Version May 2024
INTRODUCTION — Chagas disease is caused by infection with the protozoan parasite Trypanosoma cruzi; the major chronic manifestations are Chagas cardiomyopathy and gastrointestinal disease [1-6].
Issues related to the natural history, clinical manifestations, diagnosis, and management of chronic Chagas disease will be reviewed here. Issues related to acute and congenital Chagas infection are discussed separately. (See "Chagas disease: Acute and congenital Trypanosoma cruzi infection".)
Issues related to the epidemiology and prevention of Chagas disease are discussed separately. (See "Chagas disease: Epidemiology, screening, and prevention".)
Issues related to cardiac and gastrointestinal Chagas are discussed separately. (See "Chronic Chagas cardiomyopathy: Clinical manifestations and diagnosis" and "Chronic Chagas cardiomyopathy: Management and prognosis" and "Chagas gastrointestinal disease".)
NATURAL HISTORY
Overview — T. cruzi infection is characterized by two phases, acute and chronic (figure 1). The acute phase lasts 8 to 12 weeks after transmission. (See "Chagas disease: Acute and congenital Trypanosoma cruzi infection".)
When the host immune response succeeds in decreasing parasite replication, parasitemia falls below levels detectable by microscopy, acute symptoms resolve, and the patient passes into the chronic phase. In the absence of successful antitrypanosomal therapy, this usually occurs 8 to 12 weeks after the onset of infection, and the chronic phase lasts for the life of the patient. Nearly all T. cruzi-infected persons have the indeterminate (asymptomatic) form during the first one to three decades of the chronic phase; an estimated 20 to 40 percent will subsequently develop cardiac and/or gastrointestinal forms of the disease [7].
Individuals with chronic T. cruzi infection are capable of transmitting the parasite to the insect vector and to other humans via blood components, organ donation, or transplacentally, regardless of clinical manifestations [8]. (See "Chagas disease: Epidemiology, screening, and prevention", section on 'Nonvectorial transmission'.)
Indeterminate form — Patients with the indeterminate form of the chronic phase of T. cruzi infection have positive serology but no symptoms or signs of cardiomyopathy or gastrointestinal disease, as described below. (See 'Identify organ involvement' below.)
The indeterminate form may persist for decades. About 20 to 30 percent with the indeterminate form develop cardiomyopathy after a latent period ranging from 5 to 30 years [3,4,7]. Approximately 10 to 15 percent of patients with the indeterminate form develop gastrointestinal disease (within the Southern Cone, where the prevalence of gastrointestinal disease is highest), and a subset of patients develop both cardiac and gastrointestinal (cardiodigestive) disease [7].
A retrospective cohort study provided some data on the transition from the indeterminate form (asymptomatic T. cruzi positivity) to chronic Chagas cardiomyopathy (CCC); however, the initial cohort was not limited to the indeterminate form since baseline cardiac testing was not performed. Among 499 initially asymptomatic blood donors in Brazil with T. cruzi seropositivity on initial screening, 24 percent were diagnosed with CCC during mean 10.5 years of follow-up; of these, 26 percent were found to have a left ventricular ejection fraction <50 percent [9]. The estimated progression rate from the indeterminate form to Chagas cardiomyopathy was 1.85 percent per year. Among 488 seronegative donors matched by year of donation, site, age, and sex, 5 percent developed cardiomyopathy during mean 11 years of follow-up. However, the high incidence of Chagas cardiomyopathy in this study may overestimate the risk in individuals with the indeterminate form of Chagas disease; given the lack of baseline cardiac testing, some of the individuals may have had CCC at the outset of the study despite their lack of symptoms. Similarly, a systematic review and meta-analysis of 23 studies of individuals with the indeterminate form reported a pooled annual rate for development of CCC to be 1.9 percent (95% CI 1.3-3.0 percent) after a mean follow-up period of 8.5 years (range 3 to 18 years) [10].
Determinate forms
Heart disease — Chagas heart disease develops more commonly than gastrointestinal disease. Issues related to Chagas heart disease are discussed in detail separately. (See "Chronic Chagas cardiomyopathy: Clinical manifestations and diagnosis" and "Chronic Chagas cardiomyopathy: Management and prognosis".)
Gastrointestinal disease — The gastrointestinal form of Chagas disease is rare, especially outside of the Southern Cone countries (Bolivia, Argentina, Paraguay, Uruguay, Chile, Brazil). Issues related to Chagas gastrointestinal disease are discussed in detail separately. (See "Chagas gastrointestinal disease".)
