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EPIDEMIOLOGYThe diseases caused by herpesviruses are endemic, and transmission usually requires intimate contact with mucosal surfaces or abraded skin.3 Approximately 90% of primary and recurrent genital herpes infection is caused by HSV-2 and the remaining 10% by HSV-1. Malik P, Tabarraei A, Kehlenbach RH, Korfali N, Iwasawa R, Graham SV, Schirmer EC.J Biol Chem. Herpesviruses block host cell transport into the nucleus through herpes-encoded ICP27 binding to nuclear pore complex protein Nup62.
Herpes simplex is caused by the herpes simplex virus (HSV), also known as herpesvirus hominis. Reactivation and replication of latent HSV occurs in the area supplied by the ganglia in which latency was established.
HSV has many different presentations, as described below, the severity of which depends on the age, the immune status of the individual, and whether it is a primary or recurrent infection - primary HSV infections are accompanied by systemic signs, longer duration of symptoms, and higher rate of complications. The clinical presentation of a cold sore is that of grouped vesicles, especially of the lips and perioral skin.
In women, ulcers can affect the external genitalia, as well as the vagina and cervix, which is involved in 70%-90% of cases. Recurrent genital herpes simplex is very common, with up to 95% of patients with HSV-2 suffering one or more further episodes.
Those at risk are immunocompromised patients, and neonates not protected by maternally acquired antibodies. Systemic infection, such as hepatitis and encephalitis may develop with or without widespread cutaneous lesions.
EM is a hypersensitivity reaction usually triggered by infections, most commonly herpes simplex. The prevalence of genital herpes depends on the population studied, the technique used for viral identification, and whether the diagnosis is made on the basis of clinical or serologic evidence.4 There is a discrepancy in the estimated prevalence of genital herpes that depends upon whether infection is defined by the prevalence of antibody or by a history of a clinical genital infection. Once the nucleocapsid is within the cytoplasm of the cell, the virus is uncoated, and the viral genome is released and delivered to the nucleus. Considerably more persons have antibody to HSV-2 than have a history of clinical infection, indicating that the majority of persons with antibody to the genital HSV-2 serotype have always had asymptomatic primary and asymptomatic recurrent infection.7, 8, 9HSV usually is transmitted sexually. Viral genes are transcribed by cell polymerases in the nucleus and then exported to the cytoplasm, where HSV protein synthesis occurs.
During an active infection, herpesviruses ultimately kill the cells in which they replicate.3During the initial active infection, herpesvirus travels inside the axon of the nerve cell bodies to the sensory and autonomic ganglia of that nerve region. The virus then migrates back to the skin by the peripheral sensory nerve branches of that sensory ganglion. During latency, viral replication ceases, normal cell activity takes place, and the virus exists within the host cell without killing it. Prevalence of herpes simplex virus (type 2) antibody in the United States in 1978, according to age, race, and sex.In contrast to HSV-2, HSV-1 infection starts to occur very early in life among young children who acquire HSV-1 gingivostomatitis. During reactivation, the virus travels down the sensory nerve to the dermatome served by the infected sensory ganglion and is shed from the skin or mucosa. Also in contrast to HSV-2, which is not consistently correlated with socioeconomic status, HSV-1 antibody prevalence varies substantially by socioeconomic groups. Seroprevalence rates of HSV-1 increase dramatically from age 1 to 4 and peak by 15 to 20 years of age among female blacks. Rates of recurrent infection are highest after a severe and extensive primary infection and within the first several months after a primary infection.
Thus, by age 15, approximately 70% of black girls but only 25% of white girls have antibody to HSV-1.16, 17 Overall, antibody to HSV-1 is present in 75% to 90% of persons in lower socioeconomic groups by age 15 to 20, compared with only 30% to 40% of persons in middle to upper socioeconomic groups by age 25. Thus, both symptomatic and asymptomatic reactivation of HSV-2 infection is more frequent in the genital area than is HSV-1 infection. HSV-2 causes 70% to 75% of primary genital infection and up to 88% of recurrent genital HSV infection.5Herpesvirus is not eliminated by antiviral agents or by the host's defense mechanisms. Most sexual partners, however, do not report having had a typical episode of clinically recognizable HSV around the time of viral transmission.
