, age at first infection, other medical conditions, and various other factors may play roles in the pathogenesis of chronic symptomatic Chagas disease. There are no reliable predictors of whether an infected person in the indeterminate phase of T cruzi infection is likely to develop symptomatic disease, although this is an active area of research.[135, 136, 137, 138]  





Approach Considerations

The flowchart below depicts the management of risk for congenital Chagas disease.

Footnote 1. Mexico, as well as all nations of Cent Footnote 1. Mexico, as well as all nations of Central and South America, are endemic for Chagas disease. Chagas disease is not endemic in any of the Caribbean Islands. Women who were born in Chagas endemic countries or who have resided therein for a substantial period are at geographic risk for having Chagas disease and should be screened serologically.{Edwards MS, Montgomery SP. Congenital Chagas disease: progress toward implementation of pregnancy-based screening. Curr Opin Infect Dis. 2021 Oct 1. 34 (5):538-545}. In addition, women who are not themselves at geographic risk but whose mothers are at such a risk and are not known to be seronegative are in turn considered to be at risk for Chagas disease. Footnote 2. The two approaches useful in this regard are microscopic examination of anticoagulated blood and polymerase chain reaction (PCR). Serologic testing of newborns is not useful because assays for specific immunoglobulin G (IgG) will yield a positive result, reflecting the mother’s chronic infection, and because immunoglobulin M (IgM) assays lack acceptable levels of sensitivity and specificity. Footnote 3. All children born to at risk women should be tested serologically since several studies indicate that the rate of congenital Chagas disease in babies born to infected mothers is 2%-10%. Footnote 4. The latter should include periodic monitoring for signs and symptoms of chronic cardiac and gastrointestinal Chagas disease followed by appropriate interventions, when indicated. The usefulness of specific drug treatment in adults with chronic Trypanosoma cruzi infections has not been clearly demonstrated and is a matter of ongoing debate. Footnote 5. The parasitologic cure rate in babies with congenital Chagas disease approaches 100% when a full course of treatment is given during the first year of life. Footnote 6. The sensitivities of microscopic examination of anticoagulated blood and PCR are less than 100%. Thus, the occasional baby who tests negative in these approaches immediately after birth may actually be infected with T cruzi. Serologic testing for specific IgG should be delayed until maternal IgG has disappeared.

Laboratory Studies

The diagnosis of acute Chagas disease, which includes congenital Chagas disease and reactivation of chronic T cruzi infection in immunosuppressed persons, is based on direct detection of the parasites. In contrast, the diagnosis of chronic infection (indeterminate or chronic symptomatic phases) generally is based on serologic testing, since the low level of circulating parasites precludes microscopic detection and limits somewhat the sensitivity of PCR assays. 

Parasitologic diagnosis

One useful method for identification of parasites in the blood is to put 1.5 µL of anticoagulated blood under a 12-mm circular cover slip and examine 200 fields under 400 X magnification.[139] This allows for the examination of 0.44 µL of blood with each round, which should take about 30 minutes of careful looking. The mobile trypomastigotes are translucent; thus, they are usually detected based on the corresponding movement of RBCs they cause. This approach has no set threshold for deciding that the result is negative. Simply stated, the greater the number of fields examined, the greater the probability of detecting a parasite in an acutely infected person.

Stained thin and thick blood smears may also be examined microscopically. The author is not aware of any comparative data that shed light on the relative sensitivity of examining stained smears versus wet preparations, although the movement of the parasites in the latter would seem to be advantageous.

Another method of evaluation involves using heparinized microhematocrit tubes. This method has been used extensively to test for congenital Chagas disease in infants born to chronically infected mothers.[140] The tubes typically are filled directly from the source and spun. The buffy coat at the interface of the plasma and RBCs then is examined microscopically. The curvature of the tube makes this somewhat difficult, but this problem can be resolved by cutting the tube and examining the buffy coat as if it were fresh blood. This latter procedure carries a risk for accidental transmission and thus should be performed only by experienced personnel.

Indirect parasitologic methods include xenodiagnosis and hemoculture.