Reactivation due to immunosuppression — Reactivation of chronic T. cruzi infection can occur in patients with immunosuppression due to malignancy, chemotherapy, immunosuppressive regimens for solid organ or bone marrow transplantation, or human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) [11,12]. Clinical findings and management are discussed in detail separately. (See "Chagas disease in the immunosuppressed host".)
DIAGNOSIS — Chronic Chagas disease should be suspected in individuals who have lived in endemic countries of Latin America and those born to women from endemic countries [13]. Most infected individuals are asymptomatic; cardiac or gastrointestinal symptoms in a patient from Latin America should prompt consideration of chronic Chagas disease.
Groups at highest risk include those who lived in rural areas, especially in houses with adobe walls, thatched roofs, and/or known triatomine infestation. Vector-borne transmission also occurs in the southern United States, but the risk is much lower than in areas of Latin America with domestic triatomine infestation. Infection prevalence is highest in Bolivia, Argentina, Paraguay, and Ecuador, but most infected immigrants in the United States are from El Salvador and Mexico. (See "Chagas disease: Epidemiology, screening, and prevention".)
Diagnose chronic infection — Diagnosis of chronic Chagas infection requires serologic methods to detect immunoglobulin (Ig)G antibodies to T. cruzi, most commonly enzyme-linked immunosorbent assay (ELISA) and immunofluorescent antibody assay (IFA) [3]. No available assay has sufficient sensitivity and specificity to be used alone; a positive result by a single assay does not constitute a confirmed diagnosis [14]. Two serologic tests based on different antigens (eg, whole-parasite lysate and recombinant antigens) and/or techniques (eg, ELISA and IFA) are used in parallel to increase the accuracy of the diagnosis [3,5,8]. Data suggest that the sensitivity of serologic assays varies by geographic location, possibly due to T. cruzi strain differences and resulting antibody responses [15-17].
Individuals tested by two serologic assays with discordant results require further testing. In some cases, the infection status remains difficult to resolve even after a third test because there is no absolute gold-standard assay for chronic T. cruzi infection [18]. Assays such as the radioimmune precipitation assay and IgG trypomastigote excreted-secreted antigen immunoblot are promoted as reference tests, but even these do not have optimal sensitivity and specificity and may not be capable of resolving the diagnosis [19,20].
Options for T. cruzi serologic testing in the United States are relatively limited. Three ELISA kits based on parasite lysate or recombinant antigens (Ortho ELISA, Wiener Chagatest ELISA Recombinante 3.0, Hemagen ELISA) are cleared by the US Food and Drug Administration (FDA) for diagnostic application [21]. Of these three tests, the Ortho and Wiener ELISAs demonstrated high sensitivity and specificity in published evaluations [22,23]. A rapid test based on recombinant antigens (InBios ChagasDetectPlus) was also cleared by the FDA and could facilitate screening of high-risk populations [24,25]. Use of an assay with validation data (eg, a commercial kit shown to have acceptable sensitivity and specificity in a thorough study) is preferable to reliance on in-house tests for which no performance data are publicly available.
In general, polymerase chain reaction (PCR) is not a useful diagnostic test for chronic T. cruzi infection. The sensitivity is variable and depends on patient characteristics, sample volume, and PCR primers and methods [26,27]. In the BENEFIT trial (nearly 2900 patients with proven chronic Chagas cardiomyopathy (CCC) and two positive serologic tests with two different techniques), the overall rate of serum PCR positivity was approximately 60 percent [28]. However, quantitative PCR performed under rigorously standardized protocols is increasingly used as a timely indicator of treatment failure in new drug trials. (See 'Assessing response to treatment' below.)
Direct demonstration of parasite by hemoculture or xenodiagnosis in a reliable laboratory indicates true infection, but the techniques are laborious, their sensitivity in the chronic phase is generally less than 50 percent, and final results may not be available for one to two months [29]. Xenodiagnosis consists of feeding laboratory-reared uninfected triatomine bugs directly on the patient or on blood in a membrane-feeding device.
The United States Centers for Disease Control and Prevention provides consultation to health care providers concerning Chagas disease diagnostic testing and acts as a reference laboratory for Chagas disease serology and PCR (Division of Parasitic Diseases Public Inquiries line, 404-718-4745; for emergencies after business hours, 770-488-7100; email [email protected]).
