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Chagas Disease
Introduction
Chagas disease, or American Trypanosomiasis, is a potentially life-threatening zoonotic illness caused by the parasite Trypanosoma cruzi, first described in 1909 by Brazilian physician Carlos Chagas.[1] The disease is primarily found in Central and South America, Trinidad, and the southern United States, with rural areas being most affected due to the presence of the reduviid bug (also known as the triatomine or kissing bug). The vector-borne disease is transmitted primarily via contact with contaminated excrement of the reduviid bug into an open wound (eg, the bite of the bug itself), with the insect serving as the intermediate host for the parasite and humans and other mammals serving as definitive hosts.[2] Vertical transmission between mother and fetus is also possible. Other modes of transmission include transfusion of blood products, transplant of an infected organ, or consumption of infected food or drinks.
Chagas disease has 2 phases: acute and chronic. The acute phase, lasting about 2 months, often presents with mild or no symptoms, though fever, localized edema, and Romana’s sign (unilateral eyelid swelling) may occur. In the chronic phase, which affects approximately 30% of infected individuals, cardiac complications, eg, cardiomegaly, heart failure, and arrhythmias, are common, while gastrointestinal involvement may lead to megacolon or megaesophagus.[3] Diagnosis in the acute phase relies on microscopic detection of the parasite or PCR testing, while chronic cases are confirmed through serological tests.
Treatment includes antiparasitic medications, nifurtimox and benznidazole, which are most effective in the acute phase. In chronic cases, management focuses on treating complications, with some patients requiring pacemakers, defibrillators, or surgical interventions.
Etiology
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Etiology
Chagas disease is a vector-borne disease most commonly transmitted through contact with contaminated feces and urine of the reduviid bug. This insect, in turn, carries the causative agent, the parasite Trypanosoma cruzi. Currently, 11 different species of the triatomine bug have been identified. The most common species in the southern United States are Triatoma sanguisuga and Triatoma gerstaeckeri.[4] The primary vectors for Mexico, Central, and South America are Rhodnius prolixus and Triatoma dimidiata.[5]
The insects often lay dormant during the daytime, hiding in cracks in housing or agricultural structures and emerging at night to feed. Both sexes of reduviid bugs feed in this way, and female bugs must additionally take blood meals to lay their eggs. As it takes the meal or soon afterward, the insect defecates and expels parasites in the feces and urine near the feeding bite. Local irritation at the bite site causes the person to instinctively rub the area, smearing the parasite-laden excrement into the open wound. The parasite can also enter through contact with the mucous membranes if the person touches their mouth or eyes with contaminated skin. Feces of infected reduviid bugs carry the largest number of the infectious trypomastigote form.[6]
Other mode transmissions include:
- Vertical transmission from mother to fetus leading to congenital Chagas disease
- Organ transplantation
- Transfusion of blood and blood products
Epidemiology
Chagas is endemic in Latin America, from the southern United States to northern Argentina and Chile.[7] However, the distribution of the disease is changing due to the relocation of individuals from the endemic countries. The World Health Organization (WHO) estimates that 6 to 7 million people are currently infected with T. cruzi, causing 12,000 deaths annually, with 75 million people at risk of contracting the disease. Of those infected with the parasite, 1 in 10 will develop cardiac manifestations.[8]
Domestic and wild mammals are also common hosts for this parasite. The primary transmission route occurs through infected reduviid bugs, which can be found in cracks indoors or on the roofs of substandard housing made from mud, straw, or palm thatch. Outdoor locations include animal nests, agricultural buildings (eg, barns and chicken coops), and tree bark or logs.[9] Children are most commonly affected, followed by women and then men.
Pathophysiology
The T. Cruzi Parasite Life Cycle
T. cruzi, in its leishmanial (trypanomastigote) form, is ingested by the vector reduviid bug when it takes a blood meal from an infected host. The trypomastigotes transform into epimastigotes in the insect's midgut, where they multiply and become flagellated in the midgut. Finally, they mature to the infective form in the hindgut, where they are excreted to infect a new host after the insect bites again (see Image. T. Cruzi Parasite Life Cycle).
When the reduviid bug bites and takes a blood meal, the metacyclic trypomastigotes are passed in the insect's feces near the open bite wound. Local irritation causes the mammal to scratch or contact the area, introducing the trypomastigotes to the mammalian host's bloodstream through the open bite. Alternatively, the mammalian host may innoculate themselves later by touching mucous membranes with a contaminated appendage.