In xenodiagnosis, 30-40 laboratory-reared insects are allowed to feed directly or indirectly on the blood of a person suspected to have Chagas disease. At least 1 month later, intestinal contents of the insects are extracted and examined microscopically for the presence of parasites. Xenodiagnosis is tedious, requires a long time to perform, and yields a sensitivity of only 50% in the best of hands.

Hemoculture, which involves a specialized liquid culture medium that is not available commercially, takes roughly the same amount of time as xenodiagnosis and has roughly the same level of sensitivity, but it is less tedious.

Neither xenodiagnosis nor hemoculture has any reasonable role in the diagnosis of acute Chagas disease, since the results are not available in time for short-term treatment decisions. In addition, their role in diagnosing chronic T cruzi infection is largely limited because of their insensitivity. However, these tests may have a role in resolving borderline serologic results or in evaluating treatment failures. Both hemoculture and xenodiagnosis are viewed increasingly as historical oddities. 

Serologic diagnosis

Tests for anti– T cruzi immunoglobulin M (IgM) are not standardized, are not available commercially, and should play no role in the diagnosis of acute Chagas disease.

Serologic testing for specific IgG antibodies to T cruzi is the cornerstone of diagnosing chronic T cruzi infection.

Several dozen serologic assays are available in the endemic countries for testing clinical and donor specimens for chronic T cruzi infection. Several of these are available in nonendemic areas with substantial at‑risk immigrant populations. The most widely used today are indirect immunofluorescence (IIF), enzyme-linked immunosorbent assay (ELISA), and indirect hemagglutination, but assays based on other formats also are available. Most use lysates of epimastigotes as target antigens, but several are based on recombinant proteins.[82] At least a dozen rapid tests for diagnosing chronic T cruzi infection also have made it to market.[141]

To ensure accurate results, WHO Chagas experts and other authorities recommend that each specimen undergo testing with two types of assays, and this approach is generally followed for blood donor testing in endemic countries, although in Brazil a single‑assay testing protocol is used to screen donors.

In the United States, the Ortho T cruzi ELISA Test System and the Abbott Prism/Alinity Chagas Assay both are FDA‑approved for donor screening.[142]

From 2007 through 2014, the Chagas Radioimmune Precipitation Assay (Chagas RIPA) was performed by Quest Diagnostics for confirmatory testing of donor specimens that were repeat positive in the Ortho or Abbott screening assays.[81, 82] Currently, the Abbott Enzyme Strip Assay Chagas (ESA Chagas) is the only FDA‑approved assay available for confirmatory testing available in the United States. The Chagas RIPA is available for research and limited diagnostic testing in the author’s laboratory at the University of Iowa.[143]

Currently, in the United States four assays have FDA 510(k) approval for diagnostic testing for T cruzi infection: Hemagen Chagas’ Kit ELISA (Hemagen Diagnostics, Inc, Columbia, MD); Wiener Chagatest Recombinante v.3.0. ELISA (Laboratorios Wiener, Rosario, Argentina); InBios Chagas Detect Plus (CPD) rapid test lateral flow assay (LFA) (Inbios International, Inc, Seattle, WA), and as noted, the Ortho T cruzi ELISA test system (Ortho Clinical Diagnostics, Raritan, NJ).

Diagnosis via polymerase chain reaction assays

The use of PCR tests for detecting T cruzi has been studied extensively over the past 25 years, and dozens of articles have described this approach.[144, 145]

The use of many distinct primer pairs has been described; the accumulated evidence suggests that assays based on TCZ1/TCZ2 (nuclear repetitive sequence)[146] and S35/S35 (kDNA minicircle conserved region)[147] are the most sensitive.

Detailed methodologies for highly accurate PCR assays for T cruzi have been published.[148, 149, 150]  

Although PCR assays generally yield better sensitivity rates than xenodiagnosis or hemoculture, they are not sensitive enough to justify their use for primary or confirmatory testing of blood donors or in diagnostic settings. The variable sensitivity likely is due to the extremely low parasitemias in chronically infected persons, resulting in the small blood samples taken for DNA extraction not containing even a single parasite.

