Trypanosoma cruzi

Approximately 6 million people worldwide, including 300,000 US residents, are infected with Trypanoma Cruzi. T. cruzi is usually transmitted by the bite of triatome insects that inject infected feces while feeding on the blood of humans. Triatome insects inhabit continental Latin America and the southern half of the US. Transmission can also occur from mother to infant in utero or peripartum and through blood transfusion and organ transplantation. People can also become infected by ingestion of food or beverages contaminated with insect feces. Less commonly, infections may occur after an accidental laboratory exposure. Most infected persons in the US have been immigrants from Latin America, but locally acquired infections have been reported in Texas, California, Arizona, and other states.

T. cruzi infection causes acute Chagas’ disease, with fever, inflammation, subcutaneous edema, lymphadenopathy, hepatosplenomegaly, myocarditis, and in rare cases, meningoencephalitis. The acute phase of infection typically resolves within 2 to 3 months. Once the immune system halts parasite replication, an infected person enters the lifelong chronic phase. Most individuals are asymptomatic and unaware of their infection. However, 20 to 30% of patients develop cardiac manifestations (arrhythmias and conduction abnormalities, heart failure, apical aneurysms, and sudden death) or gastrointestinal manifestations (megaesophagus and megacolon). Patients with cardiac manifestations of chronic Chagas’ disease almost always have evidence of myocarditis, fibrosis, and noncaseating granulomas on histopathological examination of heart tissue. Intracellular amastigotes are identified in only a minority of patients (15%).

In the United States, Chagas disease screening should be offered to all persons with 1 or more of the following risk factors:

• Lived 6 months or longer in Mexico or in Central or South America
• Mother lived 6 months or longer in Mexico or in Central or South America
• Family member with Chagas disease
• Known contact with triatomine insects in the US or Latin America.

At-risk females of reproductive age should ideally be screened before they become pregnant because preconception antitrypanosomal therapy decreases congenital transmission risk by more than 95%.

People with chronic Chagas disease who become immunosuppressed due to HIV (CD4 <200 cells/μL), transplant anti-rejection medications, or other immunosuppressive drugs may develop T cruzi reactivation that is characterized by high levels of parasitemia. In this population, reactivation classically presents as fever, inflammatory panniculitis, and skin nodules. Less commonly, these patients develop meningoencephalitis or myocarditis that can rapidly progress to allograft rejection and congestive heart failure if it is not treated. CNS reactivation has a high fatality rate.

Polymerase chain reaction (PCR) is the preferred test to detect T. cruzi during the acute phase. Serologic tests that detect IgG antibodies against T. cruzi are recommended during the chronic phase because the disease is often associated with a low parasite burden that may not be detectable by PCR. Because serologic tests are not 100% specific, the diagnosis of chronic Chagas’ disease requires two positive tests that differ with regard to technique or antigen.

Currently, there are only two approved medications for the management of Chagas’ disease: nifurtimox and benznidazole. Benznidazole is the preferred agent because it has a better safety profile. Posttreatment reversion to negative IgG serological is the accepted surrogate for parasitological cure. It often takes years to decades to become serologically negative. 

Patients who have received an organ from a donor with Chagas’ disease be monitored by PCR testing for the development of parasitemia. Testing begins within 2 weeks after transplantation and is performed weekly for the first 2 months, then every 2 weeks or monthly until month 6. 

References

Case 20-2019: A 52-Year-Old Woman with Fever and Rash after Heart Transplantation  M.G. Ison and Others. N Engl J Med 2019;380:2564-2573

Bern C. Chagas’ disease. N Engl J Med 2015;373:456-66.

Clark EH, Bern C. Chronic Chagas Disease in the US. JAMA. 2024;331(23):2037–2038. doi:10.1001/jama.2024.3717