A 58-Year-Old Man With Congestive Heart Failure

Correct Answer: B. Cardiac complications are the most common and clinically significant manifestations of this disease.

Discussion. The presented patient has Chagas disease, a parasitic infection caused by the unicellular organism Trypanosoma cruzi, a relative of the more famous Trypanosoma brucei gambiense, which causes West African sleeping sickness.

Most of us glossed over the parasitology section of our sophomore medical school year (perhaps apart from malaria). So why invest time on this topic? The answer is that Chagas disease is another example of an infection once considered very rare in the United States that is now increasingly recognized, as with dengue, vibriosis, and other infections discussed in previous What’s the Take Home? articles. Chagas disease shares epidemiologic features with these infections, including the effects of climate change, which can expand the geographic range of endemic host animals and insect vectors, as well as the increasing frequency and ease of international travel and migration from endemic areas into the United States. Some details of these factors as they specifically apply to Chagas disease will be discussed below.

Parasitology

Parasites are an extremely successful group of infectious agents involved in mammalian and human disease. They frequently have a complex lifecycle involving multiple hosts, with distinct developmental stages that ultimately produce an infective form capable of transmission to a new host. In many infections, including T cruzi infection, the parasite does not kill the host but may cause substantial disease years or even decades later, while the infected host serves as a chronic, long-term reservoir of infection.¹

We'll start with the insect vector, a species of insect in the Triatominae family generally called "kissing bugs" because they seek a mammalian blood meal from host exposed mucosae such as lips and eyelids (face areas) most often when the host is asleep. During or shortly after a blood meal, an infected triatomine bug may defecate near the bite site. T cruzi in the feces can enter the host when the contaminated material is rubbed or scratched into the bite wound or encounters a mucous membrane. Once inside the human host, the parasite undergoes a complex lifecycle that produces large numbers of infectious flagellated forms. These forms can be ingested by another kissing bug during a blood meal, allowing the transmission cycle to continue. Importantly, once inside the human host, T cruzi trypomastigotes invade host cells and differentiate into intracellular amastigotes, which replicate within tissues. Persistent infection and the associated inflammatory and fibrotic response can contribute to chronic cardiac and gastrointestinal disease years or decades after the initial infection. As convoluted as this parasitology is, it is the way of so many human/mammalian parasites and parasitic infections such that there is no getting around it.

Demographics

Chagas disease is named for the Brazilian physician who first described it, Carlos Chagas. The tropical illness remains endemic to Central and South America. However, migration from endemic areas (again resembling vibriosis) and warmer global temperatures have resulted in increased numbers of kissing bugs not just in Texas and other border states, but well into the more northern United States, including Delaware.² Transmission of T cruzi can also occur through transfusion of infected blood products. However, screening of blood donors in the United States has substantially reduced the risk of transfusion-transmitted Chagas disease.¹ In my view, it is just a matter of time and temperature before the incidence of this once very rare illness in the United States becomes more common.

Clinical findings

Chagas disease in humans behaves clinically in an acute and chronic phase. Ther acute phase begins with the bite, which may not be noticed until irritation is seen at the bite site. Unilateral inflammation occurs with unilateral conjunctivitis and purple discoloration of the eyelid. This finding, known as Romaña sign, is characteristic of acute Chagas disease but is observed in only approximately 10% of cases.¹ The remainder of the acute phase symptomatology is a set of nonspecific findings including fever, malaise, myalgias, and regional (to the bite) inflammation, localized edema, and lymphadenopathy. These occur due to the patient's strong inflammatory response to the dividing trypanosomes and can last up to 2 months.¹ Generally, most patients will have mild or no symptoms and will likely never seek medical attention such that the initial infestation may not be known to the patient.

More ominous by numbers affected and morbidity is the chronic phase of Chagas disease because it can last for decades in humans. The main target organs of the later sequelae of Chagas disease are the heart and GI tract. Symptomatic cardiac Chagas involvement is the more common with a ratio of at least 2:1 more so than gastrointestinal (GI) involvement,^1,3 which makes Answer B the correct answer.

