I totally understand the concern - but before you run for the Valtrex check out the link below:http://www.emedicine.com/med/topic3554.htm
Towards the bottom you will find a great chart that shows that suppression therapy will reduce, but not eliminate viral shredding. It also states that Valtrex accumulates in the amniotic fluid and the baby's blood. It should also be noted that in all the studies this paper looked at (women with Herpes) 799 births, not a one passed Herpes onto her child. Just food for thought.
Before I started reading I too was all for doing supression the last month, "just in case" - I have since rethought that position.
Drug info and Study excerpts
Teratogenic Effects: Pregnancy Category B. Valacyclovir was not teratogenic in rats or rabbits at 10 and 7 times human plasma levels, respectively, during the period of major organogenesis.
There are no adequate and well-controlled studies of VALTREX or ZOVIRAX in pregnant women. A prospective epidemiologic registry of acyclovir use during pregnancy was established in 1984 and completed in April 1999. There were 749 pregnancies followed in women exposed to systemic acyclovir during the first trimester of pregnancy resulting in 756 outcomes. The occurrence rate of birth defects approximates that found in the general population. However, the small size of the registry is insufficient to evaluate the risk for less common defects or to permit reliable or definitive conclusions regarding the safety of acyclovir in pregnant women and their developing fetuses. VALTREX should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Acyclovir was not found to be teratogenic in pregnant mice, rats, and rabbits at doses resulting in systemic exposures similar to those achieved in humans with therapeutic dosing. Dosing in mid-rat gestation, however, did result in skull, eye, and tail defects. Acyclovir readily crosses the human placenta to the fetus. Numerous reports involving well over a thousand cases (the majority in the manufacturer's pregnancy registry) have described the use of acyclovir during all stages of gestation. As expected, birth defects have been reported in exposed pregnancies, but none of these have been attributed to acyclovir. The primary uses of acyclovir during pregnancy have been for the treatment of primary infections of genital herpes simplex virus (HSV) type 2 or for life threatening disseminated HSV infections. In both of these infections, the benefits of acyclovir for the mother and fetus far outweigh any known risk. Prophylactic use of acyclovir to prevent recurrent genital HSV infection, however, is controversial because a clear benefit has not been established. Acyclovir is concentrated in human breast milk, reaching levels exceeding those found in maternal serum. No adverse affects from acyclovir in milk have been reported in nursing infants or in neonates given the drug directly. The AAP classifies acyclovir as compatible with breast-feeding.
Valacyclovir therapy to reduce recurrent genital herpes in pregnant women.
Andrews WW, Kimberlin DF, Whitley R, Cliver S, Ramsey PS, Deeter R.
Department of Obstetrics and Gynecology, Center for Research in Women's Health, University of Alabama, **********, AL, USA.
OBJECTIVE: The purpose of this study was to estimate the efficacy of valacyclovir suppressive therapy in pregnant women with recurrent genital herpes. STUDY DESIGN: At 36 weeks' gestation, herpes simplex virus (HSV)-2 seropositive women were randomized to receive oral valacyclovir 500 mg or placebo twice daily until delivery. Genital tract and neonatal specimens were collected weekly for HSV culture and qualitative polymerase chain reaction (PCR) assay to detect viral DNA from the time of randomization to delivery. Both maternal and neonatal toxicity measures were obtained. RESULTS: The 112 enrolled women (57 valacyclovir, 55 placebo) had similar HSV recurrence risks, including mean number of active HSV recurrences before randomization during the index pregnancy (1.1 +/- 1.9 vs 1.5 +/- 2.1, P = .308) and days between randomization and delivery (20.3 +/- 10.2 vs 22.0 +/- 8.9, P = .344). The number of women with clinical HSV recurrences between the time of randomization and delivery was significantly lower in the valacyclovir versus placebo group (10.5% vs 27.3%; P = .023, RR 0.4, 95% CI 0.2-0.9). Shedding of HSV within 7 days of delivery was similar in the valacyclovir and placebo group (10.4% vs 12.0%, P = .804; RR 0.9, 95% CI 0.3-2.7), as was the number of women with clinical HSV lesions at delivery (5.3% vs 14.6%, P = .121; RR 0.4, 95% CI 0.1-1.3). No neonates had symptomatic congenital HSV infection before discharge or up to 2 weeks' postpartum, and no clinical or laboratory safety concerns were identified. CONCLUSION: Administration of valacyclovir beginning at 36 weeks' gestation to women with a history of recurrent genital HSV reduced the number of women with subsequent clinical HSV recurrences.