Refresh your knowledge on Herpes Complex (sorry typing error due to age) it will be H. simplex & not complex.Excuse me.!!
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  • Srimanta Pal Orolabial lesions are secondary to HSV-1, and genital lesions may be caused by either virus.Genital herpes simplex virus: Both HSV-1 and HSV-2 cause clinical maternal and neonatal disease. Most orolabial lesions are secondary to HSV-1, and genital lesions may be caused by either virus.The majority of neonatal herpes cases are born to women who have subclinical viral shedding at delivery and who often have no history of disease, making transmission prevention difficult. In utero infection occurs in approximately 5% of neonatal HSV cases. The risk of trans¬mission from asymptomatic shedding in a woman with recurrent HSV is much lower, approximately 1 in 10,000 deliveries. The duration of rupture of membranes, the use of fetal scalp electrodes and the mode of 
    Diagnosis:-The great majority of CMV infections in women are asymptomatic and can be identified only by prospective antibody testing. After primary CMV infection, virus replication may persist for many months and can be reac¬tivated months or years later, with intermittent CMV shedding from the cervix and other sites. The presence of IgM-specific CMV antibody cor¬relates quite well with infection. Immunoglobulin M antibody is detected with about 90% of primary infections; however, it may also appear with recurrent infections. CMV IgG avidity testing may be of value in assessing a patient's likelihood of recent infection too.
    Tr:-If a woman has primary infection with CMV, there is a 30% chance her child will be infected and thus, approximately a 6 to 7% chance her child will have some damage due to this infection. In about half of the cases the damage will be evident at birth. Therapeutic abortion can be consid¬ered. There can be a role for amniocentesis and amniotic fluid polymerase chain reaction (PCR) for CMV to assess for in utero infection. A negative test should rule out fetal infection; however, a positive test would not necessarily indicate that the fetus is damaged.
    Recent studies suggest that there may be role for anti-CMV-specific hyperimmune globulin as prophylaxis to reduce the risk of fetal infection after maternal infection and as treatment to prevent fetal sequelae after in utero infection. However, prospective randomized studies are needed in larger groups of infected women to examine the efficacy and safety of this therapy, before this strategy can be recommended.Women who have antibody (IgG) to CMV before being pregnant can be assured that it is very unlikely that subsequent children will have sequelae due to congenital CMV infection.
    Genital herpes simplex virus
    Both HSV-1 and HSV-2 cause clinical maternal and neonatal disease. Most orolabial lesions are secondary to HSV-1, and genital lesions may be caused by either virus.
    The majority of neonatal herpes cases are born to women who have subclinical viral shedding at delivery and who often have no history of disease, making transmission prevention difficult. In utero infection occurs in approximately 5% of neonatal HSV cases. The risk of trans¬mission from asymptomatic shedding in a woman with recurrent HSV is much lower, approximately 1 in 10,000 deliveries. The duration of rupture of membranes, the use of fetal scalp electrodes and the mode of
    delivery also influence neonatal transmission. Two-thirds of neonatal HSV infection is due to HSV-2 and the remaining one-third to HSV-1 infection.
  • Srimanta Pal Diagnosis: How?? The diagnosis of HSV infection is often made clinically. Isolation of virus by cell culture is the most sensitive test widely available. PCR is highly sensitive but not as widely available. Antibodies begin to develop within 2 to 3 weeks of infection. Serological tests now available are based on antibodies formed to type-specific G-glycoproteins. These tests allow specific typing for HSV-1 and HSV-2 and are useful for counseling.
    Management
    Antepartum management
    Late pregnancy primary HSV has the highest likelihood for neonatal transmission. Counseling the woman who is HSV serology negative about safe sexual practices may lead to a decrease in acquisition of genital her¬pes in late pregnancy. Though some experts recommend screening, at this time universal screening of all pregnant women with type-specific serol¬ogy is not recommended.
    An active lesion in the antepartum period should be cultured to confirm the clinical diagnosis. If this is an initial episode, type-specific serology should be performed to determine if this is a primary or non-primary infection. Systemic antivirals may be used to attenuate signs and symptoms of HSV, especially if this is a primary infection. However, these will not eradicate latent virus.
    Antiviral suppression therapy in the latter part of pregnancy (36 weeks until delivery) has been shown to decrease the rate of clinical HSV recur¬rences at delivery and the rate of asymptomatic shedding at delivery.
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RPES SIMPLEX VIRUS (HSV) INFECTIONS DURING PREGNANCY
A. Background
1. Twenty five to 65 per cent of pregnant women in the U.S. have genital infection with herpes
simplex virus type I or 2 (HSV-1 or HSV-2).
2. Vertical transmission to the newborn is accompanied by devastating consequences (30-60%...
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RCOG.ORG.UK
www.rcog.org.uk
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  • Srimanta Pal Intrapartum management::-A woman with a history of HSV should be asked about prodromal symp-toms and recent HSV lesions. A careful vulvar, vaginal and cervical examination should be performed. Suspicious lesions should be cultured. Currently, cesarean delivery is indicated if the woman has an active lesion or prodromal symptoms. However, a cesarean delivery does not eliminate the risk. Ten to fifteen percent of infants with HSV are born to women who have had a cesarean delivery. If a lesion is present distant from the vulva, vagina or cervix, the risk of neonatal transmission is lower. The non-genital lesions may be covered with an occlusive dressing and a vaginal delivery allowed. Cesarean delivery should not be performed in a woman solely for a history of HSV.
    The management of the woman presenting with an active HSV lesion and ruptured membranes is controversial. At term, cesarean delivery should be offered regardless of how long the membranes have been ruptured. In the setting of preterm PROM, especially remote from term, expectant management should be considered; as the risk of prematurity complications may outweigh the benefit of immediate delivery