Chagas Disease (American Trypanosomiasis) Clinical Presentation

Updated: Jul 06, 2023
  • Author: Louis V Kirchhoff, MD, MPH; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
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Incubation period

The incubation period of vector-borne acute Chagas disease is thought to be 7-14 days, but definitive data are not available because persons who live in areas of active transmission are generally continually at risk for exposure to the vectors. Although newly infected persons may be aware that their living quarters are infested by triatomine vectors, most blood meals are taken while people are asleep, so they are unlikely to recall being bitten.

The incubation period of acute T cruzi infection acquired through blood transfusion may be somewhat longer, but precise data are also lacking in this regard. 

Acute phase

In most instances of acute T cruzi infection, a specific diagnosis is not made because of the nonspecific nature of the signs and symptoms and because most cases occur in poor people who have limited access to medical care.

Acute Chagas disease carries a mortality rate of less than 5%. However, even this is likely a high estimate, since acute Chagas disease rarely is diagnosed specifically; thus, the denominator for the calculation of the fatality rate is not known. As noted above, death typically is caused by myocarditis [47, 111] and, less commonly, by meningoencephalitis. [112]

Some persons develop bothersome inflammatory lesions at the bite sites presumably caused by the injected salivary proteins, but their presence is not necessarily indicative of T cruzi infection. [113, 114, 115, 116, 117]  

In the vast majority of persons with acute Chagas disease, the manifestations resolve spontaneously within 4-8 weeks. This is followed by the chronic indeterminate (asymptomatic) phase of the disease (see image below).

Natural course of American trypanosomiasis. Courte Natural course of American trypanosomiasis. Courtesy of Dr. Patricia Paredes, Guadalajara, Jal., Mexico.

Indeterminate phase

By definition, the indeterminate phase of Chagas disease does not involve symptoms.

Most adults with T cruzi infection are unaware of their parasitosis, and a history consistent with acute Chagas disease from years prior rarely is given.

Persons who are diagnosed with indeterminate Chagas disease typically are identified through blood-donor screening or pre-employment serologic testing. 

Chronic symptomatic Chagas disease

Ten to 30% of persons with chronic indeterminate Chagas disease develop clinical manifestations due to the infection. The most common and serious problems are cardiac, which are caused by an inflammatory cardiomyopathy that results from the persistent presence of the parasites in the heart.

Cardiac symptoms

A wide variety of atrial and ventricular rhythm disturbances, including right bundle branch block, left anterior hemiblock, and third-degree atrioventricular block can result in palpitations, dizziness, syncope, and even sudden death. [118, 119]

Cardiomyopathy and consequent congestive heart failure can result in shortness of breath, decreased exercise tolerance, easy fatigability, lower-extremity edema, and nocturia, as well as other signs and symptoms.

Thromboembolism can result in stroke, as well as pulmonary and arterial embolization to areas other than the brain. [120, 121, 122]

Gastrointestinal symptoms

The gastrointestinal symptoms associated with chronic T cruzi infection typically result from denervation of hollow viscera and consequent dysfunction.

Megaesophagus is the most common anatomic finding and typically results in symptoms similar to those of achalasia, such as dysphagia, odynophagia, substernal discomfort, and a sensation that ingested food and liquids do not move forward properly.

Megacolon usually results in constipation and pain, and some affected patients can go for long periods between bowel movements. In advanced cases, bowel obstruction and/or volvulus can occur, requiring surgical treatment.

Gastric dilatation in patients with Chagas disease has been described, as has megaureter, but these manifestations are relatively rare. 



Acute phase

Symptoms of acute Chagas disease may include malaise, anorexia, myalgia, and headache, but many recently infected persons are asymptomatic.

Intermittent fevers occur, but they do not follow a specific pattern.

Some patients have lesions at the portal of entry of the parasites. Romaña sign (unilateral painless periorbital and palpebral edema) occurs when the parasites have contaminated the conjunctivae. Romaña sign is viewed as a classic sign of acute Chagas disease but develops in few newly infected persons. A chagoma, which is an indurated inflammatory skin lesion, may develop when parasites enter through a break in the skin. Romaña sign and chagomas may persist for several weeks. The lymph nodes that drain either of these lesions may be enlarged.

Hepatomegaly and splenomegaly may occur in children with acute Chagas disease, often accompanied by generalized lymphadenopathy.

Varying degrees of generalized edema may occur in acutely infected persons, particularly children.

Some patients with acute T cruzi infection develop a nonpruritic morbilliform rash called schizotrypanides.

Persistent tachycardia may be present.

Signs of acute myocarditis and resulting heart failure may develop in a small minority of patients with acute Chagas disease. [46, 47, 48]

Neurologic dysfunction may develop in acutely infected children with meningoencephalitis. [123]  

Chronic phase

Any of the physical findings of acute T cruzi infection can occur in chronically infected persons in whom the infection is reactivating due to natural (HIV infection) or iatrogenic immunosuppression. [124, 125, 126, 127, 128, 129, 130, 131, 132]  In such patients reactivation of the indolent T cruzi infection can occur in a manner and with a severity not seen in immunocompetent persons. [133, 134]

Chronic chagasic cardiomyopathy may manifest as the following:

  • Signs of congestion due to isolated left-sided heart failure may be present in the early stages of chronic chagasic cardiomyopathy. Biventricular failure with peripheral edema, hepatomegaly, ascites, and pulmonary congestion are more common in the later stages.
  • Signs of thromboembolism may appear, mostly with embolization to the brain, lungs, and extremities.

Chronic chagasic megaesophagus may manifest as the following:

  • Weight loss and, in severe cases, cachexia
  • Hypertrophy of the salivary glands
  • Pneumonitis related to regurgitation and aspiration of the food retained in the esophagus or stomach (particularly during sleep)
  • Erosive esophagitis, with increased risk for esophageal cancer

Chronic chagasic megacolon may manifest as the following:

  • Abdominal distention
  • Fecaloma
  • Signs of intestinal occlusion, sigmoid volvulus


It is not known which parasite characteristics or host factors cause some persons with chronic T cruzi infection to develop clinically apparent cardiac and gastrointestinal lesions (10‑30%), while others remain infected for life but do not develop symptoms related to the infection. This pattern of variable clinical penetrance is not particularly surprising, however, since it is similar to that observed in most other infectious diseases. Parasite strain, host immunogenetics, nutrition, age at first infection, other medical conditions, and various other factors may play roles in the pathogenesis of chronic symptomatic Chagas disease. There are no reliable predictors of whether an infected person in the indeterminate phase of T cruzi infection is likely to develop symptomatic disease, although this is an active area of research. [135, 136, 137, 138]