The cardiac and gastrointestinal manifestations of Chagas disease reflect the persistence of T cruzi in tissues and the resulting chronic inflammatory, fibrotic, and neuronal injury.⁴ In the heart, these processes may involve the myocardium and conduction system, resulting in chronic Chagas cardiomyopathy, ventricular dilation, reduced left ventricular ejection fraction, heart failure, and conduction abnormalities such as atrioventricular block and bundle branch block. Ventricular arrhythmias, including ventricular tachycardia, may also occur. In the gastrointestinal tract, injury to the enteric nervous system can impair motility and lead to manifestations such as megaesophagus, megacolon, and severe constipation.⁴ Cardiac involvement is the major driver of mortality in chronic Chagas disease.

Diagnosis

Specific diagnostic methods for Chagas disease are in the acute phase the demonstration of trypanosomes in Giemsa-stained blood smears and once again the use of polymerase chain reaction (PCR) for the presence of trypanosome DNA, currently a true referral study but as with all PCR studies generally becoming more available and perhaps becoming standard of care in time. Confirmation in the chronic phase is by demonstration of IgG antibodies in patient serum.³ According to the CDC, confirmation generally requires 2 serologic tests that use different antigens or techniques. It should be noted that in the chronic phase, Chagas should be in the differential upon appropriate clinical suspicion and "thinking about it.” So, in a patient who has immigrated from an endemic area, (eg, Central and South America); has traveled to such an area in an appropriate time frame; presents with isolated cardiomyopathy CHF, and significant heart block, then T cruzi infection should be in the differential diagnoses once more common suspects like CAD and valvular heart disease have been excluded.  

Treatment

In the acute phase, benznidazole has shown a more than 80% success rate.⁴ Despite the potentially increased range of vectors and human infection on the horizon, acute illness remains rare in the United States as well as asymptomatic in most cases. However, due to immigration and travel from endemic areas where Chagas was acquired decades previously, chronic cases are becoming more common.³

Regarding the use of benznidazole, one study found that although its use can result in "cure" (defined as clearance of IgG antibody), it did not change the course of potential chronic complications (eg, CHF, arrythmia incidence, or their cumulative expressions of morbidity or mortality).^5,6 Therefore, the role of antitrypanosomal therapy in chronic Chagas disease remains uncertain, warrants further study, and should be considered in consultation with an infectious disease specialist experienced in tropical medicine. Meanwhile, the therapeutics for patients with a chronic disease utilize aggressive modern CHF regimens. Risk stratification prophylaxis for sudden death from cardiac causes (eg, an implanter defibrillator) and thromboprophylaxis for cardiac emboli when imaging demonstrates risk (eg, direct oral anticoagulants for apical aneurysm) are also indicated.³ Mortality prognosis will be contingent upon extent of and ongoing cardiac morbidity findings, especially the CHF.

Patient follow-up. A thorough evaluation was performed, which included echocardiography and excluded primary valvular disease and coronary angiography, which ultimately ruled out CAD. The next differential included less common causes such as amyloidosis and myocarditis. Serum protein electrophoresis and cardiac amyloid protein studies were negative, essentially excluding the former, while complete rheumatological studies were negative, excluding the latter. Attention was then turned to the history of early life in an area where T cruzi is endemic. The patient does not remember either having or being told he had Chagas risk exposure events (eg, bite with ocular syndrome or serious acute phase illness). However, an IgG antibody study for T cruzi was positive, and the diagnosis of chronic phase cardiac involvement Chagas disease was made. An appropriate regimen for CHF was initiated as was thromboprophylaxis, and a defibrillator device was placed. No decision has been made regarding the use of anti-trypanosome medication. At 3-months follow-up, CHF symptoms have improved and echocardiogram EF is 27%.

