Chagas disease

Chagas disease
Other namesAmerican trypanosomiasis
A crescent-shaped Trypanosoma cruzi parasite surrounded by red blood cells
Photomicrograph of Giemsa-stained Trypanosoma cruzi
SpecialtyInfectious disease
SymptomsFever, large lymph nodes, headache[1]
ComplicationsHeart failure, enlarged esophagus, enlarged colon[1]
CausesTrypanosoma cruzi spread by kissing bugs[1]
Diagnostic methodFinding the parasite or antibodies in the blood[2]
PreventionEliminating kissing bugs and avoiding their bites[1]
MedicationBenznidazole, nifurtimox[1]
Frequency6.2 million (2017)[3]
Deaths7,900 (2017)[4]

Chagas disease, also known as American trypanosomiasis, is a tropical parasitic disease caused by the protist Trypanosoma cruzi.[1] It is spread mostly by insects known as Triatominae, or "kissing bugs".[1] The symptoms change over the course of the infection. In the early stage, symptoms are typically either not present or mild, and may include fever, swollen lymph nodes, headaches, or local swelling at the site of the bite.[1] After 8–12 weeks, individuals enter the chronic phase of disease and in 60–70% it never produces further symptoms.[2][5] The other 30–40% of people develop further symptoms 10–30 years after the initial infection,[2] including enlargement of the ventricles of the heart in up to 30%, leading to heart failure.[1] Neurological and digestive complications, including an enlarged esophagus or an enlarged colon, may also occur in 10% of people.[1]

T. cruzi is commonly spread to humans and other mammals by the blood-sucking "kissing bugs" of the subfamily Triatominae.[6] These insects are known by a number of local names, including: vinchuca in Argentina, Bolivia, Chile and Paraguay, barbeiro (the barber) in Brazil, pito in Colombia, chinche in Central America, and chipo in Venezuela.[7] The disease may also be spread through blood transfusion, organ transplantation, eating food contaminated with the parasites, and by vertical transmission (from a mother to her fetus).[1] Diagnosis of early disease is by finding the parasite in the blood using a microscope.[2] Chronic disease is diagnosed by finding antibodies for T. cruzi in the blood.[2]

Prevention focuses on eliminating kissing bugs and avoiding their bites.[1] This may involve the use of insecticides or bed-nets.[8] Other preventive efforts include screening blood used for transfusions.[1] As of 2019, a vaccine has not been developed.[1] Early infections are treatable with the medications benznidazole or nifurtimox.[1] Medication nearly always results in a cure if given early, but becomes less effective the longer a person has had Chagas disease.[1] When used in chronic disease, medication may delay or prevent the development of end–stage symptoms.[1] Benznidazole and nifurtimox cause temporary side effects in up to 40% of people[1] including skin disorders, brain toxicity, and digestive system irritation.[5][9][10]

It is estimated that 6.2 million people, mostly in Mexico, Central America and South America, have Chagas disease as of 2017.[1][3] In 2017, Chagas was estimated to result in 7,900 deaths.[4] Most people with the disease are poor,[5] and most do not realize they are infected.[11] Large-scale population movements have increased the areas where Chagas disease is found and these include many European countries and the United States.[1] The disease was first described in 1909 by the Brazilian physician Carlos Chagas, after whom it is named.[1] Chagas disease is classified as a neglected tropical disease.[12] It affects more than 150 other animals.[5]

Signs and symptoms

Black and white photo of a young boy with a swollen right eye
An acute Chagas disease infection with swelling of the right eye (Romaña's sign)

The human disease occurs in two stages: an acute stage, which occurs shortly after an initial infection, and a chronic stage that develops over many years.[13] The acute phase, which develops one to two weeks after a person is exposed to the parasite,[14] is often symptom-free.[13] When present, the symptoms are typically minor and not specific to any particular disease; most acute infections are never diagnosed.[14] Signs and symptoms include fever, malaise, headache, and enlargement of the liver, spleen, and lymph nodes.[1][13][14] Rarely, a skin nodule called a chagoma may be present at the site of the insect bite.[14] Another marker of acute Chagas disease is Romaña's sign, which is a painless swelling of the eyelids on the side of the face near the bite wound or where the insect feces were deposited.[14][15] During the acute phase of infection, Trypanosoma cruzi can be seen in stained blood smears or on direct microscopic examination of the blood.[14][16]

