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Chagas disease: Epidemiology, screening, and prevention

Chagas disease: Epidemiology, screening, and prevention
Literature review current through: Jan 2024.
This topic last updated: Apr 08, 2022.

INTRODUCTION — Chagas disease is caused by infection with the protozoan parasite Trypanosoma cruzi [1-3]. Most infected patients are asymptomatic; late manifestations include heart disease and gastrointestinal disease.

Issues related to the epidemiology, screening, and prevention of Chagas disease will be reviewed here. Other issues related to Chagas disease are discussed in detail separately:

(See "Chagas disease: Acute and congenital Trypanosoma cruzi infection".)

(See "Chagas disease: Chronic Trypanosoma cruzi infection".)

(See "Chronic Chagas cardiomyopathy: Clinical manifestations and diagnosis" and "Chronic Chagas cardiomyopathy: Management and prognosis".)

(See "Chagas gastrointestinal disease".)

EPIDEMIOLOGY AND VECTORIAL TRANSMISSION — Chagas disease is responsible for a higher burden of morbidity and mortality than any other parasitic disease in the Western hemisphere, including malaria [4]. Vector-borne transmission is the major route of Chagas transmission. Transmission can also occur vertically from mother to fetus, via ingestion of contaminated food or drink, via transfusion of infected blood components, via transplantation of an organ from an infected donor, or via laboratory exposure [5]. In the absence of successful antitrypanosomal treatment, infection is lifelong; spontaneous cure is extremely rare.

Geographic distribution — Chagas disease is endemic in 21 continental Latin American countries, from the southern United States to the north of Argentina and Chile. Vector-borne transmission occurs exclusively in the Americas, where an estimated 6 million people are infected (table 1) [6]. Historically, the disease occurred predominantly in rural areas of Latin America where residents of infested houses were repeatedly exposed to infected vectors [2,5]. The prevalence of T. cruzi is highest in Bolivia, Argentina, Paraguay, Ecuador, El Salvador, and Guatemala [1,6].

Vector transmission and life cycle — Parasite transmission via infected triatomine bugs is responsible for the majority of infections (figure 1 and picture 1). Vector control programs are discussed elsewhere. (See 'Vector control' below.)

The infective trypomastigote form of the T. cruzi parasite is present in large numbers in the feces of infected triatomine bugs. During or immediately after a blood meal, the triatomine bug defecates on the skin of the host, allowing the organism to enter through the bite wound. The organism can also enter via intact conjunctiva or mucous membranes. Most domestic triatomine species feed nocturnally and are able to complete their blood meal without awakening the host [7].

The classic epidemiology of vector-borne T. cruzi is closely linked to the biologic and ecologic characteristics of the triatomine vectors and the reservoir hosts (including both domestic and sylvatic mammals). The triatomine passes through five nymphal stages; only the adults are winged. Triatomine bugs of both sexes must take blood meals to develop through their nymphal stages to adults. In addition, females require blood meals to lay eggs. Thus, both nymphs and adults, of both sexes, may be infected with T. cruzi, but infection rates increase with developmental stage and age.

T. cruzi infection is transmitted to wild mammals by sylvatic triatomine species; these bugs often colonize the nests of rodent or marsupial reservoir hosts [7,8]. Sylvatic triatomine adults may fly into human dwellings and cause sporadic human infections [9].

Domestic transmission occurs in settings where triatomine vectors have become adapted to living in human dwellings and nearby animal enclosures. Domestic mammals such as dogs, cats, and guinea pigs play important roles as triatomine blood meal sources and T. cruzi reservoir hosts [10-12]. Some triatomine species can infest both domestic and sylvatic sites [13]. Triatomines also may feed on blood from birds and reptiles but these animals are not susceptible to T. cruzi infection.

There are more than 130 triatomine bug species in the Americas, many of which can transmit T. cruzi [7,8]. A small number of highly domiciliated vectors are of disproportionate importance in the human epidemiology of disease (table 2) [14]. In Mexico and Central America, the main domestic and peridomestic vector is Triatoma dimidiata. In northern South America, Rhodnius prolixus occurs in both domestic and sylvatic cycles [15]. R. prolixus has been certified as eliminated from Central America [16]. In Brazil, Bolivia, and farther south, the main domestic vector is Triatoma infestans. Panstrongylus megistus is an important domestic vector in Brazil and is found as a sylvatic vector in Bolivia, Paraguay, and Argentina (table 2) [17].

