A 7-day-old infant is seen in the emergency department because of a rash that was noted on the infant’s trunk and back. The rash consisted of crops of vesicular lesions on an erythematous base (Figure 187-1). The infant was born at term gestation to an 18-year-old mother who had poor prenatal care. The mother denied a history of herpes simplex infection or other sexually transmitted infections. A direct fluorescent antibody test for herpes simplex virus (HSV) was positive and an HSV culture from the lesion was positive. A lumbar puncture was normal, and blood and CSF tests for HSV DNA were negative. The infant was admitted and treated with intravenous acyclovir for 14 days and recovered without sequelae.

Many microbiological agents can cause infection in the newborn infant. These infections may be acquired in utero, at the time of delivery, or in the immediate newborn period. Although the majority of congenital infections result in inapparent infection, it is imperative to recognize infections that manifest symptomatically. Although the clinical manifestations of these infections may be similar regardless of the pathogen, specific clinical findings and patterns may serve as important clues for specific microorganisms.

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  The epidemiology varies depending on the organism responsible for the infection:

Streptococcus agalactiae (Group B Streptococci)

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  Incidence of early onset disease (presentation in the first week of life) is 0.3/1000 live births.^1,2

  
  
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  Early-onset disease is related to perinatal transmission of the organism.

  
  
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  Fifteen to forty percent of pregnant women are colonized with the organism in the genital and/or gastrointestinal tract.

  
  
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  Fifty to seventy percent of colonized mothers transmit the organism to their infants; 1 to 2 percent of colonized infants develop early-onset sepsis (if intrapartum antimicrobial prophylaxis is not provided); risk higher if risk factors are present (see the following section “Risk Factors”).

  
  
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  Incidence of early-onset GBS infection has decreased significantly since the implementation of maternal intrapartum antibiotic prophylaxis.³

Herpes Simplex Virus (HSV)

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  Incidence is estimated to be 1 per 3200 deliveries.⁴

  
  
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  Most neonates acquire the virus from an infected maternal genital tract at the time of delivery.⁵

  
  
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  HSV-2 accounts for 70 percent of neonatal cases while HSV-1 accounts from 30 percent of cases.

  
  
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  Because most maternal genital infections are asymptomatic, 60 to 80 percent of neonates who have HSV infection are born to mothers who have no history of current or past genital HSV infection.⁵

  
  
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  The transmission rate from mother to infant during maternal primary infection is 35 to 50 percent, while the transmission rate during a recurrence of HSV is 2 to 5 percent.

Enteroviruses

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  Newborns who become infected most commonly acquire these viruses at the time of delivery.

  
  
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  In temperate climates, these viruses most commonly cause infections in late summer and early autumn.

  
  
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  Recent maternal febrile illness and abdominal pain, lack of obstetrical complications, and summertime or autumn illness may serve as clues to the diagnosis.⁶

Cytomegalovirus (CMV)

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  Most common congenital infection, affecting approximately 1 percent of all newborns in the US.⁷

  
  
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  Can be acquired in utero, perinatally, or postnatally, through breastfeeding or blood transfusion.

  
  
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  Can be acquired as a result of maternal primary or recurrent infection; risk considerably higher if infection is a result of a primary maternal infection.

Toxoplasma infection

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  Incidence in the US is 1 per 1,000 to 8,000 live births.⁸

  
  
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  Maternal acquisition of the organism occurs via the ingestion of food containing cysts or by exposure to oocytes excreted by cats.

  
  
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  Congenital infection can occur when a pregnant mother has a primary infection.

  
  
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  Risk of transmission to the fetus increases with advancing gestational age; however, neonatal manifestations are more severe when the fetus is infected early in pregnancy (i.e., first trimester).⁹

Rubella

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  The incidence of congenital rubella in the US today is very low because of widespread immunization against the virus.

  
  
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  All congenital cases are due to maternal primary infection during pregnancy.

  
  
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  Overall risk of infection of the fetus is 80 to 100 percent if maternal infection occurs during the first trimester. Risk is significantly lower if maternal infection occurs in the second or third trimester.¹⁰

Syphilis

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  The incidence of congenital syphilis had declined to the lowest reported levels in 2000. Since that time, the rate of primary and secondary syphilis has increased among women, with a concomitant increase in cases of congenital syphilis since 2005.¹¹

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  Bacterial causes of perinatal infections include Streptococcus agalactiae (Group B), Escherichia coli, and Listeria monocytogenes.

  
  
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  Bacterial pathogens that cause early-onset infection are most commonly transmitted to the infant at the time of delivery.

  
  
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  HSV is most commonly acquired by the neonate at the time of delivery; infection of the neonate may occur in utero (very rare) or may occur after postnatal acquisition from an oro-labial HSV infection.

  
  
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  CMV infection in the neonate may follow a primary or recurrent maternal infection and may be acquired in utero, at the time of delivery or postnatally, through breastfeeding or blood transfusion.

  
  
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  Toxoplasma gondii and Rubella congenital infections are a result of maternal primary infection.

  
  
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  Transplacental transmission of Treponema pallidum may result in congenital syphilis; because the fetus acquires the infection from hematogenous spread, the clinical manifestations in the newborn are similar to those of secondary syphilis.

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  Risk factors for Group B Streptococcal sepsis include:

  
  
  
  
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    Maternal colonization at the time of delivery.

    
    
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    Prematurity (less than 37 weeks gestation).

    
    
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    Prolonged rupture of membranes (>18 hours).

    
    
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    Chorioamnionitis/maternal fever.

    
    
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    Group B Streptococcal bacteriuria.

  
  
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  A risk factor for neonatal enteroviral infection is exposure of a pregnant mother to a contact who is shedding enterovirus.

  
  
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  Prolonged contact with young children, especially among parents, is a risk factor for primary CMV infection during pregnancy.¹²

  
  
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  Ingestion of undercooked pork, beef, and lamb during pregnancy serve as an important source of primary Toxoplasma maternal infection.

  
  
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  Non-immunity to rubella during pregnancy—either from lack of vaccination or incomplete vaccination—is a risk factor for maternal rubella infection.

  
  
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  Untreated syphilis in a pregnant mother may result in congenital syphilis.

Clinical Features

Perinatally acquired infections

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  The clinical manifestations of infections acquired around the time of delivery usually become apparent soon after birth but may occur anytime in the neonatal period. Examples of these infections include S. agalactiae (Group B), E. coli, L. monocytogenes, herpes simplex virus, and enteroviruses.

  
  
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  Pneumonia, septic shock, and meningitis are manifestations of perinatally acquired infections; brain abscess may complicate meningitis caused by neonatal pathogens, especially gram negative organisms (Figure 187-2).

  
  
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  The clinical manifestations of infection in the neonatal period may be subtle and are similar regardless of etiology; meningitis is clinically indistinguishable from sepsis in this age group.

  
  
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  Common manifestations include temperature instability, respiratory distress, apnea, feeding intolerance, lethargy, and jaundice.

  
  
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  Herpes simplex virus infection in the newborn may manifest with localized disease (confined to the skin, eyes, or mucous membranes), disseminated infection, or infection confined to the central nervous system.¹³

  
  
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  Vesicular lesions, forming singly, or in clusters, on an erythematous base (Figure 187-3) are the hallmark features of localized HSV infection in the newborn.

  
  
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  Enteroviral infections in the newborn may be mild and nonspecific, or may be severe and life-threatening; a macular, maculopapular, vesicular, or petechial rash may be present in these infants (Figure 187-4).⁶