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Trypanosoma cruzi, a protozoan parasite, is the causative agent of Chagas disease. It is most commonly found among people, dogs, cats, and wild mammals in Central and South America, especially in rural communities where people reside in houses constructed from mud or thatch. The vector is the reduviid or kissing bug, which lives in the cracks of buildings and substandard houses8. Often substandard housing/living conditions are shown to have these structural fractures, which provide suitable habitats for reduviid bugs. The reduviid bug transmits T. cruzi by rubbing its own contaminated feces into an abrasion (wound or bug bite) or a mucous membrane of the host. Two other modes of infection are blood transfusions/organ transplants and perinatal/vertical transfer from mother to child3. In addition, there have been reports that infections originated from undercooked food that was contaminated8.
The life cycle of T. cruzi: The vector, reduviid bug, bites and defecates on host. Parasites, in the form of trypomastigotes, are able to enter the blood via mucous membranes or a cut. During cell invasion, the trypomastigotes transform into amastigotes and undergo multiplication. Parasites are then released into the blood stream as trypomastigotes where they either spread to other tissues or are taken up by the vector to perpetuate the life cycle2.
Chagas disease exists in three stages: acute, indeterminate, and chronic.
1. The acute stage manifests shortly after infection from a bite or alternate mode of transmission and is generally found in only 1% of reported cases8. Although it is often asymptomatic, symptoms can include Romaña’s sign (one swollen eye), fever, fatigue, enlarged liver/spleen, swollen lymph nodes, rash, loss of appetite, diarrhea, and vomiting. In adults, these symptoms generally subside within 4-8 weeks and may or may not require treatment. Very young children are a concern because they may sustain severe brain damage or die as a result of infection8.
2. The indeterminate stage may also be asymptomatic. Onset of this stage is reported about 8-10 weeks following infection and may persist for years.
3. The chronic stage is the most severe and the most common manifestation of Chagas disease. Chronic Chagas disease usually presents itself 10-40 years after infection, in about 30% of infected individuals. On average, developing this class of Chagas disease reduces life expectancy on average by 9 years8 . It is characterized by cardiac and digestive tract complications stemming from damage to the cardiac conduction system and the gastrointestinal autonomic nerve, respectively9. The cardiac conduction system creates electrical impulses that cause contractions in the heart and circulation of blood. The autonomic system is a part of the nervous system which regulates the activities of the heart, the glands, and the smooth muscles, including those of the intestinal tract10. Although there is a high rate of variation in symptoms, specific examples are heart attack/failure, and an enlargement of the esophagus or large intestine (digestive megasyndromes) 8.
If caught early (during acute or early indeterminate stages), Chagas disease is treatable and curable with benznidazole and nifurtimox chemotherapy2. Early detection and speedy treatment are the key to an effective remedy. However, early detection is difficult because the individual may initially be asymptomatic and parasitological screening tests have a high rate of false negatives with respect to T. cruzi4. With the onset of chronic stage Chagas disease, a cure is no longer possible and medical professionals will focus on managing and minimalizing the symptoms8.
Trypanosomes have a variable outer glycoprotein layer, allowing them to evade the immune system by frequently altering their surface antigens9. However, to date it is not clear how or why T. cruzi can cause damage to the cardiac conduction system and/or autonomic nerve of the gastrointestinal tract9. A 2003 study involving mice infected with T. cruzi clones suggested that cardiac problems stem from the parasite’s ability to sustain itself in inflamed cardiac issue. Therefore, the endurance and presence of the parasites causes the chronic inflammation. The study also concluded that the documented variation in the presentation of Chagas disease is dependent not only on the diversity of infectious agent T. cruzi, but also on host factors, including genetic makeup6.
The Centers for Disease Control estimates that of the 16-18 million people diagnosed, 50,000 will die of Chagas disease each year8. Although T. cruzi is not indigenous to the United States, it is estimated that between 25,000 and 100,000 Latin American immigrants residing in the US are infected1. No vaccine or preventative medication currently exists. However, suggested preventative measures include the usage of bed netting and insecticides5. Another preventative measure is the screening of blood products for T. cruzi serology. Although this test is actively promoted by the World Health Organization and The Pan-American Health Organization, it is not a reasonable expectation in Latin America and the United States does not screen, as it is not found indigenously. However, as of 2002, there were 6 documented instances of T. cruzi transmission via blood transfusion in the United States and Canada6.
In 1997, the National Institute of Allergy and Infectious Disease began a study to increase the understanding of people with parasitic infection and the appropriate treatment. Chagas disease was and currently is on the list of parasitic diseases included in the study7.
Images used with permission from the CDC (CDC Image Library)
1. Centers for Disease Control and Prevention. “Chagas Disease After Organ Transplantation – United States, 2001.” Morbidity and Mortality Weekly Report. 15 March 2002: 51(10); 210-212.
2. Centers for Disease Control and Prevention. Trypanosoma cruzi. 20 May 2003. 3 October 2004. http://www.dpd.cdc.gov/dpdx/HTML/TrypanosomiasisAmerican.htm.
3. Corral, Ricardo S., Jaime Altcheh, Sandra R. Alexandre, Saul Grinstein, Hector Freilij, and Alejandro M. Katzin. 1996. Detection and Characterization of Antigens in Urine of Patients with Acute, Congenital, and Chronic Chagas’ Disease. Journal of Clinical Microbiology. 34 (8): 1957-62.
4. Galvão, Lúcia M.C., Egler Chiari, Andrea M. Macedo, Alejandro O. Luquetti, Simonne A. Silva, and Ana Lúcia S. S. Andrade. 2003. PCR Assay for Monitoring Trypanosoma cruzi Parasitemia in Childhood after Specific Chemotherapy. Journal of Clinical Microbiology. 41(11): 5066-70.
5. Herwaldt, Barbara and James Maguire. “American Trypanosomiasis (Chagas Disease).” The Yellow Book: Health Information for International Travel, 2003-2004. 30 June 2003. 10 October 2003. http://www.cdc.gov/travel/disease/chagas.htm.
6. Marinho, Claudio R. F., Daniella Z. Bucci, Maria Lúcia Z. Dagli, Karina R.B. Bastos, Marcos G. Grisotto, Luiz R. Sardinha, Cristiane R. G. M. Baptista, Carlos Penha Gonçalves, Maria Regina D’Imperio Lima, And José M. Álvarez. 2004. Pathology Affects Different Organs in Two Mouse Strains Chronically infected by a Trypanosoma cruzi Clone: a Model for Genetic Studies of Chagas’ Disease. Infection and Immunity. 72(4): 2350-57.
7. National Institute of Allergy and Infectious Diseases. Evaluation, Treatment, and Monitoring of Patients with a Known of Suspected Parasitic Infection. 1997. 3 October 2004. http://www.clinical trials.gov.
8. Parasitic Disease Information. Fact Sheet: Chagas Disease. 21 September 2004. 3 October 2004. http://www.cdc.gov/chagas/
9. Schaechter, Moselio, N. Cary Engleberg, Barry I. Eisentstein, and Gerald Medoff. Mechanisms of Microbial Disease, 3rd Ed. Philadelphia: Lippincott, Williams, and Wilkins, 1999.