Acute phase: There is an incubation period of approximately two weeks after which the acute phase begins. The acute phase is characterized by non-specific symptoms such as fever and malaise. The acute phase may last eight to twelve weeks. Less than 10% of individuals get diagnosed during this phase. In a few, a chagoma may form. Inoculation via the conjunctiva causes unilateral swelling of the eyelids classically known as Romana’s sign.

Severe acute disease may occur in very few patients which presents with acute myocarditis which is clinically similar to myocarditis caused by viruses. It may also present with meningoencephalitis. Severe disease is associated with significant mortality [6].

Chronic phase: After 8-12 weeks, the patients enter the chronic phase; the intermediate phase of which is usually asymptomatic and may persist for decades. Later on, such patients progress to overt disease either in the gastrointestinal system, cardiac system or both.

Chronic Chagas cardiomyopathy: Patients that eventually develop this complication may be asymptomatic but eventually present with features of heart failure such as exertional dyspnea, palpitations and edema. They present with biventricular failure but the first presentation may be a stroke, thromboembolism or cardiac arrhythmia.

Gastrointestinal Chagas disease: This may present with esophageal manifestations such as motility disorders to mild achalasia to the most severe form being mega-esophagus. The most common symptom is dysphagia. There may also be severe regurgitation of food with risk of aspiration. Food may also lodge with the esophagus and cause local ulceration. There is an increased risk of esophageal cancer.

Colonic Chagas disease: The most common manifestation is slowly progressive constipation associated with bloating, abdominal distention and pain. There is also risk for developing intestinal obstruction due to volvulus.

• Acute phase: During the acute phase, the level of parasitemia is high and the parasites are visible on fresh preparations of blood (anti-coagulated or buffy coat). The level of parasitemia decreases with the next two months. Polymerase chain reaction is very sensitive for detecting infection even before the parasites circulate into the blood.
• Chronic phase: Usually serological methods are used to detect immunoglobulins towards the parasite. Methods used include enzyme-linked immunosorbent assay and immunofluorescent antibody assay. There is no gold standard test for the chronic phase as all the currently available test are not sensitive enough to detect infection [7].
• Imaging: Echocardiography is used to assess the structure and function of the heart in patients with chronic Chagas cardiomyopathy. Electrocardiogram is also indicated to assess for conduction abnormalities. For gastrointestinal disease, barium swallows and enemas are used to assess the extent of disease [8].

Acute and indeterminate disease: Antitrypanosomal therapy is recommended to treat acute Chagas disease. The drugs include benznidazole and nifurtimox. These are the only drug that have been shown to be efficacious in humans [9].

Chronic disease: There is no role of antitrypanosomal drugs in treating chronic disease since such therapy will not reverse existing pathology. Focus is on supportive management of cardiac or gastrointestinal disease.

The prognosis in the non-severe acute phase is better as compared to the severe form that has a variable outcome. The chronic phase of the disease is potentially fatal if no intervention is instituted, with cardiac failure or fatal arrhythmias being the cause of mortality.

The parasite Trypanosoma cruzi is transmitted into the human host by an insect vector known as reduviid bug.

Chagas disease is only found in the American continent. It is found in wild animals from the Southern part of the United States to the southern parts of Argentina. Due to the nature of transmission by infected triatomines, it tends to be a disease of the poor. Most infections occur in childhood. The true incidence is difficult to determine because most cases remain undiagnosed [2]. Blood transfusion used to be a major source of transmission in endemic areas but this has dramatically declined after screening of donated blood was implemented [3].

Trypanosoma cruzi is transmitted to it hosts (mammals) by hematophagous triatomine insect better known as reduviid bug. The insect gets infected when it feeds on a blood meal from an infected mammal. The parasites mature in the insect's gut and the infective forms of the parasite are excreted in its droppings. The infective parasite usually gains access, through broken skin or mucous membranes like the conjunctiva. This usually occurs after blood meal of the reduviid bug [4]. The parasites may also be transmitted via blood transfusions and organ transplants or orally from contaminated utensils or food. They can also be transmitted from an infected mother to her unborn child.

The parasites then infect the cells of the nearby muscles and subcutaneous tissues. These infected cells soon rupture and the infection spreads systemically. The parasites may reach the cardiac muscles and infect them causing inflammation which is initially acute but eventually becomes chronic. Aggregates of amastigotes may be seen on histology of the heart muscles. The chronic manifestations are caused by a chronic inflammatory response that eventually leads to the pathologic changes observed microscopically and clinically as organ dysfunction [5].

The best mode of prevention is breaking the transmission cycle and this may be done by using long lasting residual insecticides in the dwellings that are at risk and improving the living conditions for the inhabitants in endemic zones [10].

Chagas disease is a parasitic disease which is initially acute and treatable. If left untreated, the disease progresses into a chronic phase with primary damage to the heart and the gastrointestinal tract [1].

Chagas disease is caused by the parasite Trypanosoma cruzi that is transmitted by a bug. Chagas disease may either be acute or chronic; both of which have differet features and are managed differently. The disease can be prevented if proper measures are taken in the areas where the disease is endemic. The treatment for the acute phase is to kill the parasite by using specific medications; whereas in the chronic phase, the treatment is only supportive.

1. Brun R, Blum J, Chappuis F, Burri C. Human African trypanosomiasis. Lancet 375:148, 2010
2. Carabarin-Lima A, González-Vázquez MC, Rodríguez-Morales O, et al. Chagas disease (American trypanosomiasis) in Mexico: an update. Acta Trop. Aug 2013;127(2):126-35
3. Kirchhoff LV, Paredes P, Lomelí-Guerrero A, et al. Transfusion-associated Chagas' disease (American trypanosomiasis) in Mexico: Implications for transfusion medicine in the United States. Transfusion 46:298, 2006
4. Maguire JH. Trypanosoma. In: Infectious Diseases, 2nd ed, Gorbach S, Bartlett J, Blacklow N (Eds), Lippincott, Williams & Wilkins, Philadelphia 2004.
5. Lent H, Wygodzinsky P. Revision of the Triatominae (Hemiptera, Reduviidae), and their significance as vectors of Chagas' disease. Bull Am Museum Natural History. 1979
6. Secretaria de Vigilancia em Saude de Brasil. Doenca de Chagas Aguda. Nota Tecnica, 9 de outubro de 2007. Brasilia, Brasil, 2007.
7. Bern C, Montgomery SP, Herwaldt BL, et al. Evaluation and treatment of chagas disease in the United States: a systematic review. JAMA 2007; 298:2171.
8. Acquatella H. Echocardiography in Chagas heart disease. Circulation 2007; 115:1124.
9. Rodriques Coura J, de Castro SL. A critical review on Chagas disease chemotherapy. Mem Inst Oswaldo Cruz 2002; 97:3.
10. Moncayo A, Ortiz Yanine MI. An update on Chagas disease (human American trypanosomiasis). Ann Trop Med Parasitol 2006; 100:663.