Nonetheless, there are several settings in which PCR assays for detecting T cruzi play an important role. The first is in chronically infected patients who have been treated with benznidazole or nifurtimox. In this instance, a positive PCR result indicates treatment failure, but, given the variable sensitivity, a negative test is not meaningful unless the assay is performed repeatedly. Secondly, PCR assays for T cruzi can play a role in detecting acute Chagas disease, particularly congenital T cruzi infection, since their sensitivities have been shown to be greater than microscopic examination in several contexts.[151, 152, 153, 154] Finally, PCR assays are the method of choice for detecting T cruzi infection in insect vectors[155, 156] and in food suspected of being contaminated with parasites.[157]

Imaging Studies

No imaging studies are specific for Chagas disease. However, the manifestations of Chagas disease (eg, cardiac, esophageal, and colonic dysfunction) should be evaluated with the appropriate imaging studies, as they would be when they result from any disease process. 

Other Tests

Electrocardiography and 24-hour continuous monitoring are the cornerstones of assessing possible dysrhythmias in patients with chronic T cruzi infection, as is the case with rhythm disturbances of any cause. Infected persons should undergo electrocardiography every 6-12 months to monitor for the development of ominous arrhythmias that would require management with drugs or pacemaker placement.

Esophageal manometry and endoscopy may be useful in assessing and managing patients with Chagas disease who have symptoms that suggest esophageal dysfunction. Endoscopy can be used to differentiate chagasic megaesophagus from other causes of esophageal dysfunction (eg, cancer). 



Medical Care

The goals of therapy in persons with Trypanosoma cruzi infection are to eliminate the parasites with specific drug treatment and to manage the signs and symptoms that result from the largely irreversible lesions associated with the disease. In 2017, benznidazole was approved by the FDA for the treatment of Chagas disease caused by T cruzi in children aged 2-12 years. Its safety and efficacy were established in two placebo-controlled clinical trials in children aged 6-12 years. In these trials, antibody test results changed from positive to negative in approximately 55-60% of children treated with benznidazole, compared with approximately 5-14% who received placebo. An additional study of the safety and pharmacokinetics of benznidazole provided information for dosing recommendations in children as young as 2 years.[158, 159]

Nifurtimox gained FDA approval in 2020 for pediatric patients (birth to younger than 18 years who weigh at least 2.5 kg) for the treatment of T cruzi infection. Approval for nifurtimox was based on the number of treated patients who became IgG antibody negative or who showed an at least 20% decrease in optical density on 2 different IgG antibody tests against antigens of T cruzi.[160]  No other drugs, either alone or in combination with nifurtimox or benznidazole, have been approved for treating T cruzi infection.[161, 162, 163]

For the most part, both benznidazole and nifurtimox are limited in their capacity to effect parasitologic cure, especially in chronically infected patients (see below). It merits mention that prescribing benznidazole or nifurtimox for patients who do not fall within the age ranges specified in their corresponding FDA approvals constitutes off‑label use.

Acute Chagas disease

Consistent with WHO 2022 and current CDC recommendations, all patients with acute Chagas disease, including infants with congenital infection and persons with reactivation of chronic infections due to immunosuppression, should be treated with either benznidazole or nifurtimox. Responses to treatment of patients with reactivation is best monitored by PCR assay.[164]

In general, the younger the patient and the closer to acquisition of the infection, the higher the probability of parasitologic cure. Babies with congenital Chagas disease have the greatest chance for cure. Data from Argentina show that the cure rate exceeds 90% if treatment is given within the first year of life.[165]  Some sources have stated that the overall parasitologic cure rate in persons with acute Chagas disease is 70%, but the author is unaware of specific data that support this estimate.

The usefulness of corticosteroids or interferon-γ in patients with acute Chagasic myocarditis or meningoencephalitis has not been established. 

Indeterminate-phase Chagas disease

The current evidence‑based consensus concerning treatment of T cruzi infection is that chronically infected children and adolescents up to 18 years of age should be treated with either benznidazole or nifurtimox. Convincing data from trials in Argentina and Brazil indicate that a substantial proportion of these patients will be cured parasitologically.[36, 166, 167]

In addition, there is broad agreement that all women of child‑bearing age should be given a full course of treatment. This recommendation is based on convincing evidence that has accumulated over the last decade indicating that the treatment of girls and women of child‑bearing age infected with T cruzi markedly reduces the probability of congenital transmission to their babies conceived after treatment.[168, 169, 170, 171, 172, 173, 174]

It is noteworthy that a substantial proportion of the girls and women in these trials treated prior to pregnancy likely were not cured parasitologically, and in some instances many years had gone by between the treatment and the pregnancies. These data indicate clearly that specific pre-pregnancy treatment of chronic T cruzi infection has a marked suppressive effect on the likelihood of subsequent congenital transmission, and it seems likely that treating all infected women of child-bearing age who are not pregnant will become the standard of care. In view of the potential fetal toxicity of benznidazole and nifurtimox, care must be taken to establish that chronically infected women are not pregnant when treatment is started and that they do not become pregnant during treatment.