The virus remains protected from antiviral therapy when in the latent phase within the ganglion cells.
Because latent virus probably does not replicate in the latent phase, it is not susceptible to antiviral drugs that affect viral DNA synthesis.
However, the differential diagnosis of a genital ulcer also includes syphilis and chancroid. The duration, severity, and frequency of recurrent episodes are reduced by antiviral treatment, but the virus is not killed. Primary first-episode genital herpes is characterized by a negative clinical history for prior genital HSV infection in a patient with no preexisting antibodies to either HSV-1 or HSV-2.
Nonprimary first-episode genital herpes is characterized by the first-time acquisition of genital HSV-2 infection in a patient with preexisting antibodies to HSV-1.
Patients with primary genital HSV-1 or HSV-2 have a similar frequency of systemic symptoms, genital symptoms, and duration of lesions.22 During a primary infection, HSV-2 cannot be distinguished from HSV-1 on clinical findings.
The incubation period of HSV extends from 2 to 20 days, but symptoms usually develop 3 to 7 days after exposure (Fig. Symptomatic primary infection is characterized by prodromal symptoms of a feeling of tingling or itching in the genital area followed by painful multiple bilateral labial lesions, vaginal discharge, external dysuria, sacral paresthesia, and tender inguinal lymph node enlargement. Local symptoms increase during the first 6 to 7 days, when the skin lesions are in the vesicular stage (see Fig. Ulcers of the skin continue to develop in approximately 75% of patients for up to 10 days.22 Cervical lesions occur in approximately 90% of patients with primary genital herpes. In women with primary genital herpes, the mean duration of viral shedding from the cervix is similar to that from lesions of the vulvar skin.19 Lymphadenopathy appears in the second to third week of infection. Extragenital lesions of the hips, groin, and buttocks occur in approximately 20% of women from autoinoculation of the virus. Symptomatic pharyngitis can occur in association with primary genital herpes, and may be the presenting complaint in up to 20% of patients with either primary HSV-1 or HSV-2.25Lesions of a primary infection usually persist for 3 weeks (range, 2 to 6 weeks) and then heal completely. Dissemination of HSV can cause pneumonia, hepatitis, thrombocytopenia, or disseminated intravascular coagulation.
Physicians should be aware that pregnancy can predispose a patient to disseminated herpes infection.4, 22, 26Subclinical, first-episode genital HSV is common. Patients with nonprimary first-episode genital infection have fewer constitutional symptoms, fewer lesions, a shorter duration of pain, fewer newly developing lesions, a shorter duration of viral shedding, and a shorter duration of genital lesions than do persons with a true primary genital herpes infection.
In one study, more than 90% of patients with a primary genital HSV-2 infection had a reactivation within the first year (Fig.
Approximately 40% of patients have six or more recurrent episodes in the first year after a primary infection.Fig. The frequency and severity of recurrence vary considerably among patients and even within a single patient. Compared with primary infections, however, most recurrent infections are accompanied by fewer lesions, less pain, and a reduced duration of pain and viral shedding. Constitutional symptoms are infrequent, occurring in only 12% of women with a recurrence.22 As with the initial genital infection, symptoms of recurrent genital herpes tend to be more severe in women than in men.
HSV transmission to sexual partners or neonates can occur as a result of asymptomatic shedding.The salient differences among primary HSV-2, nonprimary first-episode HSV-2, and recurrent HSV infection among nonpregnant women are compared in Table 1. These differences help explain marked differences in rate of HSV transmission to the neonate during pregnancy.
Transmission to the neonate occurs mainly from direct contact with genital HSV during labor and at birth.