Poor-quality housing with adobe or unfinished brick walls provides crevices and other hiding places for triatomine bugs [18,19]. Roofs made of thatch are an attractive habitat for several species [20]. Domestic infestation rates in endemic areas can be high (eg, 25 to 100 percent of houses infested). A house and its immediate surroundings may support large colonies of both juvenile and adult bugs [18,19,21].

In endemic settings, T. cruzi infection is usually acquired in childhood. Infection persists for life, so the seroprevalence in an area with sustained vector-borne transmission increases with age (reflecting cumulative incidence) [22,23]. Before widespread vector control was instituted in the early 1990s, more than 60 percent of adults were infected with T. cruzi in some endemic communities [21,24]. Cross-sectional community surveys have demonstrated that most infected individuals are asymptomatic (have the indeterminate form); an estimated 70 to 80 percent remain asymptomatic throughout their lives [5,25]. The prevalence of clinical disease increases with age, reflecting onset of cardiac and gastrointestinal manifestations in early adulthood with progression over a period of years to decades [26,27].

The southern region of the United States has established enzootic cycles of T. cruzi involving several triatomine vector species and mammalian hosts, such as raccoons, opossums, woodrats, and domestic dogs [28-31]. Autochthonous vector-borne infections in humans have been documented in Texas, California, Tennessee, Louisiana, Mississippi, Arizona, and Missouri [3,32-39]. The rarity of vector-borne transmission in the United States has been attributed to housing conditions that minimize vector-human contact and lower transmission efficiency of the North American vectors [33,40]. A study of repeat blood donors in the United States demonstrated no locally acquired incident infections over 6 million person-years of follow-up, confirming that autochthonous vector-borne transmission is rare [41]. However, undetected cases certainly occur.

Changes due to migration and public health interventions — The epidemiology of Chagas disease has changed due to migration of individuals within and outside of endemic countries as well as successful programs to reduce transmission in endemic areas [2]. The following factors have altered the epidemiology of Chagas disease:

Massive rural to urban migration within Latin America

International migration of persons from Chagas disease-endemic areas to Europe and the United States

Rise of the human immunodeficiency virus (HIV) epidemic

Success of vector control in many areas

Failure of vector control and emergence of insecticide resistance, especially in the Gran Chaco

There are several consequences of these trends. Hundreds of thousands of infected individuals live in cities across Latin America and in the United States, Spain, and other European countries [42,43]. In Santa Cruz (the largest city in Bolivia), T. cruzi infection is found in 15 to 20 percent of pregnant women presenting for delivery and up to 60 percent of patients with heart disease [44,45]. An estimated 300,000 infected immigrants are thought to be living in the United States [42,46]; the prevalence of Chagas disease among Latin American-born residents of Los Angeles County was estimated to be 1.24 percent in one study [47]. In studies of Latin American immigrants presenting to health care facilities with cardiac disease, the prevalence of T. cruzi infection has ranged from 5 to 19 percent and is highest in patients with dilated cardiomyopathy [48-51]. Because of infection prevalence and immigration patterns, T. cruzi infection in the United States is most commonly found in immigrants from El Salvador and Mexico [47]. At least 40,000 infected individuals live in Spain; the largest affected group are immigrants from Bolivia [43,52].

In a study including more than 14 million units of blood screened between January 2007 and June 2008 in the United States, the overall seroprevalence was 1:27,500; the highest seroprevalence rates were observed in Florida and California [53]. Of 104 identified donors infected with T. cruzi, 28 percent were born in Mexico, 26 percent in the United States, 16 percent in El Salvador, and 11 percent in Bolivia; the remaining donors were born in nine other Central and South American countries. Among donors infected with T. cruzi who were born in the United States, 37 percent reported no specific risk factors for T. cruzi infection; all reported outdoor activities in the southern United States, suggesting autochthonous exposure to the infected vector or animal reservoirs. A subsequent study using blood bank screening data suggests that 5 to 7 percent of blood donors infected with T. cruzi may have been infected through local vector-borne transmission in the United States [54].

