ABSTRACT
BACKGROUND: Human parvovirus B19 (PVB19) infection is occasionally associated with acute myocarditis. Three cases of children with PVB19 virus-associated myocarditis occurred in a very short period and the same geographical region. OBJECTIVE: To elucidate if virological factors could be responsible for determining the course of infection, a molecular epidemiologic investigation was performed. STUDY DESIGN: The diagnosis of myocarditis was established by histology or echocardiography. In the three cases, the PVB19 DNA was detected in different samples. Eight different regions were amplified by PCR using a high fidelity Taq polymerase and sequenced on both strands. Phylogenetic analyses were performed. First, the genotypes of the PVB19 strains were determined, then the intra-patient viral variability was analysed by sequencing PVB19 detected in different specimens sampled from the same patient at the same moment. RESULTS: Nearly complete sequences of the PVB19 virus (4265nt) were obtained from different samples in the three patients. The phylogenetic analyses showed that PVB19 strains identified clustered with genotype 1a PVB19 strains referenced in GenBank. When compared to the referenced strain NC_000883, the number of substitutions (transitions and transversions) were as follows: 58 for Caen.FRA/19.09, 74 for Caen.FRA/21.09 and 60 for Caen.FRA/24.09. The strains isolated from the same patient showed 100% of similarity. CONCLUSIONS: Viral myocarditis is a frequently unrecognized cause of post-inflammatory cardiomyopathy. The detailed molecular analyses do not give rise to virological markers associated with myocarditis in these children.
Subject(s)
Myocarditis/virology , Parvoviridae Infections/virology , Parvovirus B19, Human/genetics , Acute Disease , Child, Preschool , DNA, Viral/genetics , Echocardiography , Female , Genotype , Humans , Infant , Myocarditis/physiopathology , Parvoviridae Infections/physiopathology , Polymerase Chain ReactionABSTRACT
We report the case of a 4-year-old girl, successfully treated by surgical pulmonary embolectomy for acute massive pulmonary embolism. She was known to have a congenital antithrombin III deficiency diagnosed after a familial history of thromboembolic events. Surgical embolectomy may be considered as a treatment option in selected patient with anatomically extensive pulmonary embolism.
