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Antiviral chemotherapy and neonatal herpes simplex virus infecition: a pilot study--experience with adenine
Insights
Early treatment with vidarabine (ara-A) for neonatal herpes simplex virus (HSV) infection, especially when skin vesicles appear early, significantly improves survival and prevents neurological deficits.
Area of Science:
- Neonatal infectious diseases
- Virology
- Pediatric neurology
Background:
- Neonatal herpes simplex virus (HSV) infection poses a significant threat, with varied presentations including disseminated disease, CNS involvement, or localized skin/eye infections.
- Disseminated HSV infection in neonates often leads to severe outcomes, including mortality and long-term neurological sequelae.
- The hallmark of HSV infection is often skin vesicles, but diagnosis and treatment can be delayed, particularly in cases without early skin manifestations or with delayed vesicle appearance.
Purpose of the Study:
- To evaluate the efficacy and safety of vidarabine (ara-A) in treating neonatal herpes simplex virus (HSV) infection.
- To determine the impact of early diagnosis and treatment initiation on patient outcomes, particularly neurological deficits.
- To assess the toxicity profile of vidarabine in neonates.
Main Methods:
- Retrospective analysis of 13 neonates diagnosed with HSV infection.
- Administration of vidarabine (ara-A) at 10-20 mg/kg/day via continuous intravenous drip for 10-15 days.
- Correlation of treatment timing (relative to disease onset and skin vesicle appearance) with clinical outcomes and neurological status at follow-up.
Main Results:
- Eight infants had disseminated disease, one had localized CNS disease, and four had skin/eye infections.
- Delayed diagnosis and treatment (beyond 3-8 days post-vesicle onset or in infants without vesicles) were associated with poor outcomes in disseminated disease (4 deaths, 1 severe neurological deficit).
- Eight infants (4 disseminated, 4 localized) treated early (within 3 days of neurologic signs, with early skin vesicles) survived without neurological deficits at 6-12 months. Vidarabine showed no apparent bone marrow, liver, or kidney toxicity.
Conclusions:
- Early administration of vidarabine (ara-A) in neonates with HSV infection, particularly when skin vesicles are the earliest sign, is associated with excellent survival and no neurological deficits.
- Delayed treatment initiation significantly worsens prognosis in neonatal HSV infection.
- Vidarabine (ara-A) appears to be a safe and effective antiviral agent for neonatal HSV, with no observed toxicity to major organs.
Abstract:
Among 13 neonates with herpes simplex virus (HSV) infection, eight had disseminated disease, one localized CNS disease, and in four the infection was confined to the skin and eyes. Ara-A, a purine nucleoside with anti-viral activity against DNA-VIRUSES, WAS GIVEN (10 TO 20 MG/MG/DAY) BY A CONTINUOUS 12-HOUR INTRAVENOUS DRIP FOR 10 TO 15 DAYS. In all, ara-A administration was begun within three to eight days after the appearance of skin vesicles which represented the hallmark of the disease. Both diagnosis and ara-A treatment were much delayed in one infant without skin vesicles and four infants whose skin vesicles appeared late, long after the occurrence of CNS damage. In this group of infants with disseminated disease, four died and one infant was left with severe neurological deficits. Eight infants (four with disseminated and four with localized skin disease) with skin vesicles as the earliest sign of infection received ara-A early, within three days after the onset of neurologic signs. All survived with no neurologic deficit at 6 months to 1 year of age. There was no apparent toxicity of ara-A to the bonemarrow, liver, or kidney.