An additional consequence of these migration patterns is the occurrence of congenital and organ-derived T. cruzi infection in areas without vector-borne transmission. Congenital infections have been detected in the United States, Spain, and Switzerland, and transplant transmission of T. cruzi infection has occurred in the United States [55-59].

Movement of individuals infected with T. cruzi to cities has resulted in a rise in HIV coinfection [60]. Reactivation of Chagas disease in patients infected with T. cruzi and HIV has been described in Brazil, Bolivia, Argentina, and the United States [60-64].

The success of vector control means that formerly endemic areas of Brazil, Uruguay, Argentina, Paraguay, and Bolivia no longer have domestic and peridomestic vector-borne transmission [5]. Congenital transmission therefore accounts for a greater proportion of new infections than in the past; in 2015, the Pan American Health Organization estimated that 77 percent of incident infections are due to vectorial transmission compared with 22 percent by congenital transmission [6].

Insecticide resistance and failure of vector control methods in the Gran Chaco region of Bolivia, Argentina, and Paraguay means that this area still experiences the highest incidence of T. cruzi infection [65]. In much of this area, more than half of the rural population is infected [23,66]. Innovative approaches are needed to address vector control, etiologic treatment, and management of Chagas heart disease in this region.

Molecular epidemiology — T. cruzi is recognized as a complex of seven major lineages (TcI-TcVI and TcBat), with discrete but overlapping distributions [67-69]. TcI is the principal cause of Chagas disease in Mexico, Central America, and northern South America [70-72], while TcII, TcV, and TcVI are more frequently isolated from domestic transmission cycles in southern South America [15].

Gastrointestinal Chagas disease has long been observed to occur with some frequency in the Southern Cone countries, but very rarely in Mexico, Central America, and northern South America; this distribution was observed to track closely with the related discrete typing units (DTUs) TcII, TcV, and TcVI versus the more distantly related TcI [67]. No other clinical outcome has been convincingly shown to be associated with differences in DTU. Cardiomyopathy occurs throughout the range of T. cruzi, and the distribution of genotypes in any given study does not differ between those with and without cardiomyopathy [73]. Similarly, congenital infections mirror the distribution of genotypes detected among local adult populations [73].

However, molecular data are much sparser from regions where TcI predominates, compared with the Southern Cone. Additional data are needed to determine whether rates of congenital Chagas disease differ by parasite lineage. One of the major challenges to such studies is the technical difficulty of genotyping directly from clinical specimens [73]. Serotyping has been suggested as an alternative, and a rapid test that detects TcII/TcV/TcVI has been developed [74,75]. The sensitivity of the rapid test was higher among those with cardiomyopathy compared with asymptomatic infected individuals, possibly reflecting higher antibody levels in symptomatic individuals [75]. A parallel serotyping tool for TcI has been developed [76]. Both serotyping and molecular typing are applicable only as research tools.

NONVECTORIAL TRANSMISSION

Vertical transmission — An estimated 22 percent of new Chagas infections occur through mother-to-child transmission [6]. Congenital transmission can occur via females who themselves were infected congenitally, perpetuating the disease in the absence of the vector [77].

Reported transmission rates from infected mothers to infants range from approximately 1 to 10 percent [44,78-84]. The low sensitivity of neonatal screening tests combined with low follow-up rates later in infancy may lead to substantial underestimation of the transmission rate; one study estimated that only half of all infected infants are detected by routine screening [44]. (See "Chagas disease: Acute and congenital Trypanosoma cruzi infection", section on 'Congenital Chagas disease'.)

The strongest determinant of vertical transmission risk is the level of parasitemia in the mother; females with negative polymerase chain reaction (PCR) results are very unlikely to transmit to their infants [44,85,86]. Other factors associated with increased risk of congenital transmission include younger maternal age and HIV infection, likely because they are associated with higher parasite loads [44,78,83,85-90]. Treatment of females prior to pregnancy significantly decreases parasitemia and reduces the risk of congenital transmission by an estimated 95 percent [86,91,92]. Diagnosis in females of reproductive age is therefore a high priority (see 'Summary of screening recommendations' below). Antitrypanosomal drugs are contraindicated during pregnancy and lactation; if the diagnosis is made during pregnancy, treatment should be postponed until lactation ends.