After the parasite enters through an open wound or mucous membrane, the metacyclic trypomastigote penetrates various host cells near the site of infection, where they transform into amastigotes intracellularly. The amastigote stage of the parasites is found mainly inside pseudocysts located in muscle or nerve cells, where they multiply via binary fission. The intracellular amastigotes transform into trypanomastigotes, resulting in cell rupture and the entrance of the trypanomastigotes into the host bloodstream. These circulating trypanomastigotes can then infect additional host cells, and this host auto-infection cycle repeats, leading to clinical disease. If such a host is then bitten by another reduviid bug, these circulating trypomastigotes are then uptaken with the blood meal by the reduviid vector, facilitating transmission to additional hosts.[10]
Clinical Phases
Chagas disease has 2 clinical phases: acute and chronic.
Acute infection
Signs and symptoms are directly related to the T. cruzi parasite's replication and the host immune response to this replication. During this phase, the cycle of replication and auto-infection results in circulating trypomastigotes in the bloodstream, and the host's immune system produces antibodies to combat the infection. This phase lasts several weeks after initial infection and is primarily driven by host immune cells targeting intracellular pathogens, eg, natural killer T-cells and macrophages.[11]
Chronic infection
Untreated infection leads to ongoing circulation and deposition of parasite trypomastigotes into various cells throughout the host's body, and clinical disease is the result of years of continuing replication, circulation, and immune response, ultimately leading to end-organ damage in the host.[12] The parasites show a predilection for infecting striated muscle cells, with significant parasite load detectable in cardiac muscle early in the chronic infection course. This leads to local immune response inciting fibrosis of the cardiac muscle, leading to cardiomegaly and an overall decrease of viable myocardium.
Late in the chronic phase of infection, parasite levels drop to barely detectable levels as the number of viable myocardial cells decreases.[12] This cardiomegaly and cardiac fibrosis then lead to clinical signs and symptoms of heart failure, with reduced contractility, cardiac output, and arrhythmias.[13] The parasite also routinely infects nerve cells in the gastrointestinal tract, leading to a profound loss of nerve endings in the digestive system, leading to decreased peristalsis in the esophagus and loss of function in the esophagus, as well as in the colon, with this loss of neurologic control of these organs being the underlying cause of organ dysfunction, as well as interrupting the blood supply.[13]
Histopathology
Microscopic detection of T. cruzi parasites is diagnostic for Chagas disease. Motile parasites can be detected microscopically by examining fresh, anticoagulated blood or the buffy coat of a fresh blood sample (see Image. Chagas Disease).[14] Alternatively, both thick and thin peripheral blood smears can be stained with Giemsa, where parasites can be visualized with a sensitivity ranging from 34% to 85% (see Image. Trypanosoma Cruzi).[11][15] Microscopically, the T. cruzi parasite has an undulating cell membrane with a flagellum, a visible nucleus, and a hallmark kinetoplast structure, distinguishing T. cruzi from other Trypanosoma species.[16]
History and Physical
Clinical Features of Chagas Disease
The clinical features of Chagas disease depend on its phase: acute or chronic. In either case, though possible, it is rare for a patient to remember or report a reduviid bug bite. Therefore, the astute clinician must consider Chagas disease as part of a broad differential diagnosis, especially in endemic areas.
Acute phase
The acute phase of Chagas disease lasts for approximately 2 months following infection from a bite, and symptoms may be very mild or absent altogether. Patients may rarely present with a skin lesion or visible bite with local irritation but, more commonly, will experience fever, localized edema, lymphadenopathy, myalgias, pallor, shortness of breath, and abdominal or chest pains.[17][18]
Intense local inflammation with uniocular conjunctivitis, or a purplish discoloration of 1 eyelid, is known as a Chagoma or Romana's sign and is a hallmark of Chagas disease (see Image. Romana's Sign).[19] Thus, a comprehensive physical examination is required. Care should be taken to perform a thorough skin examination and diligent heart, lung, abdominal, and extremity examinations to assess for lymphadenopathy.
