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This acronym stands for several etiologic agents of congenital infections:
T oxoplasmosis
O ther (varicella-zoster virus [VZV], parvovirus B19, Zika virus)
R ubella
C ytomegalovirus (causes most morbidity and mortality)
H erpes simplex virus, H uman immunodeficiency virus (HIV)
E nteroviruses, E pstein-Barr virus
S yphilis
Boyer S, Boyer K. Update on TORCH infections in the newborn infant. Newborn Infant Nurs Rev. 2004;4:70–80.
HSV infection usually presents as grouped vesicles on an erythematous base. These lesions may be present on any part of the skin but are more common on the face, scalp, or buttocks ( Fig. 56.1 ). They may also be generalized or disseminated or occur in the perianal region in a breech-delivered baby. They may also present as aplasia cutis congenita–like skin findings with atrophic areas and scarring.
Corey L, Wald A. Maternal and neonatal herpes simplex virus infections. N Engl J Med. 2009;361:1376–1385.
Yes. Neonatal herpetic infections are usually severe (especially if lesions are disseminated or the central nervous system [CNS] is involved) and require immediate diagnosis and treatment. The majority of infants with HSV infection acquire it in the perinatal period following contact with infectious genital mucous membrane secretions or herpetic lesions. Even with adequate treatment, the mortality rate approaches 50% in infants with disseminated disease or CNS disease, and the incidence of long-term morbidity is significant.
About 70% of infected infants display lesions shortly after birth, with disseminated disease occurring during the first 2 weeks of life. This includes infants with skin, eye, or mouth disease (40% of all neonatal HSV infections), as well as those with disseminated disease (25%) that includes the skin, of which 77% will manifest with skin lesions. If intrauterine exposure has occurred, lesions are usually present at birth. Fortunately, intrauterine transmission of HSV occurs in fewer than 5% of cases.
Jacobs RF. Neonatal herpes simplex virus infections. Semin Perinatol. 1998;22:64–71.
The majority of neonatal infections are due to perinatally acquired HSV-2 infection.
A Tzanck smear (scraping the base of a vesicle followed by staining the material with the Wright stain) can determine the presence or absence of multinucleated giant cells indicative of herpesvirus infections; however, it is unable to distinguish between VZV and HSV (see Fig. 3.5 ). Viral culture is the most accurate means of diagnosis but can take several days to be processed. HSV polymerase chain reaction (PCR) is both accurate and rapid, with results reported in 12–24 hours, and has become the gold standard in diagnosis. PCR of cerebrospinal fluid is the test of choice to rule in or out CNS involvement, but a Western blot remains the gold standard for serologic assays identifying HSV antibodies and is 99% sensitive and specific.
Strick LB, Wald A. Diagnostics for herpes simplex virus: is PCR the new gold standard? Mol Diagn Ther. 2006;10:17–28.
While the risk of vertical transmission is relatively low, 2%, intrauterine infection with VZV occurring between weeks 8 and 20 may result in congenital varicella syndrome. These infants are born with chorioretinitis, hypoplasia of limbs, and/or paresis of the extremities. Cutaneous findings appear scar-like and occur in a dermatomal distribution with underlying tissue atrophy. Maternal herpes zoster during pregnancy does not carry a risk to the fetus.
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