Congenital transmission has been reported in the United States and in Europe [55,56,58,83,93].

Breastfeeding — The risk of transmission of Chagas disease via breastfeeding is unknown, but appears to be low [94]. In general, mothers with acute or reactivated Chagas disease should not breastfeed. Breastfeeding is reasonable for mothers with chronic Chagas disease. However, for females with chronic Chagas disease, it is generally suggested that breastfeeding be interrupted if the nipples are fissured or bleeding; a reasonable alternative is expression and sterilization of breast milk by pasteurization or microwave cooking [94].

Data on the transmission of T. cruzi through lactation are limited [94,95]. In one study of breast milk samples from 78 Brazilian women with chronic Chagas disease, no infected samples were observed, even though five women had parasitemia at the time of milk collection [95].

Oral transmission — Oral transmission of acute T. cruzi infection can occur via ingestion of food or drink contaminated by infected triatomine bugs or their feces [96,97]. Vehicles of oral transmission have included açaí palm fruit, guava juice, and juice prepared from sugarcane [98,99]. However, ingestion of T. cruzi amastigotes via consumption of raw meat is an unlikely mode of transmission [100].

Acute morbidity in orally transmitted infections appears to be more severe than among patients with vector-borne infection, and case-fatality rates are higher than among patients with vector-borne infection [96].

Control of oral transmission depends on sustained vector control and improving hygiene in food and beverage preparation.

Blood transfusion — Platelet transfusions pose a higher transmission risk than other blood components such as packed red cells [53,101,102]. In one analysis that traced 350 recipients of blood components from infected donors, the risk associated with a platelet unit was estimated to be 13 percent compared with 0 percent for packed red blood cells and frozen plasma/cryoprecipitate [103].

Transfusion transmission has been reported in the United States [104-107]. At least five of the seven known instances of transfusion transmission involved platelets [3]. No instances of transfusion transmission have been reported since screening of the United States blood supply began in 2007 [3]. (See 'Reducing transfusion and transplant transmission' below.)

Organ transplantation — Uninfected organ transplant recipients who receive an organ from a donor infected with T. cruzi may develop acute T. cruzi infection. Infection rates after organ transplantation from an infected donor seem to be lower for kidney recipients (0 to 19 percent) than for liver recipients (0 to 29 percent) and heart recipients (75 to 100 percent) [59,108-111]. Transmission via unrelated cord blood transplantation has also been reported [112].

Following identification of an infected organ donor, close monitoring of the recipient is warranted. (See 'Reducing transfusion and transplant transmission' below and "Chagas disease in the immunosuppressed host", section on 'Monitoring'.)

Laboratory accidents — Laboratory-acquired T. cruzi infection has rarely occurred via needlestick inoculation or mucous membrane exposure to parasite culture, blood from infected laboratory animals, or infected triatomine fecal material [113].

Laboratory personnel should use protective equipment to prevent needlesticks and potential contamination of the face, especially the eyes. High-risk accidents comprise needlestick injuries or contamination of the eye or mucous membranes with blood from laboratory animals with known T. cruzi infection [113]. Individuals with high-risk exposures should be monitored by PCR in weekly blood specimens for four weeks and serology at four and eight weeks [113]. Presumptive treatment is not generally recommended. The United States Centers for Disease Control and Prevention provides consultation to health care providers concerning Chagas disease 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]).

Risk to travelers — The risk to short-term travelers to Latin America is extremely low. Most vector-borne transmission occurs among people living in poor housing conditions and after years of exposure to infected vectors [114,115]. The only documented case of Chagas disease in a United States traveler occurred in the setting of known triatomine exposure in a vulnerable lodging during a three-week trip to Costa Rica [116].

Travelers can minimize risk of infection by avoiding poorly constructed accommodations, sleeping under insecticide-treated bed nets with the sides tucked in to prevent entry of vectors, and avoiding consumption of potentially contaminated fruit or cane juices such as those from street vendors [1,117].