Large scale anatomy of a heart damaged by chronic Chagas disease

The acute phase typically lasts for four to eight weeks and resolves without treatment. A small proportion of infected individuals (less than 1–5%)[13] develop severe acute disease, which can cause life-threatening inflammation of the brain and surrounding tissues and the heart muscle.[14] After the symptoms resolve, if the infection is not treated the disease enters a chronic phase.[13] Of individuals with chronic Chagas disease, approximately 70–80% will never develop symptoms (called indeterminate chronic Chagas disease), while the remainder will develop organ dysfunction (called determinate chronic Chagas disease).[14] Individuals may remain in the indeterminate phase for decades before progressing to chronic disease.[17] In 10% of individuals, the disease progresses directly from the acute form to a symptomatic clinical form of chronic Chagas disease.[17] Individuals with an indeterminate form of the disease may become symptomatic if they are immunosuppressed.[16]

The symptomatic (determinate) chronic stage affects the heart, digestive system and nervous system.[13] It is estimated that 20−30% of people with chronic infections develop cardiomyopathy (disease of the heart muscle).[18] The most common manifestations of Chagas cardiomyopathy are arrhythmias, ventricular aneurysms, abnormalities of the myocardium, and thromboembolism.[17] In the later stages of the disease, individuals may develop dilated cardiomyopathy and congestive heart failure.[13][14] Sudden death (usually caused by ventricular arrhythmia) is the most common cause of death in people with Chagas cardiomyopathy, accounting for 55−60% of deaths.[13][17] The second and third most common causes are heart failure and thromboembolism.[13]

About 10–21% of people with chronic Chagas disease develop digestive system damage,[13] mainly affecting the esophagus and colon.[14] Esophageal symptoms range from mild dysfunction of the esophageal sphincter (achalasia) to severe enlargement of the organ (megaesophagus), causing difficulty swallowing, weight loss, cough, and gastroesophageal reflux.[14] Individuals with colonic involvement experience constipation and megacolon, which can lead to bowel obstruction.[17][19] It is uncommon for people to have both cardiac and gastrointestinal involvement.[13]

Up to 10% of chronically infected individuals develop neuritis that results in altered tendon reflexes and sensory impairment. Isolated cases exhibit central nervous system involvement, including dementia, confusion, chronic encephalopathy and sensory and motor deficits.[20]

The clinical manifestations of Chagas disease are due to cell death in the target tissues that occurs during the infective cycle, by sequentially inducing an inflammatory response, cellular lesions, and fibrosis. For example, intracellular amastigotes destroy the intramural neurons of the autonomic nervous system in the intestine and heart, leading to megaintestine and heart aneurysms, respectively. If left untreated, Chagas disease can be fatal, in most cases due to heart muscle damage.[19]


Life cycle and transmission of T. cruzi

Chagas disease is caused by infection with the protozoan parasite T. cruzi, typically introduced into humans through the bite of triatomine bugs, also called "kissing bugs".[14] At the bite site, motile T. cruzi forms called trypomastigotes invade various host cells.[6] Inside a host cell, the parasite transforms into a replicative form called an amastigote, which undergoes several rounds of replication.[6] The now-replicated amastigotes transform back into trypomastigotes, which burst the host cell and are released into the bloodstream.[13] Trypomastigotes then disseminate throughout the body to various tissues, where they invade cells and replicate.[13] Over many years, cycles of parasite replication and immune response can severely damage these tissues, particularly the heart and digestive tract.[13]


Rhodnius prolixus is the principal vector in Colombia, Venezuela, Guatemala, Honduras, and some parts of Nicaragua and El Salvador[citation needed]

In Chagas-endemic areas, the main mode of transmission is through an insect vector called a triatomine bug.[6] A triatomine becomes infected with T. cruzi by feeding on the blood of an infected person or animal. During the day, triatomines hide in crevices in the walls and roofs.[6][failed verification]

The bugs emerge at night, when the inhabitants are sleeping. Because they tend to feed on people's faces, triatomine bugs are also known as "kissing bugs". After they bite and ingest blood, they defecate on the person. Triatomines pass T. cruzi parasites (called trypomastigotes) in feces left near the site of the bite wound.[6]

