import json

data = {
 "topic": "Neonatal Herpes Simplex",
 "slug": "neonatal-herpes-simplex",
 "category_id": 15165,
 "summary": "Neonatal herpes simplex virus infection is a rare but severe, often initially subtle infection acquired mainly during delivery, classified into skin-eye-mouth, CNS, and disseminated disease, where early recognition and prompt IV acyclovir are critical to survival.",
 "written_by": "claude-sonnet",
 "references": [
  {"title": "2021_Fleisher_&_Ludwig's_Textbook_of_Pediatric_Emergency_Medicine.epub", "author": None, "pages": []},
  {"title": "Red Book Atlas of Pediatric Infectious Diseases", "author": "American Academy of Pediatrics,Carol J. Baker, MD, FAAP", "pages": [254, 255, 301, 305]},
  {"title": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024", "author": None, "pages": [1646, 1647]},
  {"title": "Red Book 2018", "author": "Kimberlin, David W.; Long, Sarah S.; Brady, Michael T.", "pages": [488]},
  {"title": "Red Book Atlas 4th Ed.indb", "author": "American Academy of Pediatrics;Carol J. Baker, MD, FAAP;", "pages": [305]}
 ],
 "short": [
  {"title": "In short", "content": (
   "- Neonatal HSV is rare, estimated at 1 in 3,000-20,000 live births (one source cites 1 in 3,200), and occurs in about 0.2-0.3% of febrile neonates\n"
   "- Transmission routes: intrapartum/peripartum (passage through an infected birth canal) accounts for about 85% of cases, postpartum (contact with infected oral/other secretions) about 10%, and in utero/congenital transmission about 5%\n"
   "- Most cases are caused by HSV-2, though HSV-1 also causes neonatal infection; a negative maternal history does NOT rule out neonatal herpes - most mothers of infected infants report no history of HSV, since primary infection can be asymptomatic and genital tract lesions are often not visible to the mother\n"
   "- Maternal infection classification affects transmission risk: first-episode primary (never previously exposed to either HSV type) carries the highest transmission risk; first-episode nonprimary (prior HSV-1, new HSV-2 infection or vice versa); and recurrent infection (prior exposure with protective antibody transfer to the infant, but active reactivation)\n"
   "- Three clinical categories of neonatal disease: skin, eye, and mouth (SEM) disease (about 40% of cases), central nervous system (CNS) disease, and disseminated disease\n"
   "- Timing differs by category: SEM and disseminated disease typically present earlier (days 5-12 of life, with peripartum-acquired disease overall often presenting around days 9-11), while CNS disease typically presents later (days 16-19, or the second to third week of life)\n"
   "- CNS/disseminated disease presents with fever, coma, apnea, fulminant hepatitis, pneumonitis, coagulopathy, and seizures, plus possible focal neurologic signs and ocular findings (conjunctivitis, keratitis); vesicular skin lesions are highly suggestive but present in only one-third to one-half of patients\n"
   "- HSV should be considered in any febrile neonate under 28 days old, particularly with CSF pleocytosis, elevated liver transaminases, or coagulopathy, since it substantially overlaps with bacterial sepsis/meningitis presentations\n"
   "- Diagnostics: PCR is the sensitive method for detecting virus in CSF for suspected herpes encephalitis; direct fluorescent antibody staining of vesicle scrapings is specific but less sensitive than culture; antigen detection and ELISA antibody tests are used, while Tzanck preparation has low sensitivity and is not recommended; serologic antibody testing is not useful in neonates and cannot reliably distinguish anogenital from orolabial infection\n"
   "- Even with prompt antiviral therapy, neonatal herpes carries high mortality and morbidity; mortality rates from neonatal herpes actually increased between 2004-2013 compared with the prior 20 years; about 50% of survivors develop recurrent skin lesions, often within 1-2 weeks of completing the initial IV acyclovir course"
  )}
 ],
 "long": [
  {"title": "Definition", "content": (
   "Neonatal herpes simplex virus (HSV) disease can result from infection with either HSV-1 or HSV-2. It is classified by extent of disease into three categories: skin, eye, and mouth (SEM) disease; central nervous system (CNS) disease; and disseminated disease. Disease can be acquired in utero (congenital, rare), intrapartum (during passage through an infected birth canal, the dominant route), or postpartum (contact with infected oral or other secretions after birth)."
  )},
  {"title": "Epidemiology", "content": (
   "Neonatal HSV disease is rare, with reported incidence ranging from 1 in 3,000 to 1 in 20,000 live births (one source cites approximately 1 in 3,200 deliveries), and occurring in about 0.2-0.3% of febrile neonates. Most infections are caused by HSV-2, though HSV-1 also causes a substantial share of cases. Transmission occurs intrapartum in approximately 85% of cases (through an infected maternal genital tract, or occasionally via ascending infection through ruptured or even apparently intact amniotic membranes), postpartum in approximately 10% (typically from a nongenital source such as a caregiver's mouth or hands), and in utero/congenitally in approximately 5% (rarely causing congenital malformations)."
