American trypanosomiasis, or Chagas disease, is caused by infection with Trypanosoma cruzi, which is transmitted to humans after the bite of the bloodsucking Reduviid, or kissing bug (also known as triatomine bug and cone-nosed bug). After the blood meal, the kissing bug releases trypomastigotes in its feces, which contaminate the bite wound or enter the host via an intact mucous membrane (eg, conjunctiva). The parasite then invades nucleated cells in local tissue and multiplies while spreading throughout the host. Specifically, the organisms replicate within these cells and then are released by cell lysis and infect distant cells. The parasite then spreads via blood and lymphatics and primarily targets muscle cells (cardiac, smooth, and skeletal muscle) as well as ganglion cells, establishing lifelong infection in the absence of treatment. The life cycle is continued when an infected host is bitten by an uninfected insect. Transmission can also occur during blood transfusion or organ transplant. Congenital transmission has been reported.

Natural transmission has been reported in the southern United States, in particular Texas, although the disease is much more prevalent in Mexico, Central America, and South America. Current disease control methods are significantly limiting the natural transmission in developing countries. Most primary cases in endemic areas occur in children aged younger than 10. Migration from endemic areas and rising rates of local transmission have led to an estimated 300 000 persons in the United States with chronic Chagas disease. Screening is therefore recommended for individuals born in or who have lived for a prolonged period of time in endemic areas (Mexico and Central and South America) even if they do not exhibit visible signs or symptoms.

The disease consists of an acute illness that can be followed by chronic late sequelae in long-standing infections after years or decades.

Primary infection is commonly asymptomatic, or there may be fever, malaise, and possibly hepatosplenomegaly 1-2 weeks after exposure. A nodule may develop at the site of the initial exposure (chagoma), and, if primary inoculation has occurred through the conjunctiva, patients will develop the Romana sign, painless unilateral swelling of the periocular tissue and palpebrae. Less than 1% of children develop a more severe fulminant presentation (generally in children younger than 2 years) with meningoencephalitis or myocarditis, often with pericardial effusions.

Chronic infection is also commonly asymptomatic, but 40%-50% of patients will develop clinically overt disease years to decades after the primary infection, with the heart most commonly affected (cardiomyopathy and cardiomegaly), followed by the gastrointestinal tract (organomegaly).

Chronic inflammation driven by the parasite results in fibrosis, lymphocytic infiltration, and end-organ denervation. Chagas cardiomyopathy can present with palpitations, dizziness, and even syncope and with time can progress to signs of heart failure. Chronic Chagas disease involving the esophagus has a range of presentations, from asymptomatic dysmotility to mild achalasia to severe megaesophagus, and can present with a range of symptoms including dysphagia and odynophagia, weight loss, and aspiration or regurgitation. Chronic Chagas disease involving the colon presents with constipation and can progress to volvulus in the setting of megacolon. Patients with megacolon almost always also have megaesophagus.

Asymptomatic patients in the chronic phase may develop reactivation of disease in the setting of immunosuppression, such as from HIV or cancer or after an organ transplant. Reactivated disease may be subclinical and marked only by parasitemia, or there may be acute phase-like signs and symptoms.

Related topic: African trypanosomiasis