Case Presentation:

A 63‐year‐old female presented to the emergency department with two day history of shortness of breath and lower extremity edema. She reported progressive worsening of shortness of breath for last two to three months, PND and orthopnea. She denied chest pain or any prodromal flu like illness. She was born in Guatemala, moved to the United States 10 years ago. She had recently traveled to Guatemala and returned 5 days prior to admission. Vitals were significant for hypotension and tachycardia. Physical examination revealed jugular venous distension, bibasilar crackles and bilateral lower extremity edema. Laboratory data was significant for markedly elevated pro BNP. Chest X Ray revealed pulmonary vascular congestion. Electrocardiogram showed atrial fibrillation, which was new onset. Cardiac enzymes were normal and Thyroid Stimulating Hormone was normal. Computerized Tomography of Chest showed no evidence of pulmonary embolism.

She was started on intravenous heparin for new onset atrial fibrillation. Transthoracic echocardiogram revealed severely reduced left ventricular systolic function with ejection fraction of 20‐25%, diffusely akinetic walls and left ventricular apical aneurysm. Angiography revealed normal epicardial coronaries and elevated right‐sided pressures, consistent with heart failure. Transesophageal echocardiogram (TEE) revealed thrombus in the left atrial appendage and so cardioversion could not be done. She was started on Coumadin following the TEE. She was treated with diuretics, beta‐blockers and ACE inhibitors for congestive heart failure. Given history of her origin from Guatemala and normal coronaries, there arose a suspicion for Chagas’ disease. Trypanosoma cruzi IgG serologies came back positive; confirmed by second serologic test. She was diagnosed to have Chronic Chagas’ Cardiomyopathy and was referred to CDC specialized center for further management.

Discussion:

Chagas’ disease is caused by Trypanosoma cruzi, a protozoan parasite usually transmitted by infected triatomine bugs. The diagnosis of Chagas’ disease depends on the stage of the infection and the underlying host. Thromboembolic disease, heart failure, and arrhythmias are significant contributors to the overall morbidity and mortality. Although for many years autoimmune mechanisms were thought to be responsible for most end‐organ damage, studies now point to parasite persistence as a key element in the pathogenesis of Chagas’ disease suggesting that some patients with chronic disease may benefit from anti parasitic therapy‐ Nifurtimox and Benznidazole.

Conclusions:

Chronic Chagas’ disease is a major health problem in many Latin American countries. This case report aims to increase awareness among physicians regarding Chagas’ disease, as it is considered one of the five neglected parasitic infections in USA. United States based clinicians are likely to encounter more patients with Chagas’ disease because of demographic changes and newly instituted blood bank screening.