Description

Trypanosoma cruzi is an obligate intracellular parasite that causes American trypanosomiasis or Chagas’ disease, a chronic and debilitating parasitic infection that affects millions of people in Latin America. As a result of reactivation among immigrant populations, Chagas’ disease is increasingly being reported in nonendemic settings (1). The hemato-phagous triatomine (“cone nose” or “kissing”) bugs responsible for transmitting T. cruzi to humans usually live in cracks and crevices of poor-quality houses in rural areas (1-3). These insects emerge at night to feed and then excrete vast amounts of T. cruzi in their feces, which enter the wound when it is scratched or rubbed after the blood meal (1-3). Transmission can also occur through blood transfusion (4) and organ transplantation (5), and congenitally through pas-sage of parasites across the placenta (6). Recently, an outbreak of foodborne Chagas’ disease in Brazil demonstrated yet another form of transmission (7).

Occurrence

Approximately 25% of the population of Latin America is at risk for acquiring the infection (1). Chagas’ disease occurs in Mexico, Central America, and South America; acquisition of infection in the United States is rare. An estimated 11 million people are infected worldwide; of these, 15%-30% have clinical symptoms (1-3).

Risk for Travelers

Travelers rarely acquire Chagas’ disease and will be at risk only if visiting rural areas in endemic regions. Triatomine bugs typically infest poor-quality buildings constructed of mud, adobe brick, or palm thatch, particularly those with cracks or crevices in the walls and roof (1). Because the bugs primarily feed at night, travelers can greatly reduce their risk of acquiring infection by avoiding overnight stays in such dwellings and by not camping or sleeping outdoors in endemic areas. Travelers should be aware that blood products might not be routinely or adequately tested for T. cruzi prior to transfusion (4).

Prevention

No vaccine is available. Preventive measures include insecticide spraying of infested houses. Insecticide-impregnated bed nets may reduce the risk of infection for travelers who cannot avoid camping, sleeping outdoors, or sleeping in poorly constructed houses in endemic areas. Compliance with food and water precautions in endemic areas is also recommended to prevent the extremely rare occurrence of foodborne Chagas’ disease.

Treatment

Travelers should be advised to consult an infectious disease or tropical medicine specialist for the diagnosis and treatment of Chagas’ disease. Medical therapy may be directed at eradicating the parasite or managing the symptoms of the megasyndromes or the cardiac rhythm disturbances (15,16). Treatment is recommended for all cases of acute infection, congenital infection, and reactivated infection in immunocompromised patients. Nifurtimox or benznidazole (not available in the United States) is used in the acute phase and in reactivation in immunosupressed patients (1,15-16). Chemotherapy can shorten the acute phase and achieve parasitologic cure in 60% of the cases, but because of the adverse events associated with these medications, patients being treated require careful monitoring (15-16). Nifurtimox is available from the CDC Parasitic Disease Drug Service (404-639-3670), under an Investigational New Drug protocol. (See http://www.cdc.gov/ncidod/srp/drugs/drug-service.html.)

No available data suggest that drug treatment of persons in the chronic phase can alter the natural history of the disorder (1,15). Heart failure and arrhythmias in Chagas’ disease are treated as they are in other patients with similar cardiac problems (17).