  )},
  {"title": "Etiology", "content": (
   "Maternal HSV infection is classified into three categories with different implications for neonatal transmission risk: first-episode primary infection, in a mother never previously exposed to either HSV type, which carries the highest transmission risk; first-episode nonprimary infection, in which a mother previously infected with one HSV type (e.g., HSV-1) newly acquires the other type (HSV-2) during pregnancy, benefiting from partial cross-reactive immunity between the two types; and recurrent infection, in which a mother with prior HSV exposure has protective antibodies that are transferred to the infant, but is experiencing a reactivation at the time of delivery, generally the lowest-risk scenario. A negative maternal history of herpes does not rule out neonatal herpes - primary maternal infection is often asymptomatic, and vesicular lesions deep in the female genital tract may not be visible to the mother, so most mothers of infants who develop neonatal HSV report no relevant history."
  )},
  {"title": "Clinical features", "content": (
   "Neonatal HSV disease falls into three overlapping clinical categories. Skin, eye, and mouth (SEM) disease accounts for about 40% of neonatal HSV and is the most readily diagnosed form, since it presents with obvious vesicular skin lesions; it and disseminated disease share an earlier age of onset, typically between the first and second weeks of life (days 5-12), with peripartum-acquired infection overall often presenting around days 9-11. CNS disease typically presents later, in the second to third week of life (days 16-19). Disseminated and CNS disease present with systemic symptoms including fever, coma, apnea, fulminant hepatitis, pneumonitis, coagulopathy, and seizures; focal neurologic signs and ocular findings (conjunctivitis, keratitis) may also be present. Vesicular skin lesions, while highly suggestive of the diagnosis when present, are found in only one-third to one-half of affected infants overall, meaning their absence does not exclude the diagnosis. Because HSV has substantial clinical overlap with bacterial sepsis and meningitis, it should be considered in any febrile neonate, particularly one with cerebrospinal fluid pleocytosis or elevated hepatic transaminases/coagulopathy that is not otherwise explained."
  )},
  {"title": "Diagnostics", "content": (
   "PCR testing of cerebrospinal fluid is the sensitive method of choice for detecting HSV in infants with suspected herpes encephalitis/CNS disease. Direct fluorescent antibody staining of vesicle scrapings is specific but less sensitive than viral culture. Rapid antigen detection tests and ELISA antibody assays are also used diagnostically. The Tzanck preparation has low sensitivity and is not recommended as a diagnostic tool. Serologic (antibody) testing is not useful in neonates and, more generally, herpes simplex antibody testing does not reliably distinguish anogenital from orolabial infection, since a substantial proportion of initial genital infections - and virtually all initial orolabial infections - are caused by HSV-1 rather than HSV-2. EEG and CT/MRI imaging can support the diagnosis of HSV encephalitis, with temporal lobe changes on imaging being a classic finding."
  )},
  {"title": "Treatment", "content": (
   "Prompt initiation of intravenous acyclovir is critical, since early recognition and treatment can substantially decrease the otherwise high morbidity and mortality of neonatal HSV disease. Even with parenteral antiviral therapy, neonatal herpetic infections are often severe, with attendant high mortality and morbidity rates among survivors. Notably, mortality rates from neonatal herpes increased between 2004 and 2013 compared with the preceding 20 years. Recurrent skin lesions are common even in surviving infants, occurring in approximately 50% of survivors, often within 1 to 2 weeks of completing the initial parenteral acyclovir treatment course."
  )},
  {"title": "Complications", "content": (
   "Neonatal HSV carries substantial morbidity and mortality risk despite treatment. Recurrent cutaneous lesions affect about half of survivors, typically emerging shortly after completing initial therapy. CNS disease in particular carries long-term neurodevelopmental risk from the encephalitis itself, which can progress to severe cerebral atrophy and distortion if inadequately treated (\"burned-out\" HSV encephalitis)."
  )}
 ],
 "clinical": [
  {"title": "Approach at the bedside", "content": (
   "Maintain a high index of suspicion for neonatal HSV in any febrile neonate under 28 days old, even in the absence of a maternal history of genital herpes - most mothers of affected infants have no relevant history, since primary maternal infection is frequently asymptomatic. Look specifically for cerebrospinal fluid pleocytosis, elevated liver transaminases, or coagulopathy in a septic-appearing neonate, since these findings should raise HSV alongside standard bacterial sepsis/meningitis considerations, and remember that vesicular skin lesions - while highly suggestive when present - are absent in half to two-thirds of cases, so their absence should not lower suspicion.\n\nWhen HSV is suspected, send CSF for HSV PCR (the most sensitive test for CNS disease), obtain surface/vesicle cultures or direct fluorescent antibody staining if lesions are present, and do not rely on the Tzanck smear or on serologic antibody testing, which are unhelpful in this setting. Given the time-sensitivity of outcomes, start empiric intravenous acyclovir promptly whenever clinical suspicion is significant, rather than waiting for confirmatory testing, since early treatment initiation is the strongest lever available for reducing mortality and morbidity. Counsel families of survivors that recurrent skin lesions are common (about 50%) in the weeks after completing the initial IV acyclovir course, and arrange close follow-up, particularly after CNS disease, given the risk of long-term neurodevelopmental sequelae."
  )}
 ]
}

with open("/tmp/neonatal-hsv.article.json", "w") as f:
    json.dump(data, f, indent=1)
print("written")