Chronic phase
An estimated 30% of Chagas patients will have cardiac involvement and may thus present with fever, cardiomegaly, apical aneurysms, or electrocardiography (ECG) abnormalities. Patients may present with heart failure, and subsequent cardiac workup may lead to the initial diagnosis of Chagas. Approximately 10% of patients may have gastrointestinal tract involvement and may present with fever, megaesophagus, or megacolon due to the destruction of myenteric plexus and constipation. Such gastrointestinal complaints of chronic Chagas may also be the presenting/diagnostic complaints for the patient.[20]
Patients living in or from endemic areas presenting with signs and symptoms worrisome for heart failure or with intractable constipation warrant a thorough physical examination with special attention paid to heart, lung, abdominal, and extremity examinations. Signs of cardiomegaly, eg, a displaced point of maximal impulse, diminished pulse pressures, or sinus tachycardia, may be present.[21] Features of right heart failure, including bibasilar pulmonary rales or bipedal pitting edema, may be present. Abdominal distention with a soft abdomen and diminished bowel sounds may be present. Digital rectal examination may reveal hardened or impacted stool.[22] The abdominal examination may also reveal hepatosplenomegaly, and the conjunctival exam may reveal pallor from chronic anemia.[23][24]
Evaluation
The presenting symptoms will guide the investigations when evaluating a patient for potential Chagas disease.
Laboratory Studies
Diagnosis is established during the acute phase by detecting the parasite microscopically, from a fresh preparation of anticoagulated blood or buffy coat due to the high level of parasitemia. However, levels may decrease within 90 days of infection and may be undetectable by microscopy as the sensitivity of the test decreases and as the disease progresses from acute to chronic. Polymerase chain reaction (PCR) is another diagnostic tool that may be used during the acute phase, monitoring for acute infection in organ transplant recipients or following accidental exposures. PCR assays can demonstrate positive results days to weeks before a peripheral blood smear detects circulating trypomastigotes.
Additional Diagnostic Studies
When examining a patient with suspected chronic Chagas disease, further investigations will focus on the organ system dysfunction being assessed. Long-term cardiac manifestations are most common; an initial workup will often entail an ECG, and chest x-ray and echocardiography may also be indicated. Signs of cardiomegaly will be evident on all 3, and diminished ejection fraction may be demonstrated on echocardiography.[25][26] Similarly, if a patient presents with gastrointestinal complaints, a series of abdominal x-rays may demonstrate pseudo-obstruction of the bowels, and a megacolon may be evident.[27] The diagnosis of Chagas is confirmed via the detection of IgG antibodies to T. cruzi in chronic infections.[28]
Treatment / Management
Acute Chagas Disease Treatment
Treatments for Chagas disease include nifurtimox and benznidazole, with more than 80% success during the acute phase but with no effect on the amastigote stage.[29](B3)
Management of Chronic Chagas Disease
Treatment for chronic Chagas disease is dependent on which organ is involved. Treatment of Chagas heart failure is largely symptomatic, with pacing and defibrillation used to ameliorate life-threatening arrhythmias. Simply treating the patients with antiparasitic medications does not halt or reverse the end-organ symptoms in chronic Chagas disease.[30] Current thinking revolves around a parasite-driven systemic immune response that leads to end-organ damage, and there is much ongoing research into the use of immunomodulating medications in the treatment of these patients.[31][32]
End-stage cardiac disease from Chagas is treated in much the same way as other forms of end-stage heart failure, with rate and rhythm control, prophylaxis for thromboembolism, and implanted defibrillators. Chagas cardiomyopathy is not a contraindication for heart transplantation, though the required immunosuppression makes reactivation of the latent disease highly likely.[33]
End-stage colon dysfunction, also called chagasic megacolon, may require surgical intervention. The Duhamel-Haddad procedure involves resection of the dilated, hypofunctional sections of the colon and has also been described with frozen section controls to evaluate for subclinical neuronal loss.[34][35] Other operations have been described, including partial sigmoidectomy with loop interposition, all to avoid a permanent ostomy.[36][37]
Differential Diagnosis
Differential diagnoses that should also be considered when evaluating Chagas disease include:
- Esophageal motility disorders
- Esophageal rupture
- Esophageal spasm
- Esophagitis
- Gastroesophageal reflux disease
- Leishmaniasis
- Malaria
- Meningitis
- Myocardial infarction
- Myocardial rupture
- Congestive heart failure
Prognosis
The overall prognosis depends upon when the disease is diagnosed and treatment begins. Those patients diagnosed and potentially cured in the acute phase, before end-organ damage has occurred, have an overall favorable prognosis. However, rare reports of death from acute Chagas exist, primarily due to acute myocarditis.[38]
Patients with chronic Chagas disease have a prognosis dependent upon the organ function (especially cardiac) at the time of diagnosis and treatment. Patients with Chagas cardiomyopathy have higher mortality and morbidity when compared to other causes of nonischemic heart disease, and overall, lower quality of life and lower life expectancy than those not infected.[39]
Complications
Chronic cardiomyopathy and heart failure are the principal complications of untreated Chagas disease, though megacolon and other chronic intestinal dysmotility are also well-described.[40] Other rarer complications include esophageal dilatation and dysmotility, as well as brain abscess formation.[41]
Consultations
Once the diagnosis is made, consultation with an infectious disease specialist is recommended. Other important specialists can include cardiologists and gastroenterologists.