In contrast to the largely good news related to the utility of treating children, adolescents, and women of child bearing age, the probability of parasitologic cure with a full course of either drug in adults with long-standing T cruzi infection, including persons in the indeterminate phase and those with manifest chagasic symptoms, most of whom presumably were infected while quite young, actually may be less than 10%.[175, 176, 177, 178, 179, 180, 181]  Moreover, determining which treated patients are cured is challenging, since treatment suppresses parasitemias, as reflected in reduced rates of positivity in post‑treatment PCR assays,[182]  as well as in xenodiagnosis and hemoculture. To further complicate this issue, levels of anti–T cruzi antibodies can remain positive for years even in cured patients.[149, 183]

Until recently, data from properly structured randomized clinical trials (RCTs) that assess the effect of specific treatment outcomes in chronically infected adults have been lacking. A detailed discussion of this issue took place in 2006 at a 2-day meeting convened by the CDC of an expert panel from several endemic countries and the United States, in which the author of this article was a participant. In the guidance document that resulted from that meeting,[166]  the panel recommended that treatment be offered to chronically infected adults with at most mild clinical disease, and that, after discussion of the risks and possible benefits, treatment decisions be shared by patients and caregivers. This tepid recommendation was accompanied by references to a review that summarized data suggestive of treatment efficacy from several studies[184]  and to the then recent report of a nonrandomized and unblinded benznidazole treatment trial that showed a hint of efficacy.[185]  An important background issue that was considered in the discussion of treatment efficacy at the meeting was the well-established observation that treatment of chronically infected persons generally suppressed parasitemias and prompted the hopeful assumption that this might lead to better clinical outcomes.

A major step forward in assessing the effect of specific treatment was taken in 2015 by the publication of the results of the Benznidazole Evaluation for Interrupting Trypanosomiasis (BENEFIT) trial.[186, 187]  In this blinded, placebo‑controlled trial of benznidazole versus placebo performed in Brazil, Argentina, Bolivia, and Colombia, 2,854 T cruzi–infected patients with mild cardiac disease were followed for a mean of 5.4 years. As expected, parasite detection as indicated by PCR assay was suppressed; however, benznidazole did not significantly reduce cardiac clinical deterioration or death rates. In view of these results and others published more recently,[188, 189]  specific treatment of adults with chronic T cruzi infection and mild cardiac disease cannot be recommended. Moreover, the BENEFIT results clearly showed that, at least in persons with mild cardiac disease associated with chronic T cruzi infection, suppression of parasitemias, which was clearly documented in the benznidazole arm, was not a marker for better clinical outcomes. In summary, a variety of heterogeneous trials that addressed the thorny issue of whether to treat patients with indeterminate T cruzi infection have been conducted both before and after BENEFIT, but unfortunately the question remains largely unresolved.[190]  Importantly, for technical reasons related to study design, no patients in the indeterminate phase of chronic T cruzi infection were included in the BENEFIT trial, and in the years since the report of the trial was published no convincing data from other RCTs have been published that address the question of the usefulness of treating indeterminate phase persons.[191]

To summarize the current institutional positions regarding the treatment of adults with indeterminate phase T cruzi infection, the recommendations of WHO 2022[192]  and PAHO 2023,[193]  are largely similar to those published following the 2006 CDC meeting.[166]  The lack of certainty of benefit, the long course of treatment, and the frequent and sometimes serious adverse reactions to benznidazole and nifurtimox all should be weighed carefully in the process of deciding to recommend treatment or not. A substantial proportion of patients treated with nifurtimox have bothersome side effects.[194]  Although nifurtimox lowers parasitemias and anti‑T cruzi antibody levels in a considerable proportion of treated patients, its long-term benefits have not been clearly established.[195, 196]  Finally, it merits recalling here that the FDA approvals of benznidazole and nifurtimox are limited to children and adolescents. This situation likely reflects the reality that the data suggesting that the treatment of adults with chronic T cruzi infection might be beneficial are of low quality, making any recommendations favoring treatment controversial.[197]

No information is available on which to base guidance for prophylactic treatment of chronic infection in persons who will undergo immunosuppression (eg, pre‑transplant) or in persons who are already immunosuppressed (eg, post‑transplant and persons with HIV).