What’s the Take Home? Chagas disease is a complex human illness caused by the parasitic unicellular organism T cruzi. Humans acquire T cruzi infection through a complex multispecies life cycle involving triatomine insects, commonly called “kissing bugs.”

During or after a blood meal, an infected bug deposits parasite-containing feces near the bite site. Once into a human host, its rapid multiplication causes the acute phase, which is most frequently subclinical but can cause fever, malaise, myalgias, and local inflammation with regional adenopathy in the bite area. Romaña sign, characterized by unilateral conjunctivitis and discoloration of the eyelid, is a rare but characteristic finding of acute Chagas disease. If the patient has noticed the bite, diagnosis in the acute setting is by Giemsa staining of peripheral blood for presence of flagellated forms or in recent times PCR testing for T cruzi DNA. Thereafter, T cruzi can persist in tissues as intracellular amastigotes, with chronic infection contributing to inflammatory, fibrotic, and neuronal injury. These processes can lead to the characteristic cardiac and GI manifestations of chronic Chagas disease, often decades after the initial infection. These sequelae are: (1) A cardiomyopathy type CHF with pan-cardiac dilatation and associated clinical clues such as accompanying heart block and embolic complications, and (2) intestinal dysmotility disorders such as severe constipation, megacolon and megaesophagus. Diagnosis is the chronic phase is by finding elevated IgG trypanosome antibody.

Clinicians should consider Chagas disease as a possibility when the clues include appropriate exposure to endemic areas such as Central and South America, the preliminary diagnosis of "idiopathic CHF" especially with heart blocks seen on EKG, or unexplained embolic events. The ratio of cardiac Chagas to GI chagas is about 3:1.

Treatment for the acute phase is approximately 80% effective in clearing the parasite using the medication benznidazole. However, whether this helps patients with already established chronic sequelae Chagas is conjecturable. For these patients, appropriate supportive CHF therapeutics, thrombosis prophylaxis and defibrillation measures are used.

Chagas is yet another example of a once very rare disease in the United States gaining a foothold as global warming increases the range of its vectors and immigration and travel from endemic areas occurs. The illness is here, will likely increase, and we need to be aware of it.

AUTHOR
Ronald N. Rubin, MD^1,2

AFFILIATIONS
¹Lewis Katz School of Medicine at Temple University, Philadelphia, PA
²Department of Medicine, Temple University Hospital, Philadelphia, PA

CITATION
Rubin RN. A 58-year-old man with congestive heart failure. Consultant. 2026;67(8).

DISCLOSURES
The author reports no relevant financial relationships.

CORRESPONDENCE:
Ronald N. Rubin, MD, Temple University Hospital, 3401 N. Broad Street, Philadelphia, PA 19140 (blooddocrnr@yahoo.com)

References

1. Cucunubá ZM, Gutiérrez-Romero SA, Ramírez JD, et al. The epidemiology of Chagas disease in the Americas. Lancet Reg Health Am. 2024;37:100881. Published 2024 Sep 13. doi:10.1016/j.lana.2024.100881
2. Eggers P, Offutt-Powell TN, Lopez K, Montgomery SP, Lawrence GG. Notes from the Field: Identification of a Triatoma sanguisuga "Kissing Bug" - Delaware, 2018. MMWR Morb Mortal Wkly Rep. 2019;68(15):359. Published 2019 Apr 19. doi:10.15585/mmwr.mm6815a5
3. Stewart GC, Gong J, Loria MC, et al. Case 27-2025: a 53-year-old man with embolic stroke and left ventricular apical aneurysm. N Engl J Med. 2025;393:1216-1225.
4. Pérez-Molina JA, Molina I. Chagas disease. Lancet. 2018;391:82-94.
5. Morillo CA, Marin-Neto JA, Avezum A, et al; BENEFIT Investigators. Randomized trial of benznidazole for chronic Chagas' cardiomyopathy. N Engl J Med. 2015;373:1295-1306.
6. Bern C. Antitrypanosomal therapy for chronic Chagas' disease. N Engl J Med. 2011;364:2527-2534.

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