Deterrence and Patient Education
Preventing Chagas disease primarily relies on public health initiatives and reducing exposure to the reduviid bug in endemic regions. Public health campaigns should focus on educating communities about the bug’s habitats, its nocturnal feeding behavior, and ways to minimize contact. Encouraging the use of insecticide-treated bed nets, sealing cracks in walls and roofs, and improving housing conditions—such as using plastered walls and screened windows—can significantly reduce the risk of infestation.[16] Additionally, community-based vector control programs, including insecticide spraying and environmental management, play a crucial role in reducing transmission. Proper food hygiene is also essential, as oral transmission through contaminated food or beverages has been reported in some outbreaks.
Clinician awareness is equally vital, particularly in endemic areas and among healthcare practitioners treating at-risk populations, including travelers, immigrants, and those receiving blood transfusions or organ transplants.[42] Physicians should educate patients about potential transmission routes, the importance of early diagnosis, and available treatment options. Pregnant women in endemic regions should receive counseling on congenital transmission risks, and blood banks should ensure proper screening procedures. By improving public awareness and clinician competence, preventive efforts can significantly decrease the burden of Chagas disease and reduce its long-term health consequences.[42]
Pearls and Other Issues
Currently, Chagas disease has no vaccine. The main methods for preventing transmission include education, improved housing, vector control using bed netting, and screening donated blood and children in endemic areas.
Enhancing Healthcare Team Outcomes
The diagnosis and management of Chagas disease require a collaborative, interprofessional approach to ensure timely detection, effective treatment, and improved patient outcomes. Physicians, including infectious disease specialists, cardiologists, emergency physicians, gastroenterologists, and internists, play a critical role in recognizing symptoms, ordering appropriate diagnostic tests, and implementing treatment strategies. Since the disease is rare in North America, clinicians must maintain a high index of suspicion when evaluating patients from endemic regions. Advanced practitioners and nurses are essential in patient education, monitoring treatment adherence, and providing long-term care, particularly for those with severe residual complications affecting the heart and gastrointestinal system. Pharmacists contribute by ensuring proper medication use, managing potential adverse effects of antiparasitic treatments like benznidazole and nifurtimox, and advising on drug interactions, especially for patients with cardiac involvement requiring additional therapies.
Effective interprofessional communication and care coordination are crucial to enhancing patient-centered care, improving outcomes, and ensuring patient safety. Close collaboration between healthcare professionals allows for comprehensive management, addressing both acute infection and chronic complications. Nurses and advanced practitioners serve as primary contact points for patient education, reinforcing the importance of vector control, screening, and symptom monitoring. Social workers and public health professionals are key in community outreach, helping at-risk populations access preventive resources and healthcare services. Coordinated efforts between primary care clinicians and specialists ensure that patients receive long-term follow-up, particularly those with cardiac complications requiring ongoing monitoring. A well-integrated healthcare team enhances patient safety and treatment adherence, and public health efforts can be strengthened to reduce transmission risks.
Media
(Click Image to Enlarge)
Trypanosoma Cruzi. Image of T. cruzi, the cause of Chagas disease, in Giemsa stained blood smear.
Centers for Disease Control and Prevention
(Click Image to Enlarge)
Romana’s Sign. Intense local inflammation with uniocular conjunctivitis, or a purplish discoloration of 1 eyelid, is known as a Chagoma or Romana's sign and is a hallmark of Chagas disease.
WHO/TDR
(Click Image to Enlarge)
Chagas Disease. Microscopic detection of T. cruzi parasites is diagnostic for Chagas disease. Motile parasites can be detected microscopically by examining fresh, anticoagulated blood or the buffy coat of a fresh blood sample.
Centers for Disease Control and Prevention
(Click Image to Enlarge)
T. Cruzi Parasite Life Cycle. Illustration of the various phases of the T. Cruzi life cycle.
Centers for Disease Control and Prevention, Public Domain, via Wikimedia Commons
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