Chagas disease (also known as American trypanosomiasis) is a parasitic infection caused by the protozoan Trypanosoma cruzi, transmitted primarily by triatomine insects (commonly called “kissing bugs”). It is endemic in Latin America, but cases are increasingly seen in non-endemic regions (such as the U.S. and Europe) due to migration and blood transfusion transmission. Because of its increasing prevalence in temperate climes it is receiving more attention by the popular press.

T. cruzi is typically introduced into humans through the bite of triatomine bugs. When the insect defecates at the bite site, motile T. cruzi forms called trypomastigotes enter the bloodstream and invade various host cells. Within a host cell, the parasite transforms into a replicative form known as an amastigote, which undergoes multiple rounds of replication. The replicated amastigotes transform back into trypomastigotes, which rupture the host cell and are released into the blood. Trypomastigotes then disseminate throughout the body to various tissues, where they invade cells and replicate. Over many years, cycles of parasite replication and immune response can severely damage these tissues, particularly the heart and digestive tract.

The life cycle of the disease is shown in the figure below. As the label on it shows, it’s taken from the CDC.

The first description of the disease was made by Carlos Chagas in 1909 after examining a two-year-old girl with fever, swollen lymph nodes, and an enlarged spleen and liver. Upon examination of her blood, Chagas saw trypanosomes identical to those he had recently identified from the hindgut of triatomine bugs and named Trypanosoma cruzi in honor of his mentor, Brazilian physician Oswaldo Cruz.

Clinical Features

1. Acute Phase

The acute phase develops shortly after infection and lasts about 6 to 8 weeks. It is often mild or asymptomatic, particularly in adults, but may be severe in children.

Typical features include:

  • Fever, malaise, anorexia, and lymphadenopathy
  • Hepatosplenomegaly and mild myocarditis
  • Romaña’s sign – unilateral painless swelling of the eyelid, a classic sign occurring when the parasite enters through the conjunctiva
  • Chagoma – a localized swelling at the inoculation site

In severe acute infection, patients may develop acute myocarditis, pericardial effusion, or meningoencephalitis, which can be fatal, especially in infants. Parasitemia is high during this stage, making the diagnosis easier through direct detection of trypomastigotes in blood.

2. Indeterminate (Latent) Phase

After the acute phase, most patients enter an indeterminate or asymptomatic chronic phase, which can last for decades or even a lifetime. During this period, no clinical manifestations are present, but serologic tests remain positive. The parasite persists in low numbers in tissues, and gradual organ damage may silently progress. Approximately 60–70% of infected individuals remain in this indeterminate state permanently.

3. Chronic Phase

The chronic phase manifests years or decades after initial infection and is characterized by cardiac and gastrointestinal complications, which reflect destruction of autonomic ganglia and smooth muscle as well as myocardial fibrosis.

Cardiac involvement (Chronic Chagasic cardiomyopathy):
This is the most serious and life-threatening manifestation. Key features include:

  • Cardiomegaly and progressive heart failure
  • Arrhythmias and conduction defects (especially right bundle branch block)
  • Apical aneurysm of the left ventricle
  • Thromboembolism, leading to stroke or pulmonary embolism
  • Sudden cardiac death, often due to ventricular arrhythmia

Gastrointestinal involvement:
Destruction of autonomic nerves in the digestive tract leads to megasyndromes, including:

  • Megaesophagus – dysphagia, regurgitation, and malnutrition
  • Megacolon – chronic constipation, abdominal distension, and risk of volvulus

These complications are prominent in regions such as Brazil and Bolivia.

Diagnosis

Diagnosis depends on the disease stage:

  • Acute phase: detection of T. cruzi trypomastigotes in peripheral blood via microscopy or PCR.
  • Chronic phase: detection of antibodies to T. cruzi by ELISA, indirect hemagglutination, or immunofluorescence tests.
    Additional studies such as EKG, echocardiography, barium swallow, or colonic imaging assess organ involvement.

Treatment

Treatment is most effective in the acute phase and in congenital infections. The two principal antiparasitic drugs are:

  • Benznidazole
  • Nifurtimox

Both are given for 60–90 days. They can reduce parasitemia and delay disease progression, though they may cause significant side effects. In the chronic phase, therapy focuses on managing complications—using antiarrhythmics, pacemakers, anticoagulants, and surgical interventions for gastrointestinal megasyndromes.

Prevention and Control

Because no vaccine exists, prevention relies on vector control and screening:

  • Insecticide spraying to eliminate triatomine bugs
  • Housing improvements to reduce insect infestation
  • Screening of blood donors, organ donors, and pregnant women in endemic areas
  • Health education campaigns to promote awareness and hygiene

These efforts, particularly in Latin America, have significantly reduced transmission in recent decades.

Chagas disease remains one of the most important parasitic diseases in the Americas, affecting millions and causing chronic cardiac and gastrointestinal morbidity. It ranges from asymptomatic infection to severe heart failure or digestive obstruction, reflecting the parasite’s capacity for lifelong persistence and tissue damage. Early detection and treatment, combined with sustained public health efforts, remain the cornerstone for controlling and eventually eliminating this serious tropical disease.

Chagas disease in the United States is an increasingly important public health concern, though it remains underrecognized and underdiagnosed. The Centers for Disease Control and Prevention (CDC) estimates that there are now more than 300,000 people living with Chagas disease in the U.S., most of whom were infected in endemic regions of Mexico, Central America, or South America before migrating north. However, locally acquired cases have also been documented in Texas, Arizona, California, Louisiana, and other southern states, demonstrating that transmission is possible within this country.

The insect vector (triatomine bugs) is native to parts of the southern United States. Over 30 species have been identified, and at least 11 species have been found naturally infected with T. cruzi. Most reside in wild or peridomestic environments, such as woodpiles, rodent nests, dog kennels, or chicken coops.

Most U.S. cases are chronic infections detected incidentally during blood donation screening, prenatal testing, or evaluation for cardiac disease. Clinical findings mirror those seen elsewhere.

Chagas disease in the United States is no longer a foreign problem. Although most cases are imported, domestic transmission is possible, and thousands of infected individuals remain undiagnosed. The U.S. faces a significant public health challenge: identifying and treating those already infected, preventing congenital transmission, and monitoring potential local spread. Increasing physician education and routine screening in at-risk populations are essential steps toward controlling this neglected tropical disease within the borders of the US.

My sources for the above article are:

  1. The CDC
  2. The World Health Organization
  3. Pan American Health Organization (PAHO)
  4. U.S. National Library of Medicine
  5. Wikipedia Article on Chagas Disease
  6. ChatCPT