• Title/Summary/Keyword: Viral meningitis

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Clinical fetures of kawasaki disease in school-aged children (학동기 아동에서의 가와사끼병의 임상 특징)

  • Park, Eun Young;Kim, Ji Hye;Kim, Hae Soon;Shon, Sejung
    • Clinical and Experimental Pediatrics
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    • v.50 no.3
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    • pp.292-297
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    • 2007
  • Purpose : Kawasaki disease (KD) rarely occurs in school-aged children. We clarified the characteristics of KD in this age group to provide tips for a high index of suspicion. Methods : Features of 38 patients with KD who were 7 years of age or older were retrospectively reviewed. Results : The incidence of the KD patients ${\geq}7years$ was 4.9 percent. The ratio of male to female was 2.5:1. Of the 38 patients, nine patients (24.0 percent) were diagnosed with typical KD and 29 patients (76.0 percent) with incomplete KD. In incomplete KD patients, cervical lymphadenopathy (69.0 percent) occurred most frequently, followed by conjunctival injection (62.0 percent) and polymorphous rash (45.0 percent). These patients occasionally presented with other additional symptoms including abdominal pain, headache, vomiting and arthralgia. Incomplete KD was initially diagnosed as cervical lymphadenitis (34.0 percent), viral infection (14.0 percent), scarlet fever (7.0 percent), meningitis (7.0 percent), and Kikuchi disease (7.0 percent). Coronary complications were noted in 15 patients (39.0 percent). Of the 37 patients treated with intravenous immunoglobulin, five (14.0 percent) were resistant to the therapy and all had coronary abnormalities. Conclusion : Most patients with KD ${\geq}7years$ of age have incomplete presentations. They tend to have a higher incidence of initial presentations of unilateral neck mass and coronary artery involvement. In school-aged children, fever and cervical lymphadenitis or suspected neck infection unresponsive to intravenous antibiotics should signal the possibility of KD. A high index of suspicion and prompt treatment is essential in this age group of patients.

Cloning and Sequence Analysis of the Full-length cDNA of Coxsackievirus B3 Isolated in Korea (한국에서 분리된 콕사키 바이러스 B3 cDNA의 클로닝 및 전체 염기서열 분석)

  • Chung, Yoon-Seok;Kim, Ki-Soon;Park, Jeong-Koo;Lee, Yoon-Sung;Shin, Soo-Youn;Cheon, Doo-Seong;Jee, Young-Mee;Kim, Moon-Bo;Na, Byoung-Kuk;Yoon, Jae-Deuk;Lee, Kwang-Ho;Song, Chul-Yong
    • The Journal of Korean Society of Virology
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    • v.30 no.1
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    • pp.71-81
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    • 2000
  • We have determined and analyzed the full-length cDNA sequence of a coxsackievirus B3 (CVB3) Korean isolate (CVB3-Korea/97) which has been known as a general human pathogen. The whole genome contains 7,400 nucleotides and has a single large open reading frame with 6,555 nucleotides that encodes a potential polyprotein precursor of 2,185 amino acids. The genome also contains a 5' non-coding region (NCR) of 741 bases and a 3' NCR of 104 bases followed by poly(A) tail. Sequence homologies of nucleotides and deduced amino acids between the CVB3-Korea/97 strain and the prototype (Nancy strain) were 81.7% and 91.5%, respectively. The genes encoding the functional proteins including viral protease and RNA dependent RNA polymerase showed higher homology than those encoding the structural proteins. We have further analyzed the sequences of 5' NCR, VP1 and VP2 of CVB3-Korea/97, which are known as cardiovirulent determining factors at the nucleotide and amino acid levels. Although the CVB 3-Korea/97 strain was isolated from an aseptic meningitis patient without cardiomyopathy, its 234th nucleotide and 165th amino acid were uracil and Asn as same as those of other cardiovirulent strains one. However, the 155th amino acid of VP1, which closely associated with cardiovirulence, was replaced with $Arg^{155}$ by single nucleotide substitution from $A^{2916}$ to $T^{2916}$. Moreover, additional amino acid substitutions were observed in the flanking region of $Asp^{155}$. Taken together, amino acid(s) substitution in VP1 may playa critical role in determining cardiovirulence of the CVB3-Korea/97 strain rather than individual nucleotide replacements in the 5' NCR and/or an amino acid substitution in VP2.

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