Scratching the site of the bite causes the trypomastigotes to enter the host through the wound, or through intact mucous membranes, such as the conjunctiva. Once inside the host, the trypomastigotes invade cells, where they differentiate into intracellular amastigotes. The amastigotes multiply by binary fission and differentiate into trypomastigotes, which are then released into the bloodstream. This cycle is repeated in each newly infected cell. Replication resumes only when the parasites enter another cell or are ingested by another vector.[6] Dense vegetation (such as that of tropical rainforests) and urban habitats are not ideal for the establishment of the human transmission cycle. However, in regions where the sylvatic habitat and its fauna are thinned by economic exploitation and human habitation, such as in newly deforested areas, piassava palm culture areas, and some parts of the Amazon region, a human transmission cycle may develop as the insects search for new food sources.[21]

T. cruzi can also be transmitted through blood transfusions and organ transplantation.[16] With the exception of blood derivatives (such as fractionated antibodies), all blood components are infective. The parasite remains viable at 4 °C for at least 18 days or up to 250 days when kept at room temperature. As of 2010 it was unclear whether T. cruzi can be transmitted through frozen-thawed blood components.[22]

Chagas disease can be transmitted through food or drink contaminated with triatomine insects or their feces. Unpasteurized fruit juices are the most frequent source of infection. This route of transmission, first recognized in 1960,[23] has been implicated in several outbreaks[16] and in an increase in disease incidence in the Amazon basin.[13] Orally transmitted Chagas disease is of particular concern in Venezuela, where 16 outbreaks have been recorded between 2007 and 2018.[24] The mortality rate for orally acquired disease is higher than that of the vector-transmitted form.[13]

Other modes of transmission include through breast milk[25] and by accidental laboratory exposure.[13]

Chagas disease can also spread congenitally from a pregnant woman to her baby through the placenta, and as of 1984 accounted for approximately 13% of stillborn deaths in parts of Brazil.[26]

As of 2010 Chagas disease was a growing problem in Spain, because the majority of cases with chronic infection are asymptomatic and because of migration from Latin America.[27]


The presence of T. cruzi is diagnostic of Chagas disease. During the acute phase of infection, it can be detected by microscopic examination of fresh anticoagulated blood, or its buffy coat, for motile parasites; or by preparation of thin and thick blood smears stained with Giemsa, for direct visualization of parasites.[14][16] Blood smear examination detects parasites in 34–85% of cases. If techniques such as microhematocrit centrifugation are used to concentrate the blood, the sensitivity increases to greater than 95 percent.[13] On microscopic examination, T. cruzi trypomastigotes exhibit a slender body, often in the shape of an S or U, with a flagellum connected to the body by an undulating membrane. The average length of the parasite is 20−25 μm.[28] T. cruzi can be distinguished from Trypanosoma brucei, the causative agent of African trypanosomiasis, by its smaller size and larger kinetoplast.[29] The non-pathogenic species Trypanosoma rangeli is longer and thinner than T. cruzi, with a smaller kinetoplast and non-centrally located cell nucleus.[28]

During the chronic phase, microscopic diagnosis is unreliable because the level of parasites in the blood is low. Chronic Chagas disease is usually diagnosed using serologic tests, which detect Immunoglobulin G antibodies against T. cruzi in the person's blood.[16] Two positive test results are required to confirm the diagnosis.[14] If the test results are inconclusive, additional testing methods such as Western blot (which detects antibodies) or polymerase chain reaction (which detects T. cruzi DNA) can be used.[13] Polymerase chain reaction is also used to diagnose congenital Chagas disease and to monitor T. cruzi levels in immunosuppressed people and organ transplant recipients.[13][14]

Various rapid diagnostic tests for Chagas disease are available. These tests are easily transported and can be performed by people without special training.[30] They are useful for screening large numbers of people and testing people who cannot access healthcare facilities, but their sensitivity is relatively low,[13] and it is recommended that a second method is used to confirm a positive result.[30][31]

T. cruzi can be isolated from samples through blood culture or xenodiagnosis, or by inoculating animals with the person's blood. In the blood culture method, the person's red blood cells are separated from the plasma and added to a specialized growth medium to encourage multiplication of the parasite. It can take up to six months to obtain the result. Xenodiagnosis involves feeding the person's blood to triatomine insects, then examining their feces for the parasite 30 to 60 days later.[30] These methods are not routinely used, as they are slow and have low sensitivity.[19][30]

Various immunoassays for T. cruzi are available and can be used to distinguish among strains (zymodemes of T.cruzi with divergent pathogenicities).[32] These tests include: detecting complement fixation, indirect hemagglutination, indirect fluorescence assays, radioimmunoassays, and ELISA. Alternatively, diagnosis and strain identification can be made using polymerase chain reaction (PCR).[19]


