Atlas
 

Perinatal infection



3  Neonatal pathology

3.5  Perinatal infection

Introduction:

Infections make a major contriution to perinatal mortality and morbidity. The fetus and neonate are particulary vulnerable to infection because of humotal and cellular defence mechanisms are inadequately developed. The situations resembles taht of the immunosupressed adult. The signs of infectin may be diffucult to distinguish from those of birth asphyxia or respiratory distress syndrom. Infections and sepsis as a major problem in preterm infants.

Etiology:

General routes of infection

3.5.1  Intrauterine infections (TORCH group)

Etiology:

Congenital infections of fetus and neonate with almost uniform clinical presentation and high risk of permanent handicap in survivors. The organisms spread accros the placenta. Cytomegalovirus is by far the most common.

  • T  —  toxoplasmosis
  • O  —  others (syphilis, parvovirus B19, varicella zoster etc.)
  • R  —  rubella
  • C  —  cytomegalovirus
  • H  —  herpes simplex

Clinical signs:

  • intrauterine growth retardation or failure to thrive
  • hydrops fetalis
  • jaundice or hepatosplenomegaly
  • skin rash (various)
  • CNS damage:
    • hydrocephalus (CMV, Toxoplamosis) or microcephaly (rubella)
    • intracranial calcifications, seizures
  • eye lesions:
    • microphthalmia
    • cataracts
    • chorioretinitis
  • visceral lesions:
    • pneumonitis
    • myocaridis
    • encephalitis
    • hemolytic anemia
    • bone defects (syphilis)
    • congenital heart anomalies (rubella)

On the other hand most infants have no apparent illness in the neonatal period but some of them present later during childhood with developemental delay, mental retardation or vision and hearing loss. This is particularly true for CMV infection.

3.5.2  Sepsis neonatorum

Introduction:

Bacterial sepsis occurring in the first 28 days of life characterized clinically by abrupt onset, rapid progression, often without demostrable anatomic localization and high mortality rate even with appropriate antibiotic treatment.

Clinical signs:

  • inderteminate signs
  • lethargy, irratability
  • hypothermia or hyperthermia
  • respiratory distress
  • feeding disturbances
  • mild jaundice
  • seizures
  • apnea

Etiology:

  • Gram-positive
    • group βhemolytic Streptococcus group B  —  asymptomatic vaginal colonization is found in 15 – 25 % of pregnant women. Vertical transmission is up to 60%, but only 1% of these colonized infants develop neonatal disease. IGBS is associated with both early and late onset sepsis and the most common etiologic agent of neonatal meningitis. The presentation depends on the GBS serotype Listeria monocytogenes  —  early and late onset sepsis
    • Staphylococcus aureus  —  septicemia, abscesses in the lungs, supurative skin infections, osteomyelitis
    • Staphylococcus epidermidis  —  late onset sepsis, nosocomial infections associated with intravenous catheters or invasive procedures
  • Gram-negative
    • E. coli  —  commonly encountered in sepsis, neonatal meningitis, nosocomial infections by strains with increased antibiotic resistance
    • Klebsiella, Enterobacter
    • Haemophilus influenzae

Classification:

  • Early onset sepsis
  • Late onset sepsis

Clinical signs:

  • Early onset sepsis
    • manifests in the first 7 days of life, commonly in the first hours after birth
    • associated with obstetric complications: premature delivery, chorioamnionitis, prolonged membrane rupture, prolonged labor, maternal fever
    • the organism is acquired directly from the mothers genital tract or by swallowing or aspiration of infected amniotic fluid
    • often due to group B βhemolytic Streptococcus
    • fulminant clinical course, respiratory symptoms predominate
    • mortality rate is very high
    • the main pathological finding is widespread pneumonia, hyaline membranes may be superimposed
    • lungs appear congested and airless
  • Late onset sepsis (7 – 28 days)
    • present after 7th day of life, commonly during the second to fourth week after birth
    • spread of microorganisms is either vertical (intrapartum contact with foci of maternal genital infection in most GBS sepsis) or from postnatal spread from the caregiving enviroment
    • no associaton with obstetric complications
    • mortality rate is lower than in early onset form
    • Bacteriaemia results in meningeal seeding, neonatal menignitis and ventriculitis are typical. Clinical presention of meningitis is subtle and may be dominated by nonneural signs. Nuchal rigidity and bulging anterior fontanella are late. There is high incidence of hydrocephalus in survivors.

3.5.3  Blenorrhea neonatorum

Introduction:

Gonoccocal conjunctivitis with possible severe complications. Tends to occur 3 – 5 days after birth. Neisseria gonorrhoeae is acquired during the passage through the birth canal.

Clinical signs:

  • bilateral purulent conjunctivitis, chemosis, corneal involvement with ulcer and perforation of the cornea
  • Credeƛ method of instilling silver nitrate (or other substance) solution into eyes of each newborn after birth is quite effective for prophylaxis

3.5.4  HIV infection

Introduction:

Transmission is mainly tranplacental but also occurs during labor or postnatally via brest feeding. The rate of vertical tranmission from HIV-infected mothers to infants ranges from 15 – 50%. The risk of transmission can be reduced by virostatatic therapy administration to both the pregnant woman and the neonate, cesarean section delivery. HIV-positive women should not breastfeed.

Clinical signs:

The infants are born prematurely or are growth retarded. Dysmorphic features (microcephaly, prominent forehead, flat nasal bridge) have been reported by some authors. The rate of progression varies. Children develope failure to thrive, developemental dalay, anemia, oral thrush, chronic diarrhea. Reccurent bacterial infections and opportunistic infections occur (Pnemocystis carinii).



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