PUBLIC HEALTH INTERVENTIONS

Public health interventions to address the burden of Chagas disease can be categorized as primary prevention (prevention of infection), secondary prevention (early detection and treatment to prevent sequelae), or tertiary prevention (medical and surgical management of morbidity to improve survival and quality of life) [118] (table 3). Primary prevention of Chagas disease includes vector control and donor screening to prevent transmission via blood components, organs, or tissue. Screening algorithms for control of congenital Chagas disease fall into the category of secondary prevention for the infant and their young siblings and either secondary or tertiary prevention for the mother. Diagnostic testing of patients with heart disease consistent with Chagas cardiomyopathy fits in the category of tertiary prevention.

Vector control — The first coordinated national vector control program began in Brazil in 1983 [119]. Between 1991 and 2004, four subregional control programs were established, funded largely by the governments of the countries involved and coordinated by the Pan American Health Organization. The major aims were to control transmission by domestic vectors and to prevent bloodborne T. cruzi transmission. Subsequently, programs to address congenital T. cruzi infection were added in a number of endemic countries [120,121].

Transmission by domestic vectors has been reduced via residual application of long-lasting insecticides in human dwellings and peridomestic structures. Improving the quality of domestic structures is also a useful control mechanism as this eliminates triatomine bug hiding places and decreases vector colonization and reinfestation of houses [122]. Surveys of sentinel populations are used to monitor the impact of control initiatives; such populations may include children <5 years or young individuals newly recruited to the army [123].

The Southern Cone Initiative, the first subregional control program to be established, has led to elimination of T. cruzi transmission by domestic T. infestans in Chile (1999), Uruguay (1997), Brazil (2006), and several provinces of Argentina and Paraguay [124,125]. Its success inspired the establishment of several other Chagas control initiatives (table 1) [119]. Subsequently, T. cruzi transmission by R. prolixus has been certified as interrupted throughout Central America and southern Mexico [16].

Despite this progress, foci of vector-borne transmission persist in most endemic countries of Latin America. The success of the Southern Cone Initiative has been challenged by reinfestation from residual vector colonies and the development of insecticide resistance. The Gran Chaco remains a heavily infested ecologic zone shared by Argentina, Bolivia, and Paraguay [126]. Transmission by vectors other than R. prolixus persists in Central America as well as in Mexico.

Because United States vectors are almost entirely sylvatic, the role of vector control is limited; effective screens, repair of gaps in house exteriors, and clearing brush and woodpiles around houses are recommended, especially in areas with known risk of triatomine home invasion [127].  

Reducing transfusion and transplant transmission — In the early 1990s, the prevalence of T. cruzi infection in donated blood units in Latin America ranged from 1 to 60 percent [128]. Serologic screening of blood components for T. cruzi became a component of all of the regional Chagas disease control initiatives and is mandated in all endemic countries (although compliance is variable) [129]. Since this intervention, the risk of transmission via blood transfusion has diminished greatly but has not been eliminated; in such regions, the risk of transmission is estimated to be 1:200,000 units [102,124,129].

In the United States, voluntary blood bank screening was initiated in 2007 and is estimated to cover 75 to 90 percent of the blood supply [53,104]. A small number of facilities perform screening tests only for donors who report epidemiologic risk factors. However, early studies of risk factor-based screening demonstrated suboptimal effectiveness for this approach [130]. The US Food and Drug Administration recommends screening all donations from individuals not previously screened; repeat screening is not recommended in the absence of a change in exposure history [41,131]. Infected individuals should be counseled not to donate blood.

Additional issues related to donor screening are discussed separately. (See "Blood donor screening: Medical history", section on 'Chagas disease' and "Blood donor screening: Laboratory testing", section on 'Chagas disease'.)

Recipients of an organ or blood product from a donor known to be infected with T. cruzi should be monitored for development of acute T. cruzi infection; this is discussed separately. (See "Chagas disease in the immunosuppressed host", section on 'Monitoring' and "Chagas disease: Acute and congenital Trypanosoma cruzi infection", section on 'Clinical manifestations'.)