French-language poster displaying vectors of Chagas disease and prevention methods such as use of bednets and insect screens
Awareness and prevention campaign poster in Cayenne, French Guiana, 2008

As of 2019, there was no vaccine against Chagas disease.[1] Prevention is generally focused on decreasing the numbers of the insect that spreads it (Triatoma) and decreasing their contact with humans. This is done by using insecticides (usually cypermethrin or permethrin), and improving housing and sanitary conditions in rural areas.[33] For urban dwellers, spending vacations and camping out in the wilderness or sleeping at hostels or mud houses in endemic areas can be dangerous; a mosquito net is recommended. Some measures of vector control include:

  • A yeast trap can be used for monitoring infestations of certain species of triatomine bugs (Triatoma sordida, Triatoma brasiliensis, Triatoma pseudomaculata, and Panstrongylus megistus).[34]
  • Promising results were gained with the treatment of vector habitats with the fungus Beauveria bassiana.[35]
  • Targeting the symbionts of Triatominae through paratransgenesis can be done.[36]

A number of potential vaccines are currently being tested. Vaccination with Trypanosoma rangeli has produced positive results in animal models.[37] More recently, the potential of DNA vaccines for immunotherapy of acute and chronic Chagas disease is being tested by several research groups.[38]

Blood transfusion was formerly the second-most common mode of transmission for Chagas disease, but the development and implementation of blood bank screening tests has dramatically reduced this risk in the 21st century. Blood donations in all endemic Latin American countries undergo Chagas screening, and testing is expanding in countries, such as France, Spain and the United States, that have significant or growing populations of immigrants from endemic areas.[39][40] In Spain, donors are evaluated with a questionnaire to identify individuals at risk of Chagas exposure for screening tests.[40]

The US FDA has approved two Chagas tests, including one approved in April 2010, and has published guidelines that recommend testing of all donated blood and tissue products.[40][41] While these tests are not required in US, an estimated 75–90% of the blood supply is currently tested for Chagas, including all units collected by the American Red Cross, which accounts for 40% of the U.S. blood supply.[41][42] The Chagas Biovigilance Network reports current incidents of Chagas-positive blood products in the United States, as reported by labs using the screening test approved by the FDA in 2007.[43]


There are two approaches to treating Chagas disease: antiparasitic treatment, to kill the parasite; and symptomatic treatment, to manage the symptoms and signs of the infection. Management uniquely involves addressing selective incremental failure of the parasympathetic nervous system. Autonomic disease imparted by Chagas may eventually result in megaesophagus, megacolon and accelerated dilated cardiomyopathy. The mechanisms that explain why Chagas targets the parasympathetic autonomic nervous system and spares the sympathetic autonomic nervous system remain poorly understood.


Antiparasitic treatment is most effective early in the course of infection, but is not limited to cases in the acute phase. As of 2005, drugs of choice included azole or nitro derivatives, such as benznidazole[44] or nifurtimox. Both agents are limited in their capacity to completely eliminate T. cruzi from the body (parasitologic cure), especially in chronically infected people, as of 1998, resistance to these drugs has been reported.[45]

As of 2010, studies suggested that antiparasitic treatment leads to parasitological cure in more than 90% of infants, but only about 60–85% of adults treated in the first year of acute phase Chagas disease. Children aged six to twelve years with chronic disease had a cure rate of about 60% with benznidazole. While the rate of cure declines the longer an adult has been infected with Chagas, as of 2010 treatment with benznidazole has been shown to slow the onset of heart disease in adults with chronic Chagas infections.[5][19]

As of 2010, treatment of chronic infection in women prior to or during pregnancy did not appear to reduce the probability the disease will be passed on to the infant. Likewise, it was unclear whether prophylactic treatment of chronic infection would be beneficial in persons who will undergo immunosuppression for example, organ transplant recipients or in persons who are already immunosuppressed for example, those with HIV infection.[19]


In the chronic stage, treatment involves managing the clinical manifestations of the disease. For example, pacemakers and medications for irregular heartbeats, such as the anti-arrhythmia drug amiodarone, may be life saving for some people with chronic cardiac disease,[46] while surgery may be required for megaintestine. The disease cannot be cured in this phase. Chronic heart disease caused by Chagas disease is a common reason for heart transplantation surgery. Until recently, Chagas disease was considered a contraindication for the procedure, since the heart damage could recur as the parasite was expected to seize the opportunity provided by the immunosuppression that follows surgery.[47]


