Trypanosomiasis Clinical Presentation

Updated: Nov 23, 2021
  • Author: Germaine L Defendi, MD, MS, FAAP; Chief Editor: Russell W Steele, MD  more...
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The early phase of trypanosomiasis is typically asymptomatic, as only about one-third of patients have symptoms of acute Chagas disease. A minority of patients have severe clinical disease. About 10% of patients die in the early stage of the disease due to severe myocarditis or meningoencephalitis. The vast majority of people who have clinical symptoms include the following: infants, those who are defenseless in warding off the triatomid bite, and children aged 10 years or younger. Symptoms of the acute phase disappear within 4-8 weeks in most individuals.

The incubation period for Chagas disease is 7-14 d (1-2 weeks). In transfusion-acquired disease, the incubation period is longer (20-40 d). Chronic manifestations do not appear for years after infection. 

Symptoms of parasitic infection and proliferation include the following:

  • The first symptom is a bug bite by a reduviid or triatomine insect, typically on or near the face.

  • After 1-3 weeks, the organism proliferates, producing a red nodule known as a chagoma, which develops at the site of the original inoculation. The chagoma is usually located on the face or arms and can be painful. The surrounding skin becomes indurated and, later, hypopigmented.

  • A few days after proliferation, the parasites can spread throughout the body, infecting many tissues in particular the heart, skeletal muscles, and nervous system. This spread heralds the acute phase of the illness. During this stage, the infected patient may develop a flulike illness. Symptoms include a high temperature, chills, headache, irritability, tiredness, anorexia, malaise, myalgias, lymphadenopathy, and splenomegaly. The fever can be continuous, intermittent, or remitting and may last as long as 5 weeks. Epistaxis is common in young children.

  • Cardiac symptoms are observed in almost all patients, shortly after proliferation of the parasite begins.

In chronic disease, involvement of the GI system is common. Symptoms include dysphagia, regurgitation, hiccups, constipation, and abdominal pain. Disturbances in swallowing are common. These symptoms may develop weeks to years after the initial infection and subsequent progression is typically slow.

  • Symptoms specifically of esophageal involvement include dysphagia, regurgitation, heartburn, hiccups, odynophagia, and coughing. These symptoms generally develop insidiously. Less common symptoms of megaesophagus are severe malnutrition and aspiration with bronchitis and pneumonia. Hypertrophy of the salivary glands, especially the parotids, is present in 25% of patients with chagasic megaesophagus. These patients have an excessive response to salivary stimuli and the increased volume of saliva can lead to drooling.
  • Second to the esophagus, the colon is the most frequently affected portion of the GI tract in patients with chronic Chagas disease. The rectum and sigmoid colon are affected most often. The primary symptom is slowly progressive constipation. Most patients with megacolon have a bowel movement every 10 days. Impaction, caused by a firm mass of stool or a true fecaloma, develops in a minority of cases. Symptoms can range from vague abdominal pain and rectal fullness to symptoms of large bowel distention. Other symptoms include obstipation and meteorism.
  • Megaduodenum is usually asymptomatic but can lead to nonspecific dyspepsia, prolonged nausea and vomiting, and, rarely, malnutrition.

Neurologic symptoms are present in few patients with chronic disease. Involvement of the central, peripheral, or autonomic nervous systems can occur. Symptoms include paresis, cerebellar disturbance, convulsions, alterations in the dorsal root ganglia, and polyneuritis. [26]



If the bite occurs near the eye, unilateral periorbital edema of the eyelids, known as Romaña sign, develops. This edematous eyelid skin has a violaceous coloring. Conjunctivitis and enlargement of the ipsilateral preauricular lymph node is observed. Unilateral ocular and facial edema that involves the ipsilateral preauricular lymph node is known as oculoglandular syndrome. The preauricular region can markedly swell, causing an initial impression of parotitis, such as that caused by the mumps virus. In a small number of infected individuals, the facial edema may be generalized and mistaken for nephrotic syndrome. 

The spleen and liver are palpable but, in general, are not greatly enlarged. The disease is often not recognized at this stage and is accurately diagnosed in only a minority of patients.

The younger the patient, the more severe the clinical manifestations. Occasionally, the illness is fatal, especially in children younger than 2 years old. Generalized lymphadenopathy, moderate hepatosplenomegaly, anasarca, vomiting, and diarrhea are common in infants. Meningoencephalitis is also more common in young infants.  [27]  If dermatological findings are seen, they can vary from a generalized maculopapular or morbilliform rash to urticaria.

