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Background:Infantile aseptic meningitis is a rare infection of the central nervous system. Coxsackievirus B5 (CVB5) is an enterovirus that is sometimes associated with aseptic meningitis and encephalitis.Case presentation: We report on three isolated infants with aseptic meningitis caused by CVB5 in the spring and summer of 2016 with nearly identical 404-bp CVB5 Viral Capsid Protein 1 (VP1) sequences.In addition, viral analysis of sewage samples from Chiba Prefecture in 2016 showed similar 404-bp CVB5 VP1 sequences from May to September 2016. Conclusion:These results indicate that viral screening of sewage water may help detect occult outbreaks of viral infection, particularly for enterovirus strains. (J Nippon Med Sch 2018; 85: 187 190)

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Pelizaeus-Merzbacher disease (PMD) is a rare (1.45 in 100,000 live births in Japan 1 ) X-linked disease characterized by developmental defects in the myelin sheath formation, which deeply affects the central nervous system.PMD is caused by abnormalities in the proteolipid protein 1 (PLP1) gene, which is responsible for the differentiation and myelination of oligodendrocytes 2 . Clinical findings are hypotonia, nystagmus and delayed development of motor skills, and the prognosis is dismal in later life 3 . CaseA 5-month-old boy was referred to our hospital due to delayed head control and nystagmus. Family history showed no significant hereditary diseases or neuromuscular disorders. He was born at 40 weeks and 6 days of gestation, and weighed 2,910 g. No abnormalities, including hypotonia or congenital nystagmus, were presented on delivery, and no fetal distress or abnormal findings on congenital metabolic-disorder mass screening were indicated. On referral, he showed nodding of the head, eye tracking inability, and hyper-extensiveness of the joints, although he was able to smile spontaneously, babble actively, and respond to sound. He showed no deformities, including abnormality of countenance, abnormal reflexes, or tremor. Laboratory examination results were normal for the lactic acid! pyruvic acid ratio, and tests for metabolism of amino acid, organic acid, sugar, blood gas, urine vanillylmandelic acid, and urine homovanillic acid were also normal. Ophthalmological examination also showed no abnormalities. Magnetic resonance imagining (MRI) of the brain at 7 months of age ( Fig. 1) showed hypomyelination of the white matter, but there was no progression of the myelination thereafter. Genetic analysis by fluorescence in situ hybridization showed duplication of the PLP1 gene (Fig. 2). ConclusionDifferential diagnosis of hypomyelination includes: 1) PMD, 2) spastic paraplegia type 2 (SPG2), 3) hypomyelination with atrophy of the basal ganglia and cerebrum, 4) 18q-syndrome, 5) 11q-syndrome (Jacobsen syndrome), and 6) hypomyelination with congenital cataracts. MRI findings indicating PMD are: 1) diffuse pattern of hypomyelination, 2) increased signal intensity on T2-weighted or fluid-attenuated inversion recovery (FLAIR) scans in affected white matter regions in the cerebral hemispheres, cerebellum and brainstem, 3) thinning of the corpus callosum, and 4) atrophy of the cerebral hemispheres 4 .