Chagas Disease (American Trypanosomiasis) Clinical Presentation

  • Author: Louis V Kirchhoff, MD, MPH; Chief Editor: Burke A Cunha, MD   more...
 
Updated: Jun 3, 2011
 

History

  • 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, this is likely a high estimate, since acute Chagas disease is rarely diagnosed specifically; thus, the denominator for the calculation of the fatality rate is not known. As noted above, death is typically caused by myocarditis[64] and, less commonly, by meningoencephalitis.
    • In the vast majority of persons with acute Chagas disease, the manifestations resolve spontaneously within 3-8 weeks. This is followed by the chronic latent or indeterminate (asymptomatic) phase of the disease.
  • Indeterminate phase
    • By definition, the indeterminate phase of Chagas disease does not cause any symptoms.
    • Most adults with T cruzi infection are unaware of their parasitosis, and a history consistent with acute Chagas disease from years prior is rarely given.
    • Persons who are diagnosed with indeterminate Chagas disease are typically identified by chance through blood-donor screening or pre-employment serologic testing.
  • Chronic symptomatic Chagas disease
    • Ten to 30% of persons with chronic Chagas disease develop clinical manifestations of the disease. The most common and serious problems are cardiac, which are caused by an inflammatory cardiopathy that results from the persistence presence of the parasites in the heart.
      • 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.
      • 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.
    • 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 appear to be relatively rare.
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Physical

  • Acute phase
    • Symptoms of acute Chagas disease may include malaise, anorexia, myalgia, and headache, but many recently infected persons are asymptomatic.
    • Intermittent fever occurs, but its frequency is unknown.
    • 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.[26]
    • Neurologic dysfunction may develop in acutely infected children with meningoencephalitis.[65]
    • 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.[66]
  • Chronic chagasic cardiomyopathy
    • 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
    • Weight loss and cachexia (in severe cases)
    • Hypertrophy of the salivary glands
    • Pneumonitis related to regurgitation and aspiration of the stomach contents (particularly during sleep)
    • Erosive esophagitis, with increased risk for esophageal cancer
  • Chronic chagasic megacolon
    • Abdominal distention
    • Fecaloma
    • Signs of intestinal occlusion, sigmoid volvulus
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Causes

It is not known which host factors or parasite characteristics cause some persons with chronic T cruzi infection to develop clinically apparent cardiac and gastrointestinal lesions, while others remain infected for life but develop no apparent symptoms. 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. Currently, there is no way to predict if an infected person in the indeterminate phase of T cruzi infection is likely to develop symptomatic disease.

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Contributor Information and Disclosures
Author

Louis V Kirchhoff, MD, MPH  Professor, Departments of Internal Medicine (Infectious Diseases) and Epidemiology, Carver College of Medicine and College of Public Health, University of Iowa; Staff Physician, Medical Service, Iowa City Veterans Affairs Medical Center

Louis V Kirchhoff, MD, MPH is a member of the following medical societies: American Association of Blood Banks and American Society of Tropical Medicine and Hygiene

Disclosure: Abbott Laboratories, Inc. Consulting fee Consulting; Quest Diagnostics Inc. Consulting fee Consulting; Goldfinch Diagnostics Inc. Salary Equity owner; Quest Diagnostics Inc. Royalty Licensed technology

Specialty Editor Board

Mary D Nettleman, MD, MS, MACP  Professor and Chair, Department of Medicine, Michigan State University College of Human Medicine

Mary D Nettleman, MD, MS, MACP is a member of the following medical societies: American College of Physicians, Association of Professors of Medicine, Central Society for Clinical Research, Infectious Diseases Society of America, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

John W King, MD  Professor of Medicine, Chief, Section of Infectious Diseases, Director, Viral Therapeutics Clinics for Hepatitis, Louisiana State University Health Sciences Center; Consultant in Infectious Diseases, Overton Brooks Veterans Affairs Medical Center

John W King, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Association of Subspecialty Professors, Infectious Diseases Society of America, and Sigma Xi

Disclosure: emedicine $50.00 author of chapter; MERCK None Other

Eleftherios Mylonakis, MD  Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital

Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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