Vivax malaria in an Amazonian child with dilated cardiomyopathy

Abstract

A child living in the Brazilian Amazon region who had had vivax malaria at the age of 11 months was admitted three months later with a history of progressive dyspnoea and fever, which culminated in respiratory distress and severe dilated cardiomyopathy at hospital admission in a malaria-free area. She received treatment for cardiac insufficiency and was tested for malaria with two thick blood smears, which were negative. There was general improvement of cardiorespiratory function in the next two weeks, but in the third week of hospital admission, there was re-appearance of fever, severe anaemia, severe plaquetopaenia, and respiratory distress. A third thick blood smear was positive for Plasmodium vivax mono-infection, which was confirmed by molecular methods. A serological panel with the most prevalent infectious agents known to cause myocarditis was performed, and specific anti-cytomegalovirus (CMV) IgM and elevated levels of anti-CMV IgG were also detected in the serum. After treatment for malaria, there was improvement of respiratory distress, although cardiac function did not recover. She was discharged home with drugs for cardiac insufficiency and is currently under follow-up with a paediatric cardiologist as an outpatient. This report presents a young child with several episodes of vivax malaria who suffers from cardiac insufficiency, probably related to CMV-induced myocarditis.

Figure 1

Electrocardiogram in a child with dilated cardiomyopathy. The electrocardiogram shows left ventricular and atrial overload.

Figure 2

Chest radiography showing cardiomegaly. There is marked dilation of the left ventricle and increased pulmonary blood flow.

Figure 3

Molecular diagnosis of Plasmodium vivax infection. A DNA sample of the patient was submitted to nested PCR and it was positive for P. vivax mono-infection. PS = Patient sample; VPC = P. vivax positive control; FPC = P. falciparum positive control; B = Blank; M = Molecular weight marker.

Figure 4

Clinical evolution of fever, platelet counts and haemoglobin and its relation with malaria. On admission (10/9) haemogobin level was 9.7 mmol/l and platelet count was normal. After a few days of admission axillary temperature increased, peaking on 29/9, when hourly antipyretics were prescribed. Four days later there was an acute drop on haemoglobin levels and platelet counts. The patient received a blood transfusion on 3/10, resulting in increased platelet count and haemoglobin levels. However, they declined again on 5/10. A positive smear for P. vivax was obtained in 4/10.

Figure 5

Four-chamber echocardiographic image showing marked dilation of the left ventricle. RA = right atrium, LA = left atrium, RV = right ventricle, LV = Left ventricle.

Figure 6

Echocardiographic image showing marked dilation of the left ventricle and mitral regurgitation (in blue) of moderate degree.

Figure 7

Patient history with major clinical events, diagnosis and possible causal relationship. The patient was admitted when she was 11 months old with respiratory symptoms and vivax malaria. She was treated and discharged home two days later without symptoms. After two months she started to have increasing dyspnoea and respiratory distress and was admitted again at 13 months old with a dilated cardiomyopathy and negative thick blood smears. During admission, there was an initial improvement of dyspnoea, but after a few weeks the dyspnoea worsened and she developed fever, with a positive smear to P. vivax. After malaria treatment with chloroquine and primaquine, there was important improvement of respiratory distress and fever. Positive serology for CMV suggest that she had a CMV-induced myocarditis around 11 months of age, progressing to symptomatic dilated cardiomyopathy, and later developing relapsing vivax malaria, with a severe clinical presentation.