A 34-year-old African-descendant male patient, born and raised in the urban area of the municipality of Bragança (state of Para, Brazil), an area considered endemic for Chagas' disease was assessed.
He had had fever for 30 days, associated with chills, holocranial headache and myalgia. Three weeks before admission, he noticed dark-colored urine and dyspnea, which was progressive and quickly developed to dyspnea at minimal effort, accompanied by abdominal pain, nausea and vomiting, jaundice and facial edema. On admission, he had severe dyspnea, cold extremities, mild dehydration and mucocutaneous pallor. He was neither diabetic nor dyslipidemic. He denied hypertension and smoking. The patient regularly consumed acai juice during meals. He lived in a brick house.
On clinical examination, the heart sounds were muffled and he had tachycardia with gallop rhythm. Blood pressure was 74/40 mmHg. The lungs had decreased sounds bilaterally and the abdomen was flaccid and distended, painful to deep palpation, with no visceromegalies. Pulses were palpable, with poor peripheral perfusion and cyanosis.
Biochemical assessment on the first day of hospitalization were: TB of 3.19 mg/dL; DB of 0.18 mg/dL; IB of 2,51 mg/dL; CK of 537 U/L; CKmb of 139 U/L; Hemoglobin (Hb) of 12 g; Hematocrit (Htc) of 32%; leukocytes of 15,600; lymphocytes of 30,000; platelets of 161,000/mm³; TGO of 860 U/l; TGP of 421 U/L; PT of 25; APTT of 53.
ECG showed junctional tachycardia, low-voltage complexes in classical leads and diffuse ventricular repolarization alterations.
Chest x-ray showed significant cardiomegaly with left pleural effusion, and the Doppler echocardiogram showed LVDD of 58 mm, LVSD of 39 mm, IVS of 10 mm, LVPW of 10 mm. The EF was estimated at 23% LA of 41 mm; with diffuse hypocontractility. The valves were normal and there was mild mitral, aortic and tricuspid regurgitation. Severe pericardial effusion was also observed.
The thick smear examination was positive for
On the second day of hospitalization, he developed fever (38 C), with worsening of dyspnea and required pericardial effusion drainage. He underwent endotracheal intubation and developed septic and cardiogenic shock and ventricular arrhythmias. He was treated with benznidazole, Angiotensin Converting Enzyme (ACE) inhibitors, beta-blockers, vasoactive amines, ceftriaxone and amiodarone. He went into cardiac arrest, which was refractory to resuscitation maneuvers and died.
The cause of death was septic shock and cardiogenic shock. The anatomopathological diagnosis of the necropsy study was described as heart failure due to acute Chagas myocarditis.
At the macroscopic analysis, the heart was globular, pale-gray, flaccid and congested. The presence of pericardial fluid was above normal. The assessment of the cardiac chambers showed significant chamber dilation (with predominantly dilated left chambers, mainly the left ventricle). The myocardial study showed a pinkish-gray and shiny aspect; the parietal endocardium was smooth and shiny. The heart valves were normal. The epicardium was smooth and shiny. Following the trajectory of the coronary branches, a number of small nodules was observed, described in previous studies as "rosary beads" (moliniform epicarditis),
The microscopic study showed severe acute inflammation of the epicardium and myocardium, preserving the endocardium and normal coronary arteries.
The myocardium showed intense and diffuse inflammatory activity, extensive cardiac fiber dissociation and massive destruction of the entire cardiac tissue (
The histological sections, which were stained with hematoxylin-eosin and Giemsa, disclosed the parasite-containing amastigotes (
The case described here reports on a young patient who acquired Chagas disease by oral transmission in a family micro-outbreak attributed to acai juice consumption. The case was considered as oral transmission due to the epidemiological evidence of the acai consumption and the fact that two relatives had concomitant symptoms without entry signs, considered classical of vector transmission.
The possible mechanisms of transmission of
Generally, oral
Acute myocarditis by
We report the finding of inflammatory nodules in the coronary trajectory, described in rare literature records as moliniform epicarditis or "rosary beads", which usually appear after 30 days of infection, coinciding with our patient's disease evolution stage and in accordance with reports in the literature regarding the stage of the disease.
An interesting aspect of the histological study was the massive destruction of cardiac cells, a fact that was not described in histological studies of vector transmission, which leads to the assumption about the severity of the oral transmission route.
In this case, the aggressiveness of the acute cardiac lesion involving the oral route of transmission is quite evident. We conclude that myocarditis can be extremely severe and fatal, and the implementation of public policies directed at food hygiene strategies must be implemented immediately in order to minimize the globalization of disease by this route of transmission.
The association between acai consumption and Chagas disease have been increasing annually in Para, especially in cities where there is a significant number of acai sales points, which results in increased supply of the drink throughout the year and especially during the time of the harvest, making these points a "common source", that is, the single interrelated factor among the cases.