1例早产儿在阿昔洛韦抑制治疗期间的单纯疱疹病毒性脑炎潜伏期中的应用

• 作 者: Fonseca-Aten M. Messina A.F. Jafri H.S. Snchez P.J. 王经纬
• 机 构: Department of Pediatrics University of Texas Southwestern Medical Center 5323Harry Hines Blvd Dalla
• 出 处: 世界核心医学期刊文摘(儿科学分册)
• 发表日期: 2006年11期
• 关键词: 阿昔洛韦 抑制治疗 早产儿 聚合酶链反应 皮肤病变 脑炎 脑脊液 阴性 神经系统后遗症 预防复发

Cutaneous herpes simplex virus type 2 (HSV-2) infection was recognized at 19 days of age in a 1415-g female infant born at 31 weeks of gestation. Cerebrospinal fluid (CSF) HSV polymerase chain reaction (PCR) was negative, and MRI of the brain was normal. After a 14-day course of high-dose intravenous acyclovir, the infant developed a cutaneous recurrence at 38 days of age. CSF HSV PCR again was negative. She was subsequently begun on oral acyclovir to prevent cutaneous reactivation of HSV. At 3 months of age, the infant developed HSV encephalitis as manifested by fever, seizures, abnormal CSF indices, abnormal brain MRI, and positive CSF HSV PCR. No cutaneous disease was present. It is not known whether the HSV encephalitis in our patient represented reactivation of previously unrecognized central nervous system infection or new onset of central nervous system disease as a result of spread from other tissue or site to the brain. The failure of oral acyclovir to prevent such an occurrence, however, highlights gaps in our understanding of the pathogenesis of neonatal HSV disease and questions the use of acyclovir suppression to prevent neurologic sequelae.

Cerebrospinal fluid (CSF) HSV polymerase chain reaction (PCR) was negative, and MRI was detected at 19 days of age in a 1415-g female infant born at 31 weeks of gestation. of the brain was normal. After a 14-day course of high-dose intravenous acyclovir, the infant developed a cutaneous recurrence at 38 days of age. CSF HSV PCR again was negative. She was subsequently begun on oral acyclovir to prevent cutaneous reactivation of HSV. At 3 months of age, the infant developed HSV encephalitis as manifested by fever, seizures, abnormal CSF indices, abnormal brain MRI, and positive CSF HSV PCR. No is known or the HSV encephalitis in our patient represented reactivation of previously unrecognized central nervous system infection or new onset of central nervous system disease as a result of spread from other tissue or site to the brain. The failure of oral acyclovir to prevent such an occurrenceren ce, however, highlights gaps in our understanding of the pathogenesis of neonatal HSV disease and questions the use of acyclovir suppression to prevent neurologic sequelae.