References

1. Urbina JA, Docampo R. Specific chemotherapy of Chagas disease: controversies and advances. Trends Parasitol. 2003;19:495-501.
2. Laranja FS, Dias E, Nobrega G, Miranda A. Chagas’ disease: a clinical, epidemiological and pathologic study. Circulation. 1956;14:1035-60.
3. Coura JR, de Castro SL. A critical review on Chagas disease chemotherapy. Mem Inst Oswaldo Cruz. 2002;97:3-24.  
4. Kirchhoff LV, Paredes P, Lomeli-Guerrero A, Paredes-Espinoza M, Ron-Guerrero CS, Delgado-Mejia M, et al. Transfusion-associated Chagas’ disease (American Trypanosomiasis) in Mexico: implications for transfusion medicine in the United States. Transfusion 2006;46:298-304.
5. Centers for Disease Control and Prevention. Chagas’ disease after organ transplantation – United States, 2001. MMWR Morbid Mortal Wkly Rep. 2002;51:210.
6. Moretti E, Basso B, Castro I, Carrizo Paez M, Chaul M, Barbieri G, et al. Chagas’ disease: study of congenital transmission in cases of acute malaria. Rev Soc Bras Med Trop. 2005;38:53-5.
7. PROMED-mail. Trypanosomiasis, Food-borne-Brazil (Santa Catarina). ProMED-mail March 24, 2005. Available at: [[forward label=([http://www.promedmail.org]) link=([])]]http://www.promedmail.org.; archive number: 20050324.0847. Accessed: February 13, 2006.
8. Añez N, Crisante G, Maia da Silva F, Rojas A, Carrasco H, Umezawa ES, et al. Predominance of lineage I among Trypanosoma cruzi isolates from Venezuelan patients with different clinical profiles of acute Chagas’ disease. Tropical Med Intern Health. 2004;9:1319-26.
9. Añez N, Crisante G, Rojas A, et al. La cara oculta de la enfermedad de Chagas en Venezuela. Boletín Malariologia y Salud Ambiental. 2003;XLIII(2):45-57.
10. Añez N, Carrasco H, Parada H, Crisante G, Rojas A, Fuenmayor C, et al. Myocardial persistence in chronic chagasic patients. Am J Trop Med Hyg. 1999;60:726-32.
11. Rossi MA, Bestetti RB. The challenge of chagasic cardiomyopathy. The pathologic role of autonomic abnormalities, autoimmune mechanisms and microvascular changes, and therapeutic implications. Cardiology. 1995;86:1-7.
12. Olivares-Villagomez D, McCurley TL, Vnencak-Jones CL, Correa-Oliveira R, Colley DG, Carter CE. Polymerase chain reaction amplification of three different Trypanosoma cruzi DNA sequences from human chagasic cardiac tissue. Am J Trop Med Hyg. 1998;59: 563-70.
13. Rassi A Jr, Rassi SG, Rassi A. Sudden death in Chagas’ disease. Arq Bras Cardiol. 2001;76:75-96.
14. Sartori AM, Lopes MH, Benvenuti LA, Caramelli B, DiPietro A, Nuñes EV, et al. Reactivation of Chagas’ disease in a human immunodeficiency virus-infected patient leading to severe heart disease with a late positive direct microscopic examination of the blood. Am J Trop Med Hyg. 1998;59:784-6.
15. Urbina JA. Parasitological cure of Chagas Disease: Is it possible? Is it relevant? Mem Inst Oswaldo Cruz. 1999;94(Suppl 1):349-55.
16. Andrade ALS, Zicker F, Oliveira RM, Almeida Silva S, Luquetti A, Travassos LR, et al. Randomised trial of efficacy of benznidazole in treatment of early Trypanosoma cruzi infection. Lancet. 1996;348: 1407-13.
17. Bocchi EA, Bellotti G, Mocelin AO, Uip D, Bacal F, Higuchi ML, et al. Heart transplantation for chronic Chagas’ heart disease. Ann Thorac Surg. 1996;61:1727-33.

Clinical Presentation

Chagas’ disease has three clinical stages (8,9). The acute stage follows the entry and invasion of the bloodstream by the protozoan parasite. Acute infection is usually asymptomatic but may be accompanied by local swelling at the site of inoculation, fever, and in 5%-10% of cases, meningoencephalitis, myocarditis or both. The acute phase is followed by the chronic stage, which has a variable duration but may be as long as 10-20 years (10). The disease may follow three paths: 1) the development of mega-syndromes (massive dilation of the esophagus or colon); 2) the development of myocarditis with associated fibrosis and a very high mortality; or 3) the individual may remain completely asymptomatic (1,8-10). The congestive heart failure associated with Chagas’ disease manifests as a biventricular failure with both systolic and diastolic dysfunction and associated cardiac arrhythmias or sudden cardiac death (9-12), which accounts for 55% to 65% of deaths in Chagas’ disease (13).

Chagas’ disease has become an important opportunistic infection among patients with HIV infection or other types of immunosuppression such as organ transplantation. In these cases, patients have presented with myocarditis or meningoencephalitis (5,14)