Issues related to monitoring after transplantation in a patient with chronic T. cruzi infection are discussed separately. (See "Chagas disease in the immunosuppressed host".)
Identify organ involvement — After the diagnosis of chronic T. cruzi infection is established by serologic testing, further evaluation should be pursued to determine whether the patient has evidence of chronic Chagas heart disease or gastrointestinal disease (determinate form) or lacks organ involvement (indeterminate form).
The initial evaluation includes:
●Medical history, including a review of systems with an emphasis on symptoms suggestive of cardiac arrhythmia (eg, palpitations, atypical angina), early heart failure, thromboembolism, and gastrointestinal disease [8,30,31]. Social history should include details related to potential exposure to the parasite in endemic areas or via blood transfusion or other routes.
●Complete physical examination, chest radiograph, and resting 12-lead electrocardiogram (ECG) with a 30-second lead II rhythm strip [1,3,8,32].
●Patients with symptoms consistent with gastrointestinal Chagas disease should undergo barium studies and other evaluation as indicated; such testing is not warranted in the absence of symptoms [8]. (See "Chagas gastrointestinal disease".)
Criteria — The approach to identification of determinate forms of Chagas disease is controversial. The 2011 Latin American guidelines and the 2015 Second Brazilian consensus on Chagas disease endorsed the classical approach (which does not include echocardiography) [2,4]. In contrast, some experts diagnose the indeterminate form only in patients who lack all the classical criteria for cardiac or gastrointestinal involvement and also lack echocardiographic wall motion abnormalities.
●Classical criteria — The indeterminate (or latent) form of Chagas disease is classically diagnosed in patients with serologic and/or parasitologic evidence of chronic T. cruzi infection who lack all of the following:
•Symptoms or physical signs of heart failure, arrhythmia, or thromboembolism
•Abnormalities on 12-lead-ECG with 30-second lead II rhythm strip [3,8,32]
•Any radiographic evidence (on chest radiograph or barium-contrast esophageal or colon radiographs) of cardiac or gastrointestinal involvement [1,4,33,34]
●Echocardiography — In addition to the above classical criteria for indeterminate form, some experts use echocardiography to identify patients with left ventricular (LV) regional or global wall motion abnormalities and exclude patients with these abnormalities from the indeterminate form [1,35].
Rationale for echocardiography — The rationale for including echocardiography in the evaluation of patients with chronic Chagas disease is that LV wall motion abnormalities have prognostic significance and can occur in the absence of symptoms, ECG alterations, or chest radiograph findings. Several analyses have suggested that early echocardiographic findings such as segmental wall motion abnormalities may indicate the onset of cardiomyopathy even before changes are detected on the ECG [36-38]. The presence of even minor segmental LV systolic abnormalities predicts future global LV systolic dysfunction [37]. In one study including more than 1500 patients with CCC, presence of segmental wall motion abnormalities (in spite of normal global LV systolic function) was predictive of subsequent adverse clinical outcome [38]. In addition, overt CCC may first manifest as stroke or cardiac arrhythmias including sudden cardiac arrest; many patients with these complications have only regional LV systolic dysfunction [39,40].
Given the clinical significance of LV wall motion abnormality (focal or global), this finding has the following implications for evaluation and management:
●Patients with LV wall motion abnormality should undergo further evaluation including ambulatory ECG (Holter) monitoring for arrhythmias as well as more intensive follow-up than a patient with the indeterminate form. (See "Chronic Chagas cardiomyopathy: Clinical manifestations and diagnosis", section on 'Approach to diagnosis' and "Chronic Chagas cardiomyopathy: Management and prognosis", section on 'Monitoring for disease progression'.)
●The presence of any degree of LV systolic dysfunction or an apical aneurysm is a risk factor for cardioembolism and should be considered in assessing the benefits and risks of antithrombotic prophylaxis. (See "Chronic Chagas cardiomyopathy: Management and prognosis", section on 'Thromboembolism prophylaxis'.)
●Patients with asymptomatic left ventricular systolic dysfunction with left ventricular ejection fraction ≤40 percent should be treated with pharmacologic therapy to reduce the risk of progressive adverse remodeling and development of heart failure. (See "Chronic Chagas cardiomyopathy: Management and prognosis", section on 'Management' and "Management and prognosis of asymptomatic left ventricular systolic dysfunction".)