Chagas disease in Latin America (endemic zones)

In 2017, Chagas disease affected an estimated 6.2 million people worldwide, with approximately 162,000 new infections occurring per year.[3] The disease resulted in approximately 7,900 deaths in 2017, a 3.8% increase from 2007.[4] As of 2010, 14,400 infants were born with congenital Chagas disease annually.[5][19] Chagas disease has a serious economic impact; as of 2013, the global cost was estimated at $7 billion.[48]

As of 2019, Chagas disease was endemic to 21 countries in continental Latin America (Argentina, Belize, Bolivia, Brazil, Chile, Colombia, Costa Rica, Ecuador, El Salvador, French Guiana, Guatemala, Guyana, Honduras, Mexico, Nicaragua, Panama, Paraguay, Peru, Suriname, Uruguay, and Venezuela).[1] The endemic area ranges from the southern United States to northern Chile and Argentina, with Bolivia, Argentina, and Paraguay exhibiting the highest prevalence of the disease.[13] The prevalence of the disease is increasing in non-endemic areas such as the United States, Canada and Europe, primarily due to migration from Latin America,[1] and it is considered a global epidemic.[13]

Chagas exists in two different ecological zones: In the Southern Cone region, the main vector lives in and around human homes. In Central America and Mexico, the main vector species lives both inside dwellings and in uninhabited areas. In both zones, Chagas occurs almost exclusively in rural areas, where triatomines breed and feed on the more than 150 species from 24 families of domestic and wild mammals, as well as humans, that are the natural reservoirs of T. cruzi.[49]

Although Triatominae bugs feed on them, birds appear to be immune to infection and therefore are not considered to be a T. cruzi reservoir. Even when colonies of insects are eradicated from a house and surrounding domestic animal shelters, they can re-emerge from plants or animals that are part of the ancient, sylvatic (referring to wild animals) infection cycle. This is especially likely in zones with mixed open savannah, with clumps of trees interspersed by human habitation.[50]

Chronic Chagas disease remains a major health problem in many Latin American countries, despite the effectiveness of hygienic and preventive measures, such as eliminating the transmitting insects. Landmarks have been achieved in the fight against it in Latin America, including a reduction by 72% of the incidence of human infection in children and young adults in the countries of the Southern Cone Initiative, and at least three countries (Uruguay, in 1997, and Chile, in 1999, and Brazil in 2006) have been certified free of vectorial and transfusional transmission.[19][51][52] In Argentina, vectorial transmission has been interrupted in 13 of the 19 endemic provinces,[51] and major progress toward this goal has also been made in both Paraguay and Bolivia.[citation needed]

As of 2009, screening of donated blood, blood components, and solid organ donors, as well as donors of cells, tissues, and cell and tissue products for T. cruzi was mandated in all Chagas-endemic countries and has been implemented.[53]

In the United States

As of 2008, about 300,000 infected people were living in the United States, which is likely the result of immigration from Latin American countries.[54] As of 2020, locally acquired Chagas disease in the US has been exceedingly rare. Only 28 autochthonous infections were documented from 1955 to 2015. In 2017, the first documented autochthonous case of Chagas disease in Missouri occurred, as a blood donation screened positive for antibodies to Trypanosoma cruzi.[55]

From 1998 to 2018, seven cases of transfusion-transmitted Chagas disease were documented in the United States and Canada.[56] As of 2019, all blood donors in the U.S. are tested for antibodies against Trypanosoma cruzi prior to blood donation to address and minimize the risk of disease transmission by blood transfusion.[16][56]

The primary wildlife reservoirs for Trypanosoma cruzi in the United States include opossums, raccoons, armadillos, squirrels, woodrats, and mice.[57] Opossums are particularly important as reservoirs, because the parasite can complete its life cycle in the anal glands of this animal without having to re-enter the insect vector.[57] In 1991/92 from 8.3%[57] to 37.5% of opossums were infected.[58] Studies on raccoons in the Southeast yielded infection rates ranging from 15% in 1992[57] to 47% in 2009[59] In Armadillos from Louisiana prevalence ranged from 1% in 1991[58] to 28% in 1988.[60] Small rodents, including squirrels, mice, and rats, are important in the sylvatic transmission cycle because they are bloodmeal sources for the insect vectors. A 1980 Texas study revealed 17% percent T. cruzi prevalence in 75 specimens representing four small rodent species.[61]