Chronic symptomatic Chagas disease

There is a general consensus among Chagas experts that persons who have already developed cardiac or gastrointestinal symptoms should not be given antiparasitic treatment. 

General medical treatment

As with diagnostic procedures, the medical treatment of cardiac and gastrointestinal signs and symptoms attributable to Chagas disease is similar to that instituted for similar problems caused by other etiologies. Such patients should be referred to appropriate subspecialists for evaluation and management. 

Surgical Care


Atrial and ventricular rhythm disturbances may require pacemaker placement. Ablation procedures for tachyarrhythmias, as well as implanted defibrillators, have been used in some patients with Chagas disease. However, the benefits and risks of implantable cardioverter devices (ICDs) in patients with advanced Chagas heart disease is controversial and requires further study in properly structured trials.[107, 198, 199, 200, 201, 202, 203, 204, 205]  The usefulness of resection of the left ventricular apical aneurysms that develop in some patients with Chagas cardiomyopathy has not been established.

Cardiac transplantation is an option for some patients with end-stage Chagas heart disease, and hundreds of such patients have undergone this procedure in Argentina, Brazil, and the United States.[206, 207, 208]  Not surprisingly, T cruzi has been found in endomyocardial biopsies of transplant recipients, thus raising the possibility of early failure of the transplanted hearts due to invasion of parasites.[209]  It is notable that the survival rate among patients with Chagas disease who have undergone cardiac transplantation is comparable to that in the general group of patients who have undergone cardiac transplantation for other reasons.[210, 211]


Patients with chagasic megaesophagus in whom esophageal dilatation is inadequate often undergo wide esophagocardiomyectomy of the anterior gastroesophageal junction, combined with valvuloplasty to reduce reflux.[58, 212, 213]  Laparoscopic myotomy is being used increasingly to manage severe megaesophagus. Partial esophageal resection with reconstruction with esophagogastroplasty has been used in extreme cases.[214, 215]


Patients with severe chagasic megacolon may benefit from the Duhamel-Haddad operation typically used in the treatment of idiopathic congenital megacolon.[216]

In some cases, patients with sigmoid volvulus awaiting the Duhamel-Haddad procedure have undergone anterior sigmoidostomy with an eventual resection of the necrosed segment.[217]


Depending on the phase of T cruzi infection, the following consultations may be appropriate:

  • Infectious diseases specialist
  • Cardiologist and cardiac surgeon
  • Gastroenterologist and general surgeon


A diet appropriate for patients with congestive heart failure should be recommended as appropriate.

Ingestion of warm and pasty food, in small volumes with water, is recommended in patients with megaesophagus. Such patients should not eat in the hours before bedtime to reduce the likelihood of regurgitation and aspiration.

A high-fiber diet is recommended in patients with chagasic megacolon.


Activity should be as tolerated.



Medication Summary

The goals of pharmacotherapy are to eradicate the infection, to prevent the development of or progression of clinical manifestations, and to reduce morbidity and mortality. 

Antiprotozoal agents

Class Summary

These agents are used to treat infections caused by the protozoan T cruzi.

Benznidazole (Rochagan, Radanil)

Nitroimidazole antimicrobial. Generates radical species in both aerobic and anaerobic conditions that are capable of damaging parasitic DNA. Inhibits DNA, RNA, and protein synthesis within the T cruzi parasite. Studies suggest benznidazole is reduced by a type I nitroreductase (NTR) enzyme of T cruzi, producing a series of short-lived intermediates that may promote damage to several macromolecules, including DNA. Approved by the FDA for treatment of Chagas disease in children aged 2-12 years. There is a general consensus in favor of antiparasitic treatment for all cases of acute or reactivated Chagas disease, for chronic T cruzi infection of children up to age 18 years, and for all women of child‑bearing age. Data regarding the efficacy of treating adults aged 50 years or younger with benznidazole are of low quality, and thus such treatment is controversial. As noted, there is a general consensus that persons who already have developed cardiac or gastrointestinal symptoms should not be given antiparasitic treatment. Repeated PCR testing can be used to look for treatment failure.

