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Paeds Vivasinfectious-diseases

Paeds Vivas · infectious-diseases

Herpes simplex infection in children — branching viva

Branching structured-oral viva on herpes simplex infection in children: the neurotropic latency-and-reactivation biology, the clinical syndromes (gingivostomatitis, eczema herpeticum, ocular HSV, neonatal HSV, encephalitis), host-risk stratification, PCR diagnosis, tiered aciclovir therapy, post-treatment suppression and the maternal-neonatal prevention pathway.

branching clinical structured oral5 min readVerification in progress

Target exams

RACP DCEMRCPCH ClinicalRCPSC Pediatrics
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Study tools

Target exams

RACP DCEMRCPCH ClinicalRCPSC Pediatrics
Prompt
You are the general paediatric registrar in the emergency department. A 12-day-old term infant presents with fever, poor feeding and lethargy; the mother had a first episode of genital herpes at 38 weeks and delivered vaginally through active lesions, and there is a vesicle on the infant's scalp. The examiner asks you to take the candidate through the diagnosis, investigations and treatment of neonatal HSV, then to discuss herpes simplex encephalitis, eczema herpeticum and the maternal-neonatal prevention pathway.

Opening question

Examiner: Take me through this infant. What is the diagnosis, and what is your frame for managing him? [2]

Candidate: The leading diagnosis is neonatal herpes simplex virus disease. A 12-day-old with fever, poor feeding and lethargy has bacterial sepsis on the differential, but this infant has the highest-risk HSV exposure: a maternal primary genital HSV at 38 weeks with vaginal delivery through active lesions, because a primary infection means the mother has not yet made antibody to transfer to the baby. The scalp vesicle clinches it. My frame is to treat this as neonatal HSV from the first minute — start high-dose intravenous aciclovir, run the full HSV workup, and treat empirically because outcome worsens with every hour of delay. [2] [7]

Examiner: Why is a primary maternal infection so much more dangerous than a recurrent one? [1]

Candidate: Because neonatal HSV transmission is far higher from a primary genital infection — around forty-four percent — than from a recurrent one, which is only a few percent. In a primary infection the mother lacks antibody, so the neonate receives neither transplacental antibody nor the cell-mediated advantage of maternal immunity. The baby meets a large viral inoculum unprotected, and the immature neonatal immune system cannot contain it. [1] [7]

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References7ShowHide
  1. [1]Corey L; Wald A Maternal and neonatal herpes simplex virus infections. N Engl J Med, 2009.PMID 19797284
  2. [2]Pinninti SG; Kimberlin DW Neonatal herpes simplex virus infections. Semin Perinatol, 2018.PMID 29544668
  3. [3]James SH; Kimberlin DW Neonatal Herpes Simplex Virus Infection. Infect Dis Clin North Am, 2015.PMID 26154662
  4. [5]Kimberlin DW; Whitley RJ; Wan W; Powell DA; et al Oral acyclovir suppression and neurodevelopment after neonatal herpes. N Engl J Med, 2011.PMID 21991950
  5. [7]Kimberlin DW; Baley J; Committee on Infectious Diseases; Committee on Fetus and Newborn Guidance on management of asymptomatic neonates born to women with active genital herpes lesions. Pediatrics, 2013.PMID 23359576
  6. [8]James SH; Kimberlin DW; Whitley RJ Antiviral therapy for herpesvirus central nervous system infections: neonatal herpes simplex virus infection, herpes simplex encephalitis, and congenital cytomegalovirus infection. Antiviral Res, 2009.PMID 19414035
  7. [12]Hsu DY; Shinkai K; Silverberg JI Epidemiology of Eczema Herpeticum in Hospitalized U.S. Children: Analysis of a Nationwide Cohort. J Invest Dermatol, 2018.PMID 28927889
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