Neonatal herpes is uncommon in the United Kingdom, in contrast to the USA and a few other European countries. Active surveillance by the BPSU (British Paediatric Surveillance Unit) discovered seventy-six cases over the 5.5 year surveillance period (between 1986 and 1991) with a frequency of 1.65/100 000 live births per year (95% CI 1.3 to 2.0).
Subsequent surveillance (from 2004 to 2006) demonstrated an approximate two-fold number of incidence with eighty-six cases witnessed over the 3-year surveillance period. This rise could reflect the increase in the occurrence of STDs, social and demographic changes within the population as well as enhancements in diagnostic methods. More of the published occurrence data are expected.
Subsequent surveillance (from 2004 to 2006) demonstrated an approximate twofold number of incidence with eighty-six cases witnessed over the 3-year surveillance period. This rise could reflect the increase in the occurrence of STDs, social and demographic changes within the population as well as enhancements in diagnostic methods. Further published occurrence data are expected.
The incidence in the United Kingdom is approximately 50% of that report from other countries in Europe. In the United States, the reported incidence averaged 1 in 15 000, but there are considerable disparities between populations, and rates of 1 in 7500 have been accounted in particular to disadvantaged inner-city populations.
Neonatal herpes could be a result of HSV-1 (herpes simplex virus type 1) or HSV-2 (herpes simplex virus type 2) as either viral type can result in genital herpes to the mother. Around half of neonatal herpes cases are because of HSV-1 and the other half as a result of HSV-2.
The majority of cases of neonatal herpes happen due to direct contact with the infected secretions of the mother, though, in 25% of herpes cases, a possible postnatal infection source was identified; typically the mother’s close relative. Postnatal infection could occur due to exposure to the oro-labial herpes infection.
Factors associated with the transmission take in the kind of maternal infection (recurrent or primary), the presence of transplacental maternal neutralizing antibodies, the rupturing of membranes before delivery, using fetal scalp electrodes, as well as the delivery mode. The risks are highest when a mother contracts a new infection (initial) in the last trimester, especially within six weeks of delivery, since viral shedding could persist and the infant could be born before the development of maternal antibodies.
Occasionally, congenital herpes could occur due to transplacental intrauterine infection. Case reports indicate that the CNS, eyes, and skin could be affected, and there could be fetal death or fetal growth restriction.
Disseminated herpes is a more common infection in preterm babies and happens almost exclusively due to primary herpes infection in mothers.
Although recurring genital herpes is linked with a low susceptibility to neonatal herpes, recurring herpes at the time of the delivery, which is commonly unrecognized or asymptomatic, could cause the localized types of neonatal herpes: both mouth, eye and skin infection and local CNS disease. Transplacentally-acquired HSV antibodies don’t prevent herpes virus from spreading to the neonate’s brain.
Data from the United States indicates that approximately 2% of women contract genital HSV infection during pregnancy and the majority of these infections are unrecognized or asymptomatic. On the other hand, acquisition of herpes during pregnancy could vary due to the different neonatal herpes rates between the USA and the UK. It could be hard to differentiate clinically between primary and recurrent genital HSV infections since many of the initial episode HSV infections aren’t considered as primary infections.