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Lindsey H. Malik, DO
4860 Y Street, Suite 2820
The Epidemiology, Clinical Manifestations, Sacramento, CA 95817
lindsey.malik@ucdmc.ucdavis.edu
Chagas disease results from infection by the protozoan parasite Trypanosoma cruzi and is endemic in Latin
America. T cruzi is most commonly transmitted through the feces of an infected triatomine, but can also be
congenital, via contaminated blood transfusion or through direct oral contact. In the acute phase, the disease
can cause cardiac derangements such as myocarditis, conduction system abnormalities, and/or pericarditis.
If left untreated, the disease advances to the chronic phase. Up to one-half of these patients will develop a
cardiomyopathy, which can lead to cardiac failure and/or ventricular arrhythmias, both of which are major
causes of mortality. Diagnosis is conrmed by serologic testing for specic immunoglobulin G antibodies. Initial
treatment consists of the antiparasitic agents benznidazole and nifurtimox. The treatment of Chagas cardiac
disease comprises standard medical therapy for heart failure and amiodarone for ventricular arrhythmias, with
consideration for implantable cardioverter-debrillator. Chagas disease causes the highest infectious burden
of any parasitic disease in the Western Hemisphere, and increased awareness of this disease is essential to
improve diagnosis, enhance management, and reduce spread.
Introduction Epidemiology
Chagas disease (CD) was discovered in 1909 by Carlos Cha- Until recently, CD was confined to those areas of South
gas and was thought to be limited to Latin America, where it and Central America in which T cruzi is endemic. In
is the leading cause of nonischemic cardiomyopathy.1 With these regions, the triatomine bugthe main vector for
the migration of infected individuals from Latin America to human transmissionthrives in poor housing conditions;
the United States, the Centers for Disease Control and Pre- therefore, rural populations are most commonly infected.2
vention (CDC) estimates that more than 300,000 persons In the 1980s, the number of individuals infected with T
with Trypanosoma cruzi infection reside in this country, cruzi in endemic areas of Latin America was estimated
where it now poses a major public health concern because at 16 to 18 million. However, following the institution of
of its rising prevalence and limited awareness within the parasite and vector control programs along with blood-bank
medical community. For this reason, the CDC has classified screening in this region, there has been a steady decline
CD as 1 of the 5 neglected parasitic infections in the United in the prevalence of CD to about 11 million cases in the
States, a group of diseases that has been targeted for public mid-to-late 1990s, and 7.6 million cases in 2006. Conversely,
health action.2 The importance of CD in this country is as the prevalence of CD in Latin America decreased, the
illustrated by a recent study of immigrants in Los Angeles number of Latin American immigrants in the United States
County. Of 135 persons from Central and South America rose, with more than 7 million people from T cruzi-endemic
with nonischemic cardiomyopathy of unknown etiology, countries becoming legal US residents from 1981 to 2005,
20% were found to have Chagas heart disease. Further, this resulting in a surge of this disease in the United States.5
report showed that individuals with Chagas cardiomyopa- According to preliminary estimates, the United States now
thy died at a younger age and had fourfold higher all-cause ranks seventh in the Western Hemisphere in number of
mortality than patients with more conventional causes of individuals infected with T cruzi.4
heart failure.3 Through both globalization and immigration,
the prevalence of CD in the United States is expected to Transmission/Life Cycle
increase.4 T cruzi is excreted in the feces of an infected triatomine bug
onto human skin or near mucous membranes. The parasites
breach the dermis though excoriations in the skin and gain
All authors had access to the data and a role in writing the systemic access. Once within host cells they reproduce,
article. which leads to cell lysis and hematogenous dissemination,
The authors have no funding, financial relationships, or conflicts at which point parasites are apparent on peripheral blood
of interest to disclose. smear. The cycle is complete when a triatomine vector
Received: February 12, 2015 Clin. Cardiol. 38, 9, 565569 (2015) 565
Accepted with revision: April 1, 2015 Published online in Wiley Online Library (wileyonlinelibrary.com)
DOI:10.1002/clc.22421 2015 Wiley Periodicals, Inc.
