Neurologic Infections in Travelers

Malveeka Sharma, MD, MPH; Joseph R. Zunt, MD, MPH


Semin Neurol. 2019;39(3):399-414. 

In This Article

American Trypanosomiasis (Chagas Disease)


Chagas disease, or American trypanosomiasis, was first described in 1909 by Dr. Carlos Justiniano Chagas, a Brazilian physician. Chagas disease is caused by the protozoan Trypanosoma cruzi and is endemic mainly in Latin America and South America, with an estimated 8 million people infected.[10,11] Infection occurs primarily through the bite of the triatomine bugs; however, infection can occur via contact with contaminated blood, congenital transmission, or ingestion of infected guinea pig.[5] Approximately 300,000 cases have been reported in the United States, mainly in immigrant populations who acquired infection in endemic countries.[11] The vector thrives under poor housing conditions, such as mud walls and thatched roofs.[11]

Life Cycle, Ecology, and Species

The triatomine bug infected with T. cruzi excretes the parasite eggs along with its feces near the site of the bite wound. The T. cruzi eggs are introduced through the human skin through scratching the bite site. The eggs mature and are replicated within cells; once cell rupture occurs, the host inflammatory response leads to clinical symptoms.[5]

Clinical Manifestations

Chagas disease produces acute and chronic phases, with the majority of neurologic symptoms occurring during chronic infection. Although relatively rare, CNS manifestations can include meningoencephalitis, a tumor-like chagoma, and neuropathy in upwards of 10% of infected patients.[12,13] Congenital Chagas can produce neonatal meningoencephalitis, microcephaly, or brain calcifications.[13] CNS involvement during the chronic phase varies according to the degree of the host immune system activation elicited by the infection.[5] The most common CNS manifestation during the chronic phase is meningoencephalitis. There are rare case reports of chronic Chagas disease producing chronic encephalopathy and sensorimotor deficits.[12] Stroke can occur due to dilated cardiomyopathy and cardiac thrombus formation. In addition, case–control and large, population-based cohort studies have demonstrated an association between Chagas disease and cognitive impairment.[13]


Clinical history and travel or residence in an endemic country is required for exposure to T. cruzi. Definitive diagnosis of CNS Chagas disease in the acute phase is based on the presence of trypanosome in CSF. Visualization of the parasite in the chronic phase is rare, and detection of serum antibody is the diagnostic test of choice. Neuroimaging findings are variable and nonspecific.[5,12]


Treatment of Chagas disease is strongly recommended for all phases of disease in patients less than 18 years of age and in patients less than age 50 without advanced cardiomyopathy. There is currently only one FDA-approved therapy, benznidazole. Nifurtimox is not currently FDA-approved, but is available through an investigational protocol from the Centers for Disease Control and Prevention (CDC). Both medications have numerous side effects, including neuropathy, dermatitis, and weight loss. Length of treatment is anywhere from 60 to 90 days.[11,12] Intravenous tissue plasminogen activator (IV tPA) was found to be safe with no increase in symptomatic intracranial hemorrhage in stroke related to Chagas disease.[14] Primary prevention strategies have been targeted to vector control with improved housing and household insecticide use. Screening of blood donations and early detection and treatment of new mothers have also been employed to reduce the burden of disease.[10,11]