The likelihood of transmission to the neonate increases when there is a large concentration of virus and when there is no serum antibody from the mother. Because the fetus is in contact with the cervix much longer than with the vulva, virus from cervical lesions is especially likely to be transmitted to the neonate as opposed to virus from vulvar lesions. Systemic symptoms, often indicative of a viremia, are for the most part limited to primary infection. As can be seen in Table 1, the duration of pain, number of lesions, and surface area of the lesions progressively decrease in primary versus nonprimary first-episode versus recurrent HSV infection.
Patients with primary first-episode HSV infection compared with those with recurrent disease have higher fetal transmission rates in part because of a 3-fold higher number of lesions (more virus), a 10-fold increase in mean surface area of lesions (more virus), a 4-fold increased duration of viral shedding from both genital and cervical lesions (longer time the virus is present), and a 7-fold increased rate of cervical shedding (a critical area for fetal exposure).22TABLE 1.
Ann Intern Med 98:958, 1983)HERPES SIMPLEX VIRUS IN PREGNANCYNeonatal HSV infection is the most feared consequence of genital HSV infection because it carries a high rate of mortality and morbidity.
The increased prevalence of adult HSV between the 1960s and the 1980s was associated with a parallel increase in the prevalence of neonatal HSV in the United States.4, 30, 31 Annually, 1500 to 2000 cases of neonatal HSV occur in the United States. Only 2% to 5% of pregnant women are aware of a previous episode of genital herpes; however, characteristic of the asymptomatic nature of both first-episode and particularly recurrent infection, most persons carrying the virus do not recognize having had an episode of HSV infection.
Only about 1 in 1000 women have HSV in the genital tract at delivery from a primary HSV infection. NeonatalHSV infection, however, occurred in 6 (33%) of the 18 infants exposed to first-episode genital herpes versus only 1 (3%) of the 34 infants exposed to recurrent genital herpes (Fig.
N Engl J Med 324:1247, 1991)The high rate of neonatal infection during a primary maternal infection is related to an increase in the concentration of virus, a larger surface area of lesions, and a high degree of cervical shedding during primary versus recurrent genital infection, as previously mentioned (see Table 1).


A high rate of neonatal infection with exposure to primary HSV also is related to the lack of a protective effect from HSV serum antibody. HSV antibodies neutralize the virus, mediate cytotoxicity, and produce type-specific inhibition. Adverse pregnancy outcomes occurred in 6 of 15 neonates born of mothers with primary firstepisode infections.
One of five first-trimester infections resulted in spontaneous abortion because of herpetic chorioamnionitis, one of five secondtrimester infections resulted in preterm delivery, and four of five third-trimester infections were associated with preterm delivery, growth retardation, and neonatal herpes. No abnormalities were noted in the 14 neonates born of mothers with nonprimary first-episode infection.36The majority of neonatal infections will not only result from primary infection at or shortly before delivery,34 but the majority of women with a primary infection will be asymptomatic at delivery.
These asymptomatic women with a primary infection at delivery may have had a recent asymptomatic primary or, occasionally, a very recent primary infection where symptoms develop only after delivery.
In the study by Brown and associates,27 of 29 women who presented with first-episode genital HSV-2, 15 had a primary infection and 14 had a nonprimary first-episode infection.
All six infected infants were born of mothers with a primary first-episode infection in which asymptomatic shedding of HSV-2 at delivery accounted for nearly all the cases of neonatal infections.
In a second study by Prober and co-workers,38 none of 34 neonates born to mothers with a history of recurrent genital HSV-2 acquired neonatal herpes. In 31 cases of neonatal herpes, 26% of mothers had a history of recurrent genital herpes, 29% had primary infections, 35% had antibody to HSV-2 but no clinical history of genital herpes, and in 10% of cases the mother was not the source of the infection.18, 34, 36As many as 80% of women with a history of recurrent infection have a recurrence of HSV during pregnancy. Asymptomatic shedding at delivery cannot be predicted on the basis of prior antenatal culture data. Only 1 of 17 women with asymptomatic shedding during pregnancy had viral shedding at delivery, and that woman had a visible lesion.41 Five other women had asymptomatic shedding of HSV at delivery but were culture-negative during the pregnancy.
