WHO; Bill & Melinda Gates Foundation.

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ABSTRACT. Objective. To clarify the relationship between enteroviral infection and febrile seizures.Study Design. Cerebrospinal fluid (CSF), serum, throat swab, and rectal swab samples were collected for virologic examination from 67 children with febrile seizures from April 1997 to March 1999. Those samples were examined for the presence of enterovirus using cell culture and 2 polymerase chain reaction (PCR) methods.Results. No enterovirus was isolated from cell culture of CSF, throat swab, or rectal swab samples. All samples were screened for the presence of enteroviral sequences using a sensitive PCR method (PCR-Fukushima). We obtained positive results from 14 of 67 CSF samples, 10 of 62 serum samples, 12 of 64 throat swab samples, and 13 of 64 rectal swab samples. Of 21 patients in whom febrile seizures had developed during the summer months (June through August), 13 (61.9%) had positive PCR results in the CSF. Forty-seven of the 49 samples with a positive result using PCR-Fukushima were reexamined independently for the presence of the enteroviral genome using another PCR method (PCR-Mitsubishi). PCR-Mitsubishi had slightly lower sensitivity than PCR-Fukushima but identified genotypes of enterovirus by subsequent sequence analysis of the PCR products. The presence of the enteroviral genome was confirmed in 39 of the samples (83.0%). In 8 of the 9 enteroviruses detected in the CSF and/or serum samples using PCR-Mitsubishi, the genotypes were identified as coxsackieviruses group A, which are usually difficult to isolate using cell culture methods.Conclusions. These findings proved that the causative agents of febrile illness associated with seizures in summer were primarily enteroviruses, especially coxsackieviruses group A, and that febrile seizures might be caused by enteroviral infection in the central nervous system. Pediatrics 2001;107(1). URL: http://www. pediatrics.org/cgi/content/full/107/1/e12; enterovirus, coxsackievirus group A, febrile seizures, polymerase chain reaction.ABBREVIATIONS. CNS, central nervous system; CSF, cerebrospinal fluid; PCR, polymerase chain reaction; bp, base pair. E nteroviruses-polioviruses, echoviruses, coxsackieviruses group A and group B, and enteroviruses-are responsible for significant and frequent human illness, including various neurologic manifestations. The most common neurologic illness is aseptic meningitis. Encephalitis and other manifestations, such as paralysis, Guillain-Barré syndrome, transverse myelitis, cerebellar ataxia, and peripheral neuritis, also occur. 1 The association of enteroviral infection in the central nervous system (CNS) with febrile seizures, however, has not been demonstrated. In general, the causative agent of the infection is not detected in the CNS of patients with febrile seizures using standard techniques.We previously reported that the enteroviral genome was detected in cerebrospinal fluid (CSF) samples collected from some children with transient neurologic complications, such as seizures and altered states of consciousness associated ...

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RSV and RV infections are factors in the development and exacerbation of wheezing after virus-induced lower respiratory tract infections. Moreover, RV-induced wheezing may be associated with subsequent recurrent wheezing and the development of asthma.

It has not been clarified if there is a correlation between rhinovirus (RV) load and disease severity in the lower respiratory tract infections of hospitalized children. This study was undertaken to elucidate the contribution of the viral load to the development of disease severity in 412 children ≤3 years of age who were hospitalized with lower respiratory tract infections. The RV load in nasopharyngeal aspirates obtained from the patients at the time of admission was measured by real-time quantitative reverse-transcription polymerase chain reaction (PCR), and the clinical symptoms of the patients were assessed using a severity scoring system. Of the 412 patients, 43 (10.4%) were diagnosed with RV infections only, and 15 were determined to have high severity scores. When all patients infected with RV were assessed, there was no correlation between the viral load and the disease severity. However, there was a significant negative correlation between the disease severity and age among children <11 months of age (n = 15, ρ = -0.677, P = 0.006) and a significant positive correlation between the viral load and the disease severity among children ≥11 months of age (n = 28, ρ = 0.407, P = 0.032). Among the patients infected with RV <11 months of age, the disease severity may be associated with an immature immune response and the small diameter of their airways rather than viral load. By contrast, in the patients ≥11 months of age, viral load may contribute to the development of disease severity.

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Background : To evaluate the recent frequency of onset and severity of IgA vasculitis with nephri-tis (IgAVN) in Fukushima Prefecture, we examined the epidemiology and clinico-pathological manifestations of IgAVN in our hospital over a 10-year period. Methods : We enrolled 18 patients with IgAVN treated between 2004 and 2013 in the Department of Pediatrics, Fukushima Medical University School of Medicine. These patients were divided into two groups ; Group 1 consisted of 12 patients with IgAVN hospitalized between 2004 and 2008 and Group 2 consisted of 6 patients with IgAVN hospitalized between 2009 and 2013. The epidemiology , clinical features, laboratory data, pathological findings, and outcome were retrospectively compared between the two groups. Results : The numbers of patients with IgAVN per year in Group 2 were lower than that in Group 1. The frequency of patients with higher than grade IIIb disease in Group 2 (50%) was lower than that in Group 1 (94%) ; furthermore, the frequency of patients with higher than grade IV disease in Group 2 (0%) was lower than that in Group 1 (50%). Conclusions : Our findings suggest that the incidence of onset and severity of IgAVN in patients diagnosed between 2009 and 2013 were lower than those in patients diagnosed between 2004 and 2008.