Chagas disease is infection with Trypanosoma cruzi, transmitted by Triatominae bug bites. Symptoms begin with a skin lesion or unilateral periorbital edema, then progress to fever, malaise, generalized lymphadenopathy, and hepatosplenomegaly; years later, some patients develop chronic cardiomyopathy, megaesophagus, or megacolon. Diagnosis is by detecting trypanosomes in peripheral blood or aspirates from infected organs. Antibody tests are sensitive and can be helpful. Treatment is with nifurtimox or benznidazole.
T. cruzi is transmitted by Triatominae (reduviid, kissing, or assassin) bugs.
While biting, infected bugs deposit feces containing metacyclic trypomastigotes on the skin. These infective forms enter through the bite wound or penetrate the conjunctivae or mucous membranes. The parasites invade macrophages at the site of entry and transform into amastigotes that multiply by binary fission; the amastigotes develop into trypomastigotes, enter the bloodstream and tissue spaces, and infect other cells. Cells of the reticuloendothelial system, myocardium, muscles, and nervous system are most commonly involved.
Infection can also be transmitted by blood transfusion, organ transplantation, or ingestion of uncooked food or drink (eg, drinks made from sugar cane juice) contaminated by infected reduviid bugs or their feces. Transplacental transmission is also possible.
Infected Triatominae bugs are present in North, Central, and South America. More than 20 million people in the Americas are infected with T. cruzi, but the prevalence has been decreasing because of control measures. In some rural parts of South America, Chagas disease has been a leading cause of death. Nonhuman reservoirs include dogs, cats, opossums, rats, and many other animals.
Vector-borne disease is rare in the US, but some Latin American immigrants living in the US are chronically infected. These people are potential sources of transmission by blood transfusion or organ donation.
Symptoms and Signs
Acute infection is followed by a latent (indeterminate) period, which may remain asymptomatic or progress to chronic disease. Immunosuppression may reactivate latent infection, with high parasitemia and a 2nd acute stage, skin lesions, or brain abscesses. Congenital transmission occurs in 1 to 5% of pregnancies and results in abortion, stillbirth, or chronic neonatal disease with high mortality.
Acute infection in endemic areas usually occurs in childhood and can be asymptomatic. When present, symptoms start 1 to 2 wk after exposure. An indurated, erythematous skin lesion (a chagoma) appears at the site of parasite entry. When the inoculation site is the conjunctiva, unilateral periocular and palpebral edema with conjunctivitis and preauricular lymphadenopathy are collectively called Romaña's sign.
Acute Chagas disease is fatal in a small percentage of patients; death results from acute myocarditis with heart failure or meningoencephalitis. In the remainder, symptoms subside without treatment.
Primary acute Chagas disease in immunocompromised patients, such as those with AIDS, may be severe and atypical, with skin lesions and, rarely, brain abscesses.
Chronic disease develops in 20 to 40% after a latent phase that may last years or decades. The main effects are
Chronic cardiomyopathy leads to flaccid enlargement of all chambers, apical aneurysms, and localized degenerative lesions in the conduction system. Patients may present with heart failure, syncope, sudden death due to heart block or ventricular arrhythmia, or thromboembolism. ECG may show right bundle branch or complete heart block.
GI disease causes symptoms resembling achalasia or Hirschsprung's disease. Chagas megaesophagus manifests as dysphagia and may lead to pulmonary infections caused by aspiration or to severe undernutrition. Megacolon may result in long periods of obstipation and intestinal volvulus.
The number of trypanosomes in peripheral blood is large during the acute phase and readily detected by examining thin or thick smears. In contrast, few parasites are present in blood during latent infection or chronic disease. Definitive diagnosis may be made by examining aspirates from organs such as lymph nodes.
Serologic tests including indirect fluorescent antibody (IFA) and enzyme immunoassays (EIA) are sensitive but may yield false-positive results in patients with leishmaniasis or other diseases. Other diagnostic approaches include xenodiagnosis (examination of the intestinal contents of laboratory-raised bugs after they take a blood meal from a patient suspected of having Chagas disease) and detection of PCR-amplified parasite DNA in blood or tissue fluids.
Treatment in the acute stage rapidly reduces parasitemia, shortens the clinical illness, and reduces risk of mortality due to chronic infection.
For indeterminate infections, treatment of children and young adults has been recommended but is not always curative. Treatment of older adults with indeterminate disease is controversial.
Once the signs of chronic Chagas disease appear, antiparasitic drugs are not helpful.
Supportive measures include treatment for heart failure, pacemakers for heart block, antiarrhythmic drugs, cardiac transplantation, esophageal dilation, botulinum toxin injection into the lower esophageal sphincter, and GI tract surgery.
The only effective drugs are
Both drugs have substantial toxicity. The long treatment courses are often associated with GI adverse effects, peripheral neuropathy, poor tolerance, and low compliance.
Plastering walls and replacing thatched roofs or repeated spraying of houses with residual insecticides (those that have prolonged duration of action) can control Triatominae bugs. Infection in travelers is rare and can be avoided by not sleeping in adobe dwellings or by using bed nets if sleeping in such dwellings is unavoidable.
Blood and organ donors are screened in many endemic areas and, since 2006, in the US to prevent transfusion and organ transplant–related Chagas disease.
Last full review/revision December 2009 by Richard D. Pearson, MD