A word of caution is in order for patients with a recent primary infection because they are more likely to shed HSV asymptomatically than are those who had HSV before becoming pregnant.
The attack rate of neonatal HSV is estimated to be 50% when exposure to virus in a primary HSV lesion occurs. In contrast to primary HSV, the odds of HSV transmission to the neonate after exposure to a recurrent lesions is about 100-fold less. Only approximately 20% of cultures from recurrent lesions contain HSV, and with the attack rate estimated to be 2%, approximately 1 in 250 of neonates exposed to a recurrent HSV lesion would develop neonatal HSV. Approximately 2.5% of patients with HSV lesions remote from the genital area shed HSV from the genital area.
If 5% is used as a high end of the range of attack rate for recurrent HSV, about 1 in 800 neonates exposed to a remote HSV lesion would develop HSV. Asymptomatic shedding of the virus at delivery occurs in approximately 1% of women with recurrent HSV.
The attack rate of neonatal herpes is not known, but the attack rate of neonatal herpes is probably even lower in the setting of asymptomatic shedding than with a recurrent HSV lesion. Neonates with congenital infection also may have elevated levels of immunoglobulin M (IgM) in the cord blood as well as viremia. Congenital infection is unusual, but it was reported to have occurred in 9 (5%) of 192 neonatal infections.44Symptomatic first-episode HSV infection also has been associated with preterm birth, although the number of cases reported has been too small to permit an accurate assignment of the risk. Signs of disseminated HSV in the mother should be treated with intravenous acyclovir to reduce the severity of maternal disease.Management of Recurrent Herpes Simplex Virus in PregnancyPregnant women with recurrent HSV often have periodic outbreaks of genital HSV, and their outbreaks may even become slightly closer together in late pregnancy, but there is a limited chance of an HSV outbreak at the time of labor. Cesarean section for delivery is indicated only for an active HSV lesion, but only about 1 in 500 women in labor have HSV in the genital tract from a recurrent HSV lesion.28 Cesarean section is unnecessary for the patient with prior recurrent HSV who has no prodromal symptoms and no lesions at the onset of labor or with rupture of membranes because the rate of neonatal infection is so small (see Table 2).
All women with a known history of prior HSV infection require a detailed physical evaluation during labor or upon rupture of membranes to establish whether or not HSV lesions are present. It has been recommended that HSV cultures be obtained from women with a history of prior HSV, even in the absence of lesions.42 The quality of these screening cultures for HSV in the absence of lesions has not been established and do not represent the standard of care. A single Dacron applicator can be used to swab the cervix, the vulva, and the genital area usually involved in recurrent lesions. A positive culture identifies neonates potentially exposed to HSV, but there is a 48-hour waiting period for culture results.
It is not known whether prophylactic treatment of asymptomatic infants exposed to HSV is of benefit. These infants do benefit, however, from very close evaluation for early symptoms of neonatal HSV. Some physicians also perform surface and oropharynx cultures of the neonate.42 Serial cultures of high-risk infants after birth, including infants born of mothers with an HSV-positive culture taken during labor, also are recommended by some pediatricians. An HSV-positive culture from the neonate 24 hours after delivery is considered evidence of neonatal infection, rather than contamination from secretions from the mother. These infants should be considered candidates for acyclovir treatment.Approximately 1 in 250 neonates exposed to an active recurrent HSV lesion will acquire HSV (see Table 2), and cesarean section is recommended for the few patients with recurrent HSV who have active genital lesions at the time of labor or rupture of membranes. Cesarean might also be considered if typical prodromal symptoms are present in patients with no genital lesions. Cesarean delivery within 4 to 6 hours of membrane rupture reduces the rate of HSV transmission to neonates of mothers with an active recurrent HSV lesion.37 Cesarean section does not prevent all cases of neonatal HSV, even when it is performed within 4 to 6 hours of membrane rupture or even before membrane rupture. In a recent survey, 15 (8%) of 184 infants with neonatal HSV were delivered by cesarean before membrane rupture.13 However, patients with active lesions generally are delivered by cesarean section, even after a prolonged period of membrane rupture, because cesarean delivery may slightly reduce HSV transmission to the neonate. If the cesarean section is performed 6 hours or more after membrane rupture, the mother and neonate should be cultured for HSV and counseled that neonatal infection could still occur.Management becomes problematic for the patient in labor with an active extragenital HSV lesion present some distance from the genital area.