feeds on the human host, ingesting T cruzi from the Table 1. Clinical Manifestations of Chagas Disease
blood.6 Chagas disease can also be transmitted through Acute phase (duration: weeks)
nonvectorial mechanisms, such as blood transfusion or
vertically from mother to infant. Cases of direct oral Fever
transmission have also been documented.7 Transfusion- Malaise
based and congenital transmissions are the main forms
of human infestation in urban zones and nonendemic Lymphadenopathy
countries, and are therefore the major targets for the
Chagomainammatory nodule at site of inoculation
reduction of spread.8
Romanas signperiorbital swelling
Pathogenesis ECG abnormalities: sinus tachycardia, rst-degree AV block
Inoculation is followed by a short incubation period of 1
Myocarditis (rare)
to 2 weeks after which the acute phase of the disease
begins. This phase typically lasts 8 to 12 weeks and Indeterminate phase (duration: decades)
is characterized by parasitemia and subsequent immune
response. Following the acute phase, about 30% of patients Asymptomatic (most)
directly enter the determinate (final) phase, but the majority Conduction abnormalities, regional LV wall motion abnormalities,
of patients proceed to the indeterminate phase (Figure or sudden cardiac death (rare)
1). The latter phase involves host-parasite equilibrium
Chronic phase (duration: decades)
and is without progressive host damage.9 Approximately
one-third of patients progress from indeterminate to Asymptomatic
determinate phase, in which cardiac symptoms and signs
arise from progressive myofibril fibrosis and conduction Cardiac: LV dilatation, congestive heart failure, conduction
abnormalities, ventricular arrhythmias, thromboembolic disease,
system injury.10 Remodeling of the collagenous matrix with
sudden cardiac death
fibrosis leads to increased myocardial stiffness, systolic
and diastolic dysfunction, and ultimately a severe, dilated Abbreviations: AV, atrioventricular; ECG, electrocardiogram; LV, left
cardiomyopathy. ventricular.
The level of parasitemia decreases within the first 90 days of monitoring has been suggested for patients with an abnor-
infection and T cruzi is not detectable in the chronic phase, mal resting ECG or ventricular wall motion abnormalities
during which diagnosis focuses on detection of serum anti- on echocardiography. If nonsustained ventricular tachy-
bodies to the parasite for which there are 3 serologic tests: cardia is detected, invasive electrophysiologic study has
indirect hemagglutination, indirect immunofluourescence, been considered.19 However, at this time, a uniform and
and enzyme-linked immunosorbent assay. consensus-based approach to screening patients has not
Although its findings are nonspecific, the ECG provides been established.
the initial evidence of cardiac involvement. The most
common abnormalities are right bundle branch block, left
Treatment
anterior fascicular block, and diffuse ST-T changes.8 Patients
who exhibit ECG changes suggestive of cardiac involvement Anti-infective Agents
should undergo further assessment to determine severity The 2 antiparasitic drugs available for the treatment of CD
of disease. Excellent prognosis for almost a decade are benznidazole and nifurtimox. These agents are most
has been reported for patients with a normal ECG.19 effective in the acute phase of the disease, with the rates of
Echocardiography can demonstrate both structural and parasitological cure of 60% to 80% (Figure 1). Treatment
functional alterations in the early stages of cardiac is recommended for all cases of acute, reactivated, or
involvement, including regional wall motion abnormalities congenitally transmitted infection, and also for children
and diastolic dysfunction. With progression of the disease, up to age 18 years old with chronic infection.8 Indications
ventricular dilation and severe, global hypokinesis ensue.20 for treatment of patients in the chronic phase are currently
Due to the high incidence of ventricular arrhythmias unclear. A meta-analysis of 9 studies showed that compared
and sudden death in chronic Chagasic patients, screen- with placebo or no treatment in patients with chronic
ing of those at risk has been proposed. Ambulatory ECG Chagas infection, benznidazole increases the probability