SCREENING FOR CHAGAS DISEASE IN NONENDEMIC CLINICAL AND COMMUNITY SETTINGS

Summary of screening recommendations — Selection of populations who can be expected to benefit from screening for Chagas disease is based on epidemiologic risk factors, risk of transmission to others, and risk of morbidity and mortality from reactivation. Screening test modalities include serology, microscopy, and molecular testing with polymerase chain reaction (PCR); selection of appropriate testing modality is determined by the individual’s age and immune status, and the suspected phase of T. cruzi infection (table 3).

We suggest screening with a single, highly sensitive immunoglobulin (Ig)G serologic test for individuals who are nine months of age or older and meet one or more of the following criteria:

Persons who were born in or lived for at least six months in an endemic country of Latin America (high priority should be given to screening females of reproductive age, either prenatally or during routine care)

Persons born to a mother with confirmed T. cruzi infection

Persons with evidence of a bite or other exposure to a triatomine bug in Latin America or regions of United States with known enzootic cycles

Living organ donors with any of the above epidemiologic risk factors

Individuals who have any of the epidemiologic risk factors above and are transplant candidates/recipients or have HIV

Individuals with positive results by the screening test should undergo confirmatory testing with one or more additional distinct serologic assays. Confirmed diagnosis requires positive results by at least two distinct tests, preferably based on different antigens. Those with a confirmed diagnosis should undergo evaluation and potentially treatment for chronic Chagas disease. (See "Chagas disease: Chronic Trypanosoma cruzi infection", section on 'Diagnosis'.)

Individuals with profound immunosuppression may have false negative serology; in such cases, molecular testing may be warranted when the suspicion for Chagas disease remains high despite a negative screening IgG assay.

We suggest screening infants born to mothers with T. cruzi infection with PCR (plus microscopy if available) twice in the first three months of life, followed by IgG serology at nine months or later (algorithm 1). (See "Chagas disease: Acute and congenital Trypanosoma cruzi infection", section on 'Diagnosis'.)

We suggest serial monitoring with PCR for the following groups:

Recipient of an organ or tissue from a donor infected with T. cruzi (See "Chagas disease in the immunosuppressed host", section on 'Monitoring'.)

Transplant recipients with pre-existing chronic T. cruzi infection at risk for reactivation (See "Chagas disease in the immunosuppressed host", section on 'Monitoring'.)

We suggest that patients with epidemiologic risk factors and cardiac findings (arrhythmias, conduction abnormalities, congestive heart failure and/or reduced ejection fraction, regional wall motion abnormalities [particularly basal inferolateral or apical aneurysm], and thromboembolic phenomenon) suggestive of Chagas cardiomyopathy and/or gastrointestinal findings (megaesophagus, megacolon) suggestive of digestive Chagas disease undergo diagnostic testing with two distinct serologic assays. (See "Chronic Chagas cardiomyopathy: Clinical manifestations and diagnosis", section on 'Diagnosis' and "Chagas gastrointestinal disease", section on 'Diagnosis'.)

Rationale for screening

Rationale for screening asymptomatic persons with epidemiologic risk – We suggest serologic screening in primary care settings targeted to those with epidemiologic risk [132]. Because the majority of infected persons are asymptomatic for many years, if not throughout their lives, the only way to detect infection early is to screen populations at risk, either in community settings [47,133] or through primary care providers [134]. The expected prevalence of infection depends on the age groups screened and predominant source countries. The prevalence of Chagas disease in the United States among those born in Latin America is estimated to be 1 to 3 percent [47,133,135]. (See 'Geographic distribution' above.)

The major epidemiologic risk factor for T. cruzi infection in the United States and other nonendemic areas is prolonged exposure in endemic countries of Latin America [3]. Other risk factors include being born to a woman with prolonged exposure and/or birth in an endemic country and evidence of a bite or other exposure to a triatomine bug in Latin America or United States regions with known enzootic cycles. If a person’s mother is known to have epidemiologic risk factors but her infection status cannot be determined, it is reasonable to screen that person as well.  

As reviewed above, risk within endemic countries is extremely heterogeneous, with essentially no transmission risk in most urban centers. In rural areas, transmission risk varies greatly with triatomine species, density and behavior, house vulnerability to infestation, and presence of nonhuman animal reservoirs. However, given the lifelong nature of the infection and lack of detailed geographic risk data, the most prudent approach is to assume anyone born in or who has spent prolonged time in an endemic country may be at risk and should be screened at least once. Many publications use a cutoff of six months to define an exposure period warranting testing, although data informing a specific exposure period are minimal [132]. (See 'Geographic distribution' above.)

All individuals confirmed to have Chagas disease should undergo evaluation for cardiac or gastrointestinal involvement [136]. As an example, in a study of 302 women (median age 27 years) in Bolivia infected with T. cruzi, 28 (9.3 percent) had electrocardiography changes characteristic of Chagas cardiomyopathy [85].

Screening females of childbearing age and infants – Prenatal screening and screening for females who may become pregnant in the future is suggested for those with epidemiologic risk factors in order to prevent and treat congenital Chagas disease [132]. Treatment of infection prior to pregnancy decreases the risk of subsequent congenital transmission by an estimated 95 percent [86,92]. As with all other patients, females diagnosed with infection should undergo evaluation for cardiac or gastrointestinal involvement. Identification of T. cruzi infection in a female should prompt testing of all biological children; a mother with one infected infant may have a higher risk for transmission of infection to her other children [85,137,138].  

Congenital Chagas disease screening requires a multistep algorithm: (1) serologic screening and confirmation of T. cruzi infection in pregnant females (and females planning pregnancy), followed by (2) testing of infants of infected mothers with microscopy and/or molecular methods at birth and in the early months of life, and (3) for infants with negative screening earlier in infancy, IgG serology at nine months or later [137] (algorithm 1). The multistep process is necessary to identify congenital Chagas disease since one step testing is not sensitive enough to detect all cases early in life. Microscopy and PCR have a sensitivity of ≤50 percent and 70 to 75 percent in a single specimen, respectively [139]. An additional infant specimen tested at 30 to 90 days increases the likelihood of early detection. Follow-up with IgG serology at 9 to 12 months of age (when maternal IgG has cleared) is necessary to rule out infection in the infant.

Screening females of child-bearing age at high risk for Chagas disease in the United States has been shown to be cost effective. A study that compared the costs of testing and treating mothers and infants with the lifetime societal costs in the absence of testing found screening of high risk females to be cost-effective when maternal prevalence of Chagas disease is greater than 0.06 percent [140]. Among pregnant Latin American-born females in one Houston hospital, the prevalence of Chagas disease was estimated to be 0.3 percent [141,142].

Countries with a high burden of Chagas disease, such as Bolivia and Argentina, have large-scale congenital Chagas disease screening programs [79,143-146]. The weakest aspects of current screening programs are the low sensitivity of microscopy, lack of availability of reliable molecular laboratories in endemic zones, and low rates of follow-up (<20 percent) at the 9 to 12 month visit; at least half of congenital infections are likely missed by current screening [139,147,148]. (See "Chagas disease: Acute and congenital Trypanosoma cruzi infection", section on 'Congenital Chagas disease'.)

Screening persons with epidemiologic risk who are or may become immunosuppressed – Screening is suggested for individuals with epidemiologic risk for Chagas disease who are transplant candidates, are transplant recipients, or have HIV.

T. cruzi infection in the immunosuppressed patient can result in life-threatening reactivation disease. Patients receiving a kidney, liver, or heart transplant from an infected donor have up to 19, 29, and 100 percent risk, respectively, of developing T. cruzi infection [59,62,108-111]. Molecular monitoring can detect infection prior to the onset of symptoms, allowing for prompt antitrypanosomal therapy.

For transplant candidates who have chronic Chagas disease prior to transplantation, risk of reactivation after transplantation is approximately 20 percent [108].

Immunosuppression may cause falsely negative serology [149]. If suspicion for Chagas disease remains high despite negative serology, molecular testing for Chagas disease with PCR may be warranted. (See "Chagas disease in the immunosuppressed host".)

Diagnostic testing in persons with epidemiologic risk and evidence of existing cardiomyopathy or gastrointestinal Chagas disease – Diagnostic testing is suggested for patients with epidemiologic risk and cardiac or gastrointestinal findings consistent with Chagas disease. Five to nearly 20 percent of Latin American-born patients with nonischemic cardiomyopathy have Chagas disease [48-51]. Even though antitrypanosomal therapy does not significantly slow progression of established cardiomyopathy [150], knowledge of the etiology remains important for cardiac medical management and is crucial prior to heart transplantation to enable prospective monitoring for reactivation when immunosuppression occurs [136,151]. (See "Chronic Chagas cardiomyopathy: Clinical manifestations and diagnosis", section on 'Diagnosis' and "Chagas gastrointestinal disease", section on 'Diagnosis'.)  

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.

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Basics topic (see "Patient education: Chagas disease (The Basics)")

SUMMARY AND RECOMMENDATIONS

Introduction − Chagas disease is caused by infection with the protozoan parasite Trypanosoma cruzi, principally transmitted by triatomine bugs endemic to Latin America and the southern regions of United States. (See 'Introduction' above and 'Geographic distribution' above.)

Epidemiology – An estimated 6 million people are infected with Chagas disease, mostly due to vector-borne transmission in poor housing conditions in endemic regions of Latin America. The epidemiology of the disease is changing due to successful reduction of transmission in endemic areas as well as migration of individuals within and outside of endemic areas. Hundreds of thousands of infected individuals live in cities across Latin America and in the United States, Spain, and other European countries. (See 'Epidemiology and vectorial transmission' above.)

Vector transmission and life cycle − The infective trypomastigote form of the T. cruzi parasite is present in large numbers in the feces of infected triatomine bugs. During or immediately after a blood meal, the triatomine bug defecates on the skin of the host, allowing the organism to enter through the bite wound or via intact conjunctiva or mucous membranes. The risk of infection in the setting of short-term exposure is low; mathematical models estimate that, on average, 900 to 4000 contacts with infected vectors are needed to result in infection. (See 'Vector transmission and life cycle' above and 'Risk to travelers' above.)

Other modes of transmission – In addition to vector transmission, Chagas disease transmission can also occur vertically from mother to fetus, via breastfeeding, via transfusion of infected blood components, via organ transplantation from an infected donor, via ingestion of contaminated food or drink, or via laboratory exposure.

Vector control − Transmission by domestic vectors has been reduced via residual application of long-lasting insecticides in human dwellings and peridomestic structures. Despite this progress, foci of vector-borne transmission persist in most endemic countries of Latin America. (See 'Vector control' above.)

Blood transfusion screening − Serologic screening of blood components for T. cruzi became a component of all of the regional Chagas disease control initiatives and is mandated in all endemic countries (although compliance is variable). Since this intervention, the risk of transmission via blood transfusion has diminished greatly but has not been eliminated; in such regions, the risk of transmission is estimated to be 1:200,000 units. The US Food and Drug Administration recommends screening all donations from individuals not previously screened. (See 'Reducing transfusion and transplant transmission' above.)

Screening recommendations in nonendemic clinical and community settings

We suggest screening with a single, highly sensitive immunoglobulin (Ig)G serologic test for individuals who are nine months of age or older and meet one of the following criteria (table 3) (Grade 2C):

-Persons who were born in or lived for at least six months in an endemic country of Latin America (high priority should be given to screening females of reproductive age, either prenatally or during routine care).

-Persons born to a mother with confirmed T. cruzi infection

-Persons with evidence of a bite or other exposure to a triatomine bug in Latin America or regions of United States with known enzootic cycles

-Living organ donors with any of the above epidemiologic risk factors

-Individuals who have any of the epidemiology risk factors above and are transplant candidates/recipients or have HIV. (See 'Summary of screening recommendations' above and 'Rationale for screening' above.)

For infants born to mothers with T. cruzi infection, we perform screening with PCR (plus microscopy if available) twice in the first three months of life, followed by IgG serology at nine months or later (algorithm 1). (See 'Rationale for screening' above.)

We perform serial surveillance with PCR for recipients of an organ or tissue from a donor infected with T. cruzi and transplant recipients with pre-existing chronic T. cruzi infection at risk for reactivation. (See 'Rationale for screening' above.)

In patients with epidemiologic risk factors and findings suggestive of Chagas cardiomyopathy and/or digestive Chagas disease, we perform diagnostic testing with two distinct serologic assays. (See 'Rationale for screening' above.)

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Topic 5698 Version 35.0

References

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