Many experts recommend that a cesarean section be performed when extragenital lesions are present, and this recommendation appears prudent.42The management of women with active recurrent HSV and membrane rupture before term is particularly difficult. The physician must weigh the chance of a preterm infant developing an ascending HSV infection versus the chance of serious morbidity or death from respiratory distress syndrome. A summary of the management of patients with recurrent genital HSV is provided in Table 3.42TABLE 3.
Considerations for the Management of Pregnant Women with Recurrent Genital Herpes Sequential cultures during late gestation are not indicated unless they are done after clinically evident recurrent infection to document cessation of virus excretion.
Symptomatic recurrences of genital herpes during the third trimester will be brief; vaginal delivery is appropriate if no active lesions are present at delivery. Obtaining specimens for culture at delivery from women with a history of HSV infection may help in identifying exposed infants, but the clinical benefit of this procedure has not been established. Clin Infect Dis 15:1031, 1992)Management of Primary Herpes Simplex Virus Infections in PregnancyNeonatal exposure to a primary maternal HSV infection results in a 50% rate of neonatal HSV.
First-episode infection is associated with a large number of viral lesions, often comprising a large surface area, and a 90% chance of cervical HSV infection.
Cesarean section should be offered to all women with active first-episode HSV, even if it was a nonprimary first-episode infection. Transplacentally acquired heterologous antibodies to HSV-1 does little to influence the acquisition of HSV-2 by the neonate.28 Cesarean section should be done immediately in the patient has a membrane rupture.
Commercial serologic testing is discouraged because of inaccuracies in distinguishing between HSV-1 antibody and HSV-2 antibody.48, 49 Accurate differentiation of these antibodies has a potential advantage because many first-episode infections will be nonprimary ones, which are associated with less maternal morbidity and fewer complications of pregnancy than are primary infections. The patient with a primary infection should be advised of the limited data on spontaneous abortion, congenital infection, growth retardation, and preterm labor.
36, 41, 50 This high risk of viral shedding immediately after a primary infection means that HSV may still be present in the cervix or genital area if the patient goes into labor within 2 months of a primary HSV infection. Patients with primary genital HSV late in pregnancy should be followed with weekly cervical or vaginal cultures, or both. If viral shedding stops by the time of delivery and no lesions are present, vaginal delivery can be undertaken with the precautions in place for recurrent HSV, including careful examination for lesions and cultures of patients without lesions. A cesarean section should be performed, however, for the patient in labor with a recent primary HSV infection if viral shedding continues until delivery or if lesions are present. Sexual contact obviously should not occur when the sexual partner has an active HSV lesion or prodromal symptoms where the risk of infection increases further.
Condom use also should be considered for any sexual contact with a male partner with a known history of genital herpes to protect the pregnant woman from acquiring HSV during asymptomatic shedding by the male partner. There is a small but definite rate of primary HSV during pregnancy transmitted even by stable asymptomatic partners.
In a study of private obstetric patients, 32% of women and 25% of their husbands had antibody to HSV-2.
Of the 190 couples, 73% were serologically concordant; of these couples, 57% were both antibody negative and 16% were both antibody positive. Rate of condom use by the asymptomatic male with no known history of prior HSV would be very low.
Thus, prevention of much of HSV infection becomes problematic short of abstinence.Postnatal infection appears to account for approximately 10% of neonatal HSV.
The higher rate of HSV-1 isolation from neonatal infection (30%) than from genital infection (10% to 25%), is suspected to be related to postnatal transmission from adults with active oral HSV-1. Parents, other relatives, friends, and hospital personnel with active oral labial HSV should avoid direct contact with newborns when they have active lesions, and they should wash their hands with soap to reduce the chance of HSV transmission to the newborn from free virus contaminating the hands. Because postnatal HSV infection is preventable, all attempts should be made to reduce exposure by advising unsuspecting adults about the contagious nature of active oral lesions.Neonatal Morbidity and MortalityNeonatal HSV is one of the most life-threatening of all infections in newborns.