In the acute phase, tachycardia is present and may not be related to fever; rather, it may result from destruction of the heart's parasympathetic innervation. As many as 30% of patients have cardiovascular abnormalities, which include cardiac enlargement, functional murmurs, and conduction blocks. Evidence of myocarditis is almost always found. Myocarditis is mild in the majority of cases. Biventricular heart failure rarely develops. Death from acute myocarditis occurs in 2-3% of patients. Prognosis is poor with early development of premature ventricular contractions, atrial fibrillation, heart block, or congestive heart failure.

The manifestations of the acute phase of Chagas disease generally last 2-4 weeks. In those who survive, the disease progresses to the indeterminate, or asymptomatic, phase. A low level of parasitemia is present. This phase can persist for years or even for the rest of the patient's life. As many as 30% of persons with disease in the indeterminate phase have cardiac, GI, or neurologic damage 10-20 years after infection. 

Clinical manifestations of chronic disease can develop years after the initial acute infection. During the chronic phase, the most serious aspect of Chagas disease is the delayed damage that it can inflict on the heart and GI system. Serious sequelae can be cardiomyopathy, heart failure, megaesophagus, and megacolon. 

  • Cardiac abnormalities are the most frequent manifestations of chronic Chagas disease.
  • Cardiac disease is the most serious cause of morbidity and mortality.
  • Chagas cardiomyopathy develops in 30% of patients. 

Congestive heart failure is the first sign of chagasic heart disease. Once heart failure occurs, it usually is intractable and difficult to control. Signs of right-sided heart failure are more common than signs of left-sided heart failure. Heart sounds may be distant, and functional murmurs of mitral and tricuspid insufficiency can develop. Other signs and symptoms include dyspnea upon exertion, peripheral edema, ascites, hepatomegaly, chest pain, and palpitations.

Patients with cardiac abnormalities typically do not have acute pulmonary edema. Orthopnea is also uncommon. The most important complications are systemic and pulmonary embolism and sudden death. Sudden death frequently occurs from a fatal dysrhythmia, such as ventricular fibrillation, or, less frequently, from a third-degree heart block or an embolism.  

In advanced cases of cardiac disease, the typical aneurysm develops at the apex of the left ventricle. Predictors for poor prognosis include impaired left ventricular function, New York Heart Association class III/IV, cardiomegaly observed on radiographs, left ventricular systolic dysfunction observed on echocardiographs, nonsustained ventricular tachycardia on 24-hour Holter monitoring findings, low QRS voltage on electrocardiography findings, apical aneurysms, and male sex.  QT interval dispersion, a marker of inhomogeneous myocardial repolarization, has been shown to be an independent predictor of sudden cardiac death in patients with Chagas disease.

Abnormalities in the GI system are the second most common manifestation of chronic Chagas disease. These occur in 8-10% of patients and vary from minor changes in motility to severe dilatation of the esophagus or colon.

  • Esophageal disease is the most common cause of symptoms in chronic disease. Most patients have symptoms at age 20-40 years, and the rate of progression widely varies.
  • Less commonly involved organs include the stomach and duodenum; rarely, the gallbladder and biliary tree. Involvement of the stomach leads to hypotonia, hypoperistalsis, delayed emptying and decreased acid secretion; and, rarely, dilatation.
  • Abdominal examinations reveal abdominal distention and tympanism.

Other rare findings ascribed to Chagas disease include bronchiectasia, hemosiderosis, and dilatation of the ureter or urinary bladder.

Intrauterine infection can cause spontaneous abortion or premature delivery. In its acute stage, congenital Chagas disease often resembles the acquired disease. The onset might be at birth or a few months later. [28]

  • The affected infant has a low birth weight, hepatosplenomegaly, jaundice, anemia, fever, and edema.
  • Neurologic involvement includes meningoencephalitis with convulsions, hypotonia, hyporeflexia, and tremors.
  • Some patients have metastatic hemorrhagic chagomas in the skin or mucous membranes.
  • Intracranial calcifications and ocular lesions have been described.
  • Cardiac involvement is rare.
  • GI abnormalities from megaesophagus present as dysphagia and cause death by aspiration. 
  • Death frequently occurs within the first few weeks of life. Those who survive have severe neurologic sequelae with mental deficiency or behavioral and learning disabilities.

The differential diagnosis of intrauterine infection includes erythroblastosis fetalis, congenital toxoplasmosis, cytomegalovirus, parvovirus B19, lymphocytic choriomeningitis virus, and herpes simplex infections. A positive serologic result for specific immunoglobulin G (IgG) at 6-12 months for Chagas disease is an indication for treatment. Transmission of this infection through infected mother's milk has been observed in breastfed babies.

Immunosuppression as a result of organ transplantation or human immunodeficiency virus (HIV) infection can lead to reactivation of the infection. Severe myocarditis and neurologic disease with brain abscesses, meningoencephalitis, and seizures caused by T cruzi have been major findings in patients infected with HIV. Clinical findings of neurologic involvement are nuchal rigidity, convulsions, paralysis, and coma. [27]  





T cruzi, a protozoan hemoflagellate, causes American trypanosomiasis. T cruzi belongs to the order Kinetoplastida, suborder Trypanosomatina, genus Trypanosoma, and subgenus Schizotrypanum.

These organisms undergo an obligatory developmental and reproductive cycle in the alimentary tract of a reduviid or triatomine insect. The reduviid or triatomine insects commonly are called assassins, cone-nose, or kissing bugs because of their predilection for biting the victim's face while he or she is sleeping. The insects are large (2-3 cm in length), obligate hematophages that hide in crevices in mud walls, windows, door frames, and dark corners of poorly constructed adobe-style huts. These insects come out at night to feed on the blood of sleeping humans. They require blood to grow and mature.

The vector (ie, reduviid or triatomine insect) becomes infected by ingesting trypomastigotes present in the bloodstream of an infected mammal. Infection lasts for the life of the vector, which can be as long as 2 years.

The developmental cycle of T cruzi includes 3 morphologic forms: epimastigotes, trypomastigotes, amastigotes. The entire cycle takes place in the insect gut lumen over 6-15 days.

  • Within a few hours after the ingestion of infected blood, short, spindle-shaped forms lacking a free flagellum can be found in the insect's foregut. These develop into small epimastigote forms that divide and elongate, resulting in large (35-40 µm long) epimastigotes.
  • By the third or fourth day, the epimastigotes attach to the rectal epithelium.
  • By the fifth day, the epimastigotes become rounded, short trypomastigotes, which then elongate.
  • By the seventh and eighth days, they become infective metacyclic trypomastigotes that are long (17-22 µm), slender, and spindle shaped. They have a large kinetoplast posterior to the nucleus and a flagellum. 

Human transmission occurs through contact with infected insect excreta. These insects defecate while ingesting human blood, thereby excreting the infective trypanosomes. Each microliter of insect excreta may contain 3000-4000 organisms. The person who is bitten is inoculated by inadvertently rubbing the insect's feces into the site of the bite. The organism can also enter through abraded skin or intact mucous membranes of the mouth, nose, and conjunctiva. T cruzi invades cells near the inoculum. Once inside the cell, the infective metacyclic trypomastigote moves from the digestive vacuole to the cytosol. Next, they transform into intracellular amastigote forms and multiply by binary fission.

Amastigotes have a short flagellum, are spherical or oval, and 2-4 µm in diameter. After a period of multiplication, amastigotes transform back into trypomastigotes; rupture the cell; enter the bloodstream; and invade other cells, predominantly reticuloendothelial, cardiac, skeletal and smooth muscle, and neuroglial cells.

The parasite can be transmitted congenitally,  [29, 30, 31]  transmitted through organ transplantation [32] , via infected breast milk, via blood transfusion, [33] or accidentally in the laboratory. As much as 6.5% of blood stored in some blood banks in Latin America is contaminated by T cruzi. In highly endemic areas, this figure can be as high as 20%. Transplacental transmission occurs in 2-10.5% of infected mothers. [34]

Natural infection occurs in a wide variety of animals, including guinea pigs, opossums, foxes, squirrels, armadillos, anteaters, porcupines, rats, mice, bats, and monkeys. After humans, birds are the most important blood sources; however, birds are not susceptible to infection. Domestic cats and dogs are the most important domestic reservoirs for human infection.

The parasite can also be transmitted orally. [35, 36, 37, 38]

  • Ingestion of food contaminated by triatomine feces or entire insects

  • Consumption of raw or undercooked blood and/or meat of reservoir hosts

  • Eating food contaminated by the anal gland secretions of the common opossum