Nifurtimox (Lampit)

Trypanocidal drug that acts on circulating trypomastigotes, as well as intracellular amastigotes. The mechanism of action may depend on the formation of nitro anion radicals, but precise details are not known. Approved by the FDA for treatment of Chagas disease in children from birth to age 18. The guidance regarding which groups of T cruzi‑infected persons can be treated with nifurtimox are the same as those listed above for benznidazole. As is the case for persons treated with the latter, evidence of treatment failure can be sought with repeated PCR testing.



Further Outpatient Care

Monitor infants born to mothers with T cruzi infection. Infants who are parasite-negative at birth should be tested serologically at 6 and 9 months, after maternal antibodies have disappeared. Treatment should be instituted when results are positive.

Persons with chronic T cruzi infection should undergo electrocardiography every 6-12 months to look for dysrhythmias (see Other Tests).

Patients with clinically manifest cardiac or gastrointestinal Chagas disease should be managed by appropriate specialists (see Consultations).

Weekly white blood cell counts should be performed in patients being treated with benznidazole to evaluate for agranulocytosis.

Immunosuppressed persons with T cruzi infection who have unexplained febrile illnesses should be evaluated parasitologically for reactivation of the infection.

Further Inpatient Care

The level of care depends on the clinical condition of the patient.


Collective prophylaxis

No vaccination is available for T cruzi infection, and primary chemoprophylaxis in persons who plan to visit endemic regions is not recommended because of the extremely low risk for the infection in such circumstances (Only 5 such cases have been reported.).[218, 219, 220]

It has been demonstrated in much of the endemic range that a major reduction of vector-borne transmission of T cruzi to humans can be achieved through improvement of housing conditions, use of residual insecticides, and education of persons at risk of acquiring the infection.

Transmission of T cruzi via transfusion of contaminated blood has been largely eliminated with serologic identification and permanent deferral of infected donors.

Although some risk factors for congenital transmission of T cruzi have been identified,[38, 221]  no approaches for reducing this risk during pregnancy have been defined. As noted, the rate of congenital transmission of T cruzi is markedly reduced by prior treatment. The critical elements in controlling congenital Chagas disease, beyond reducing the prevalence of chronic T cruzi infection in women of childbearing age and treating them with benznidazole prior to pregnancy, are the thorough parasitologic and serologic evaluation of babies born to mothers with T cruzi infection and treating the ones who are determined to be infected.

Personal prophylaxis

Secondary chemoprophylaxis to reduce the risk for reactivation of T cruzi infection in persons with concomitant HIV infection is not recommended.

Laboratory personnel who work with T cruzi or infected vectors should take protective measures appropriate for this risk group 2 organism.

Persons who travel to endemic areas should avoid sleeping in primitive buildings and should take general measures to protect themselves from insects. 


Complications include the following:

  • Acute phase - Myocarditis, meningoencephalitis
  • Chronic chagasic cardiomyopathy – Rhythm disturbances, congestive heart failure, apical aneurysm, thromboembolism, sudden death
  • Chronic chagasic megaesophagus - Poor nutrition, esophagitis, esophageal cancer
  • Chronic chagasic megacolon - Fecaloma, volvulus of sigmoid colon, toxic megacolon


The overall prognosis among persons in the indeterminate phase of T cruzi infection is good, given that only 10-30% of infected persons ever develop signs and symptoms attributable to the disease, and those who do are generally asymptomatic for decades prior to developing cardiac or gastrointestinal problems. 

Patient Education

Education of at-risk persons living in areas of active transmission is a key element in reducing the incidence of new infections. Data suggest that making dogs sleep outside homes can be an important factor in reducing transmission,[28]  although a much more important measure would be to exterminate the domiciliary vectors.


Questions & Answers


Which mammals are infected with T cruzi?

What is Chagas disease (American trypanosomiasis)?

What causes Chagas disease (American trypanosomiasis)?

What is the lifecycle of T cruzi?

What are vectors of T cruzi?

How is Chagas disease (American trypanosomiasis) transmitted?

What is the pathophysiology of Chagas disease (American trypanosomiasis)?

Which organ systems are affected by Chagas disease (American trypanosomiasis)?

What is the prevalence of Chagas disease (American trypanosomiasis) in the US?

What is the global prevalence of Chagas disease (American trypanosomiasis) internationally?

What is the mortality and morbidity associated with Chagas disease (American trypanosomiasis)?

What are the racial predilections of Chagas disease (American trypanosomiasis)?

What are the sexual predilections of Chagas disease (American trypanosomiasis)?

How does the morbidity of Chagas disease (American trypanosomiasis) vary by age?


What is the incubation of acute Chagas disease (American trypanosomiasis)?

Which clinical history findings are characteristic of acute Chagas disease (American trypanosomiasis)?

Which clinical history findings are characteristic of chronic Chagas disease (American trypanosomiasis)?

What are the cardiac symptoms of Chagas disease (American trypanosomiasis)?

What are the GI symptoms of Chagas disease (American trypanosomiasis)?

Which physical findings are characteristic of acute Chagas disease (American trypanosomiasis)?

Which physical findings are characteristic of chronic Chagas disease (American trypanosomiasis)?

Which physical findings are characteristic of cardiomyopathy in chronic Chagas disease?

Which physical findings are characteristic of megaesophagus in chronic Chagas disease?

Which physical findings are characteristic of megacolon in chronic Chagas disease?

What causes Chagas disease (American trypanosomiasis)?


What are the differential diagnoses for Chagas Disease (American Trypanosomiasis)?


How is the risk for congenital Chagas disease (American trypanosomiasis) managed?

What is included in the serologic diagnosis of Chagas disease (American trypanosomiasis)?

How is Chagas disease (American trypanosomiasis) diagnosed?

What is included in the parasitological diagnosis of Chagas disease (American trypanosomiasis)?

What is the role of polymerase chain reaction assays in the diagnosis of Chagas disease (American trypanosomiasis)?

What is the role of imaging studies in the workup of Chagas disease (American trypanosomiasis)?

What is the role of cardiac testing in the workup of Chagas disease (American trypanosomiasis)?

What is the role of esophageal manometry and endoscopy in the workup of Chagas disease (American trypanosomiasis)?


How is the indeterminate-phase of Chagas disease (American trypanosomiasis) treated?

How is Chagas disease (American trypanosomiasis) treated?

How is acute Chagas disease (American trypanosomiasis) treated?

What are the CDC guidelines for the medical treatment of Chagas disease (American trypanosomiasis)?

How is congenial transmission of Chagas disease (American trypanosomiasis) prevented?

When is prophylactic treatment of chronic Chagas disease (American trypanosomiasis) indicated?

When is antiparasitic treatment contraindicated in chronic Chagas disease (American trypanosomiasis)?

How are the cardiac and GI symptoms of Chagas disease (American trypanosomiasis) treated?

How is cardiopathy treated in Chagas disease (American trypanosomiasis)?

How is megaesophagus treated in Chagas disease (American trypanosomiasis)?

How is megacolon treated in Chagas disease (American trypanosomiasis)?

Which specialist consultations are beneficial to patients with Chagas disease (American trypanosomiasis)?

Which dietary modifications are used in the treatment of Chagas disease (American trypanosomiasis)?

Which activity modifications are beneficial in the treatment of Chagas disease (American trypanosomiasis)?


What are the goals of drug treatment for Chagas disease (American trypanosomiasis)?

Which medications in the drug class Antiprotozoal agents are used in the treatment of Chagas Disease (American Trypanosomiasis)?


What is included in the long-term monitoring of Chagas disease (American trypanosomiasis)?

When is inpatient care indicated for Chagas disease (American trypanosomiasis)?

How is Chagas disease (American trypanosomiasis) prevented?

What are the possible complications of Chagas disease (American trypanosomiasis)?

What is the prognosis of Chagas disease (American trypanosomiasis)?

What is included in patient education about Chagas disease (American trypanosomiasis)?