High death rates (60% to 80%) occur with disseminated infection, moderate rates (20% to 30%) with local central nervous system infection, and low rates (15%) with HSV localized to the skin or eye.


Death rates are increased with concomitant prematurity, reduced level of consciousness, and disseminated intravascular coagulopathy.32 Permanent neurologic sequelae are common among survivors of neonatal HSV, but sequelae vary with the invasiveness of infection. The neurologic impairment in survivors is 63% after disseminated disease, 41% after localized central nervous system infection, and 6% after localized skin infections.32Fig.
The parents should be advised of symptoms and signs of lethargy, poor feeding, or lesions (Table 4). If exposure occurred to a primary maternal infection, where the risk of neonatal infection is high, it is advised that viral cultures be taken of the eyes, throat, urine, stool, and cerebrospinal fluid.42 Some physicians culture the infant's eyes, nose, mouth, and skin weekly thereafter for 4 to 6 weeks (see Table 4). Therapy using acyclovir is recommended if any HSV culture is positive 48 hours after delivery or the cerebrospinal fluid is abnormal.42 Acyclovir can be given prophylactically to an inadvertently exposed infant, but acyclovir appears to have limited ability to prevent all of the manifestations of neonatal infection. The infrequency of transplacental passage of HSV and the problems of diagnosis of congenital HSV make identification and management of possible congenital HSV experimental.TABLE 4.
Clin Infect Dis 15:1031, 1992)DIAGNOSISViral cultures provide the most sensitive and specific method to diagnose HSV. HSV-1 and HSV-2 can be distinguished by culture techniques.52 To establish the diagnosis of HSV with certainty in pregnancy, cultures should be performed on persons with typical lesions and no prior history of herpes and on patients with atypical lesions.
Cultures are not necessary during pregnancy for patients with atypical lesions and a prior history of herpes.Vesicles are the lesions most likely to contain virus.
For the asymptomatic patient in labor with a history of recurrent HSV, one swab should be used to culture the cervix, and the same swab should be used to swab vigorously the usual site of recurrence as well as the labia minora. The single swab is then placed in transport media.The most sensitive rapid test uses monoclonal antibody to HSV. For vesicular and ulcerated lesions, the direct monoclonal antibody test for HSV is 65% to 90% more sensitive compared with the culture technique. Tsank and Papanicolaou smears are only approximately 50% sensitive compared with the culture, and these older rapid tests should no longer be used. Most commercially available serologic tests consist of enzyme-linked immunosorbent assays or latex agglutination, which cannot distinguish between HSV-1 and HSV-2 antibodies.
These assays have been used by researchers to distinguish primary from nonprimary first-episode infections and to study the effect of maternal antibody on neonatal outcome.TREATMENTAcyclovir is the drug recommend for genital HSV. Acyclovir is activated by specific viral thymidine kinase, and activated acyclovir inhibits HSV-specific DNA polymerase. Inhibition occurs at lower concentrations than is required to inhibit the patient's cellular DNA. Another theoretic but unknown concern of acyclovir use is a blunting of the maternal antibody response, which could reduce the protective effect of antibody for the neonate.Intravenous acyclovir, however, should be given to women with disseminated HSV to reduce morbidity. Acyclovir also could be considered in an attempt to reduce viremia when pregnant women have severe systemic symptoms during a primary infection.
Systemic acyclovir promotes lesion healing, reduces viral shedding, and reduces new lesion formation.
Nonpregnant patients with six or more annual episodes of HSV are candidates for suppressive acyclovir therapy. Suppressive regimens of 400 mg, two to three times daily, and 200 mg three to five times daily cause a 70% to 90% reduction in the frequency of recurrent HSV. Suppressive acyclovir regimens have been used in research settings in an attempt to reduