In utero transmission ofHSV-l or HSV-2 is rare and is part of the TORCH (roxoplasmosis, Qther, rubella, �ytomegalovi rus, herpes virus) collection of infections. Intrauterine HSV infection classically leads to disease involving the skin (blisters, scarring), the central nervous system (hydranencephaly, micro cephaly, intracranial calcification), or the eyes (chorioretini tis, microphthalmia) (Hutto, 1987). Bone and viscera can be involved (Marquez, 2011). If seen sonographically, indings should prompt viral serological testing as described next. PCR analysis of an amniocentesis sample is another potential tool (Diguet, 2006).
Several organizations recommend against routine serological HSV screening in asymptomatic gravidas (American College of Obstetricians and Gynecologists, 20 16b; Workowski, 2015;
U.S. Preventive Services Task Force, 2016). However, for those with a clinically suspicious lesion, a diagnosis should be conirmed by laboratory testing. Available HSV tests are either virological or type-speciic serological tests.
Direct virological tests are can be performed on a specimen from the mucocutaneous lesion. PCR or culture of the sample is a testing option. Of the two, PCR assays are more sensitive, the results generally are available in 1 to 2 days, and specimen handling is easier. In contrast, for viral culture, the sensitivity of HSV isolation is relatively low as vesicular lesions ulcerate and then crust. Also, results sometimes are not available for 7 to 14 days (Strick, 2006). Regardless of the test performed, HSV viral types should be diferentiated (LeGof, 2014). Importantly, a negative culture or PCR result does not exclude infection. In contrast, false-positive results are rare.
Serological assays are available to detect antibodies produced against speciic HSV glycoproteins, Glrand G2. These proteins evoke type-speciic antibody responses to HSV-l and HSV-2 infection, respectively, and they reliably diferentiate the two. IgG antibodies develop 1 to 2 weeks after a primary infection and then persist. This permits conirmation of clinical infection and identiication of asymptomatic carriers. Providers should request type-speciic glycoprotein G-based assays when serology is being performed. Sensitivity approaches 90 to 100 percent, and speciicity is 99 to 100 percent (Wald, 2002). IgM antibody detection is not a useful test.
In nonpregnant patients, antiviral therapy with acyclovir, vala cyclovir, or famciclovir is used to treat irst-episode genital herpes. Oral or parenteral preparations attenuate clinical infec tion and viral shedding duration. Suppressive therapy is also an option to limit recurrent infections and to reduce heterosexual transmission (Corey, 2004).
In pregnant women, acyclovir is safe (Briggs, 2015).
Through 1999, the manufacturers of acyclovir and valacyclovir maintained a registry of outcomes following exposure to these drugs during pregnancy. More than 700 neonates exposed dur ing the irst trimester were evaluated, and there were no adverse efects attributable to acyclovir (Stone, 2004). At this time, data are insuicient regarding famciclovir exposure, although a pregnancy registry is being maintained (1-888-669-6682).
For a primary outbreak during pregnancy, women may be given antiviral therapy to attenuate and decrease the duration of symptoms and viral shedding (Table 65-4). Women with
HIV co-infection may require a longer duration of treatment.