As of 2013, the cost of treatment in the United States was estimated to be $900 million annually (global cost $7 billion), which included hospitalization and medical devices such as pacemakers.[48]


Black and white photo of Charlos Chagas, in his lab coat, sitting next to his microscope and surrounded by flasks and jars

The earliest detection of a T. cruzi infection comes from a 9000-year-old Chinchorro mummy. Other exhumed mummies in the Andean region as well as pre-Columbian Peruvian ceramics shed light on the existence of Chagas Disease and have provided anthropologists reasons for how and why the illness spread.[62] In 1707, the Portuguese physician, Miguel Dial Pimenta, was the first individual to provide a clinical report relating to the possible intestinal symptoms of Chagas Disease.[62]

The disease was named after the Brazilian physician and epidemiologist Carlos Chagas, who first described it in 1909.[63][64][65][66] The disease was not seen as a major public health problem in humans until the 1960s (the outbreak of Chagas disease in Brazil in the 1920s went widely ignored[67]). Dr Chagas discovered that the intestines of Triatomidae (now Reduviidae: Triatominae) harbored a flagellate protozoan, a new species of the genus Trypanosoma, and was able to demonstrate experimentally that it could be transmitted to marmoset monkeys that were bitten by the infected bug. Later studies showed squirrel monkeys were also vulnerable to infection.[68]

Chagas named the pathogenic parasite as Trypanosoma cruzi[63] and later that year as Schizotrypanum cruzi,[65] both honoring Oswaldo Cruz, the noted Brazilian physician and epidemiologist who successfully fought epidemics of yellow fever, smallpox, and bubonic plague in Rio de Janeiro and other cities in the beginning of the 20th century. Chagas was also the first to unknowingly discover and illustrate the parasitic fungal genus Pneumocystis, later infamously linked to PCP (Pneumocystis pneumonia in AIDS victims).[64] Confusion between the two pathogens' life-cycles led him to briefly recognize his genus Schizotrypanum, but following the description of Pneumocystis by others as an independent genus, Chagas returned to the use of the name Trypanosoma cruzi.

In Argentina, the disease is known as mal de Chagas-Mazza, in honor of Salvador Mazza, the Argentine physician who in 1926 began investigating the disease and over the years became the principal researcher of this disease in the country.[69] Mazza produced the first scientific confirmation of the existence of Trypanosoma cruzi in Argentina in 1927, eventually leading to support from local and European medical schools and Argentine government policy makers.[70]

It has been hypothesized that Charles Darwin might have suffered from Chagas disease as a result of a bite of the so-called great black bug of the Pampas (vinchuca) (see Charles Darwin's illness). The episode was reported by Darwin in his diaries of the Voyage of the Beagle as occurring in March 1835 to the east of the Andes near Mendoza. Darwin was young and generally in good health, though six months previously he had been ill for a month near Valparaiso, but in 1837, almost a year after he returned to England, he began to suffer intermittently from a strange group of symptoms, becoming incapacitated for much of the rest of his life. Attempts to test Darwin's remains at Westminster Abbey by using modern PCR techniques were met with a refusal by the Abbey's curator.[71]


As of 2007, Several experimental treatments showed promise in animal models. These included inhibitors of oxidosqualene cyclase and squalene synthase,[72][73] cysteine protease inhibitors,[72][74] dermaseptins collected from frogs in the genus Phyllomedusa (P. oreades and P. distincta),[75] the sesquiterpene lactone dehydroleucodine (DhL), which affects the growth of cultured epimastigote-phase Trypanosoma cruzi,[76] inhibitors of purine uptake,[72] and inhibitors of enzymes involved in trypanothione metabolism.[77]

New drug targets may be revealed following the sequencing of the T. cruzi genome.[78]

Megazol in a study seems more active against Chagas than benznidazole but has not been studied in humans.[79] A Chagas vaccine (TcVac3) has been found to be effective in mice with plans for studies in dogs. It is hoped that it will be commercially available by 2018.[80]

See also


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Further reading

  • Hotez PJ, Dumonteil E, Woc-Colburn L, et al. (29 May 2012). "Chagas disease: 'The new HIV/AIDS of the Americas'". PLoS Neglected Tropical Diseases. 6 (5): e1498. doi:10.1371/journal.pntd.0001498. PMC 3362306. PMID 22666504. An editorial.

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