Excluded tests — In patients with the indeterminate form, we do not use additional testing (beyond ECG, chest radiography, and echocardiography) for evaluation of cardiac disease. While additional tests (such as ambulatory ECG [Holter] monitoring, stress testing, radionuclide ventriculography, cardiovascular magnetic resonance imaging, autonomic evaluation, electrophysiologic testing, cardiac catheterization, and endomyocardial biopsy) may demonstrate significant abnormalities in some patients considered to have the indeterminate form [4,8,35,41,42], data are lacking to support such testing. Abnormalities detected with these tests in individuals fulfilling the other criteria for the indeterminate form have not been demonstrated to have prognostic meaning. Moreover, some longitudinal studies show that as long as the ECG remains normal, infected individuals have the same life expectancy as noninfected controls [7].
Parasympathetic autonomic dysfunction (including decreased respiratory heart rate changes and blunted heart rate responses to orthostatic changes) may be detected on specific testing in infected individuals with no signs of cardiomyopathy or digestive Chagas disease [41]. One study including more than 500 individuals with T. cruzi noted presence of subclinical peripheral neuropathy (manifested as decreased tendon reflexes and/or sensory impairment) in 10 percent of cases; there was no reported association with cardiomyopathy or gastrointestinal Chagas disease [43].
The role of additional testing in patients diagnosed with CCC is discussed separately. (See "Chronic Chagas cardiomyopathy: Clinical manifestations and diagnosis".)
DIFFERENTIAL DIAGNOSIS — The differential diagnosis for positive T. cruzi serology includes cross reactivity with other antigens (eg, Leishmania species) [44,45]. For this reason, two serologic tests (based on different antigens and/or techniques) are used to reduce the risk of false positive results. (See 'Diagnose chronic infection' above.)
The differential diagnosis of the determinate forms of chronic Chagas disease, including cardiomyopathy and gastrointestinal disease, is reviewed separately. (See "Chronic Chagas cardiomyopathy: Clinical manifestations and diagnosis", section on 'Differential diagnosis' and "Chagas gastrointestinal disease", section on 'Differential diagnosis'.)
MANAGEMENT OF INDETERMINATE FORM — The approach to management of Chagas disease varies by patient characteristics and phase and form of disease. Management of immunocompetent patients with the indeterminate form of chronic Chagas disease is discussed here. Management of immunosuppressed patients with Chagas disease (including indeterminate form) is discussed separately. (See "Chagas disease in the immunosuppressed host".)
Management of patients with determinate forms of chronic Chagas disease is discussed separately. (See "Chronic Chagas cardiomyopathy: Management and prognosis" and "Chagas gastrointestinal disease".)
Antitrypanosomal therapy
Indications and rationale for therapy — For most patients with the indeterminate form of chronic T. cruzi infection (including children and adults), we suggest antitrypanosomal treatment. For older adults (eg, >50 years), treatment should be considered on a case-by-case basis as comorbidities may decrease tolerance of the prolonged drug course [2,8]. This approach differs from major society guidelines which include a strong recommendation for antitrypanosomal treatment in children and a weak recommendation in adults [2,3,5,7,8]. As discussed below, given that available evidence reflects a surrogate outcome (eg, seroconversion rates), rather than patient-related outcomes, the quality of this evidence is low and thus supports a weak recommendation for children as well as adults. (See "Chagas disease: Antitrypanosomal drug therapy".)
For women who wish to become pregnant, treatment prior to conception is particularly important since observational data suggest that treatment likely reduces the probability of congenital transmission [5,46,47]. Antitrypanosomal drugs are contraindicated during pregnancy, so effective contraception should be assured while on treatment. Additional contraindications to antitrypanosomal drugs include severe renal or hepatic dysfunction. (See "Chagas disease: Antitrypanosomal drug therapy".)
Evidence supporting the use of antitrypanosomal agents for treatment of patients with the indeterminate form of chronic Chagas disease comes from randomized and nonrandomized clinical trials in children and adults [48-52]. Most of the available clinical trials found that treatment increases the likelihood of becoming seronegative, but there are only limited data on the effect of treatment on progression to cardiomyopathy, in part because of the difficulty of achieving the decades of follow-up necessary.
In one trial including more than 100 children randomly assigned to a 60-day treatment course with benznidazole or placebo, 62 percent of patients in the treatment arm were seronegative at four years (compared with none in the placebo arm) [49]. The incidence of new ECG abnormalities was similar in both groups (2.5 and 2.4 percent, respectively), limiting the ability to draw any conclusions about the efficacy of benznidazole in preventing onset of cardiomyopathy. An earlier trial had similar findings, reporting 58 percent seronegativity at three years in the benznidazole arm compared with 5 percent in the placebo arm [48]. The frequency of new ECG abnormalities or incident cardiomyopathy was not reported in this trial.
In another trial, 120 adults were randomly assigned to one of four 60-day treatment arms (benznidazole monotherapy, benznidazole plus posaconazole, posaconazole monotherapy, or placebo) [53]. At one year, 96 percent of patients treated with benznidazole had negative parasitemia status (measured by polymerase chain reaction [PCR]) compared with 17 percent in the placebo arm (the efficacy of posaconazole was similar to that of placebo). The effect of benznidazole on progression to cardiomyopathy or development of ECG abnormalities was not reported. In an earlier nonrandomized prospective study involving more than 560 adults (ages 30 to 50 years) assigned in alternating sequence to either 30 days of treatment with benznidazole or no treatment, those who received benznidazole had reduced risk of disease progression (4 versus 14 percent; hazard ratio [HR] 0.24, 95% CI 0.10-0.59) and onset of new ECG abnormalities (5 versus 16 percent; HR 0.27, 95% CI 0.13-0.57) [54]. Treated patients more frequently converted to negative serology (15 versus 6 percent; HR 2.1, 95% CI 1.06-4.06). Mortality was lower in the benznidazole group, but the finding was not statistically significant (1.2 versus 4.2 percent; HR 0.2, 95% CI 0.03-1.2). Limitations of this study include its nonrandomized design and the relatively large number of patients lost to follow-up (20 percent of patients in both arms).
A major barrier to clinical trials in adults is the lack of a true test of cure and the fact that reversion to negative serology in cured patients takes many decades in those treated as adults [18,46,55]. Nevertheless, data from clinical trials indicate that 85 to 95 percent of adult patients who complete a course of benznidazole have sustained negative parasitologic tests at 12 months post-treatment based on rigorously standardized quantitative PCR assays [53,56]
Regimen selection — Antitrypanosomal drugs include benznidazole and nifurtimox; in general, benznidazole is favored as the first-line treatment because it is better tolerated. There are also more contemporary data and clinical experience with benznidazole. Dosing and adverse effects are outlined in the tables (table 1 and table 2). Issues related to antitrypanosomal drugs are discussed further separately. (See "Chagas disease: Antitrypanosomal drug therapy".)
Benznidazole is typically given for 60 days for chronic indeterminate Chagas disease; most trials and studies have evaluated this duration of treatment (see 'Indications and rationale for therapy' above). Although further confirmatory data are needed, emerging evidence suggests that shorter courses (and in some cases, lower doses) may achieve similar treatment outcomes and reduce the severity of side effects. In a phase II, multicenter, randomized controlled trial of 210 adults with chronic indeterminate Chagas disease, high rates of sustained parasitologic response (persistently negative blood PCR at six months) were achieved when benznidazole was given at 300 mg daily for eight weeks (89 percent of 28 individuals), four weeks (89 percent of 28 individuals), two weeks (83 percent of 29 individuals), or at 150 mg daily for four weeks (83 percent of 30 individuals) [57]. Overall, severe adverse events were uncommon, but there were trends towards fewer events in the shorter-duration and lower-dose groups. If these results are confirmed in larger phase III trials, shorter- and/or lower-dose treatment regimens may be recommended in the future.
Adverse effects — Side effects are fairly common with antitrypanosomal agents. In the available clinical trials, approximately 20 percent of patients discontinued treatment because of adverse effects, most commonly cutaneous and gastrointestinal reactions [50]. Side effects are more common in adults than children and in women than men [58]. Adverse effects of antitrypanosomal drugs are summarized in the table and are discussed in greater detail separately (table 2). (See "Chagas disease: Antitrypanosomal drug therapy".)
Antitrypanosomal agents are contraindicated in pregnancy and in patients with severe renal or hepatic dysfunction.
Assessing response to treatment — There is no sensitive, timely assay for monitoring response to treatment in patients with chronic T. cruzi infection [8]. The length of time required to achieve sustained negative serologic test results following treatment is proportional to the duration of infection; because most individuals who grew up in an area with endemic vector-borne transmission become infected as children, patient age is often used a proxy for the presumed duration of infection. As an example, among females treated by age 15 years, the median time to negative serology in one study was 15 years, whereas among women treated after age 15 years, the median time to negative serology was 27 years [46]. The two randomized trials of benznidazole in children used experimental assays measuring lytic antibodies to demonstrate response at three to four years post-treatment, but these assays are not available outside a few research settings [48,49]. Evaluation of other diagnostic tools is ongoing [59]. Thus, there is no practical method to prove treatment success in the chronic phase, and serologic monitoring post-treatment is usually not recommended for those treated in the chronic phase [8].
In trials of posaconazole and the ravuconazole pro-drug E1224, the main outcome was parasite detection by carefully standardized real-time PCR in multiple specimens [60-62]. Positive PCR results during post-treatment follow-up provided an early indicator of treatment failure for the experimental arms in these trials. However, negative PCR does not provide proof of cure, and molecular methods are not appropriate for routine clinical use to monitor response to treatment in patients with chronic T. cruzi infection.
Monitoring — Patients with the indeterminate form should be monitored for development of cardiac or gastrointestinal dysfunction.
Cardiac involvement — For patients with the indeterminate form, the optimal approach to monitoring for development of left ventricular dysfunction is uncertain. We suggest the following approach:
●Patients should undergo annual history and physical examination and ECG to monitor for new abnormalities that may herald development of Chagas cardiomyopathy or gastrointestinal disease [1,3,8].
•The development of symptoms or signs of heart failure, thromboembolic disease or arrhythmia should prompt further cardiac evaluation including ambulatory ECG (Holter) monitoring. Diagnosis and management of chronic Chagas cardiomyopathy is discussed separately. (See "Chronic Chagas cardiomyopathy: Clinical manifestations and diagnosis", section on 'Diagnosis' and "Chronic Chagas cardiomyopathy: Management and prognosis".)
●We suggest echocardiographic assessment at regular intervals (eg, every three to five years) [35], given the importance of identifying even minor wall motion abnormalities. (See 'Rationale for echocardiography' above and "Chronic Chagas cardiomyopathy: Clinical manifestations and diagnosis".)
The utility of brain natriuretic peptide (BNP) plasma levels as a means of identifying patients who should undergo echocardiography has not been established. In a controlled study of 151 patients seropositive for Chagas disease (90 percent of whom had a left ventricular ejection fraction >40 percent), among those with an abnormal ECG or chest radiograph, plasma BNP ≥60.7 pmol/L had good sensitivity and specificity for detection of LV dysfunction (80 and 97 percent, respectively) [63]. Further studies are needed to determine the utility and cost-effectiveness of this approach prior to implementation in endemic areas.
●If echocardiography is not available, we suggest repeating a chest radiograph every three to five years.
Gastrointestinal involvement — For patients with the indeterminate form, the approach to monitoring for development of gastrointestinal involvement depends on the prevalence of digestive involvement in the country of origin. Asymptomatic patients should be reassessed annually for gastrointestinal symptoms. In patients from countries where the gastrointestinal form occurs most frequently (mainly the Southern Cone of South America), radiographic evaluation for gastrointestinal involvement using barium esophagram and colon enema may be appropriate. The presence of gastrointestinal tract symptoms (eg, dysphagia, constipation) should prompt evaluation with barium contrast studies. Diagnosis and management of Chagas gastrointestinal disease is discussed separately. (See "Chagas gastrointestinal disease".)
Family screening and patient counseling — Diagnostic screening should be offered for family members with a similar history of potential exposure to the parasite in endemic settings and for all children of infected women [8]. In one study including 86 T. cruzi-infected individuals in Los Angeles, 189 family members underwent screening; 7.4 percent of these individuals were seropositive. The mean age of infected relatives was 48 years; the mean age of uninfected relatives was 24 years [64]. (See "Blood donor screening: Medical history", section on 'Chagas disease'.)
Infected individuals should be counseled not to donate blood or organs.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Chagas disease".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Chagas disease (The Basics)")
SUMMARY AND RECOMMENDATIONS
●Trypanosoma cruzi infection is characterized by two phases, acute and chronic. The acute phase of T. cruzi infection lasts 8 to 12 weeks following transmission and is characterized by presence of circulating trypomastigotes. When the host immune response succeeds in decreasing parasite replication, parasitemia falls below levels detectable by microscopy, acute symptoms resolve, and the patient passes into the chronic phase, which lasts for the life of the patient. (See 'Natural history' above.)
●Nearly all T. cruzi-infected persons have the indeterminate (asymptomatic) form during the first one to three decades of the chronic phase. Patients with the indeterminate form of the chronic phase of T. cruzi infection have positive serology but no signs or symptoms of cardiomyopathy or gastrointestinal disease. Such patients have normal 12-lead electrocardiogram (ECG) findings and normal radiographic examinations of the chest, esophagus, and colon. An estimated 20 to 40 percent subsequently develop clinically evident cardiac and/or gastrointestinal forms of the disease. (See 'Indeterminate form' above.)
●Chronic Chagas disease should be suspected in individuals who have lived in endemic countries of Latin America and those born to women from endemic countries, especially including those who lived in rural areas in houses with adobe walls, thatched roofs, and/or known triatomine infestation. Most infected individuals are asymptomatic; cardiac or gastrointestinal symptoms in a patient from Latin America should prompt consideration of chronic Chagas disease. Vector-borne transmission also occurs in the southern United States, but the risk is much lower than in areas of Latin America with domestic triatomine infestation. (See 'Diagnosis' above.)
●Diagnosis of chronic infection requires serologic methods to detect immunoglobulin (Ig)G antibodies to T. cruzi. Two tests based on different antigens and/or techniques are used in parallel to increase the accuracy of the diagnosis; no available assay has sufficient sensitivity and specificity to be used alone. (See 'Diagnose chronic infection' above.)
●After the diagnosis of chronic T. cruzi infection is confirmed by serologic testing, the initial evaluation consists of medical history, including a review of systems with an emphasis on symptoms suggestive of cardiac arrhythmia (eg, palpitations, atypical angina), early heart failure, thromboembolism, and gastrointestinal disease. Social history should include details related to potential exposure to the parasite in endemic areas or via blood transfusion or other routes. Clinical evaluation should include complete physical examination and resting 12-lead ECG with a 30-second lead II rhythm strip. (See 'Identify organ involvement' above.)
●The approach to identification of the indeterminate form of Chagas disease is controversial. We diagnose the indeterminate form using classical criteria (exclusion of cardiac symptoms and signs and abnormalities on ECG, chest radiograph, or gastrointestinal radiographs) plus echocardiographic findings. (See 'Diagnosis' above.)
●Management of the indeterminate form of Chagas disease includes antitrypanosomal therapy and monitoring for development of cardiac or gastrointestinal dysfunction. (See 'Management of indeterminate form' above.)
●The approach to antitrypanosomal therapy for Chagas disease varies by phase and form of disease:
•Indeterminate form – For most patients with the indeterminant form of chronic T. cruzi infection, including children and adults, we suggest antitrypanosomal treatment (Grade 2C). Treatment of older adults (eg, >50 years old) should be considered on a case-by-case basis since drug tolerance may be lower. (See 'Indications and rationale for therapy' above.)
•Chagas cardiomyopathy – Antitrypanosomal therapy may be beneficial to patients with early or mild chronic Chagas cardiomyopathy but it does not appear to be beneficial for patients with advanced cardiomyopathy. This is discussed separately. (See "Chronic Chagas cardiomyopathy: Management and prognosis", section on 'Management'.)
•Chagas gastrointestinal disease – Management of Chagas gastrointestinal disease focuses on symptom amelioration. Antitrypanosomal therapy generally does not play a role. This is discussed separately. (See "Chagas gastrointestinal disease".)
•Reactivation in an immunosuppressed host – Treatment and prevention of T. cruzi reactivation in immunosuppressed patients is discussed separately. (See "Chagas disease in the immunosuppressed host".)
●Antitrypanosomal drugs include benznidazole and nifurtimox. We suggest benznidazole as the first-line treatment for Chagas disease (Grade 2C). The basis for our recommendation is that benznidazole is generally better tolerated, the available data on it are more recent, and there is greater experience using it in the contemporary era. Dosing and adverse effects are outlined in the tables (table 1 and table 2). Issues related to antitrypanosomal drugs are discussed further separately. (See 'Regimen selection' above and "Chagas disease: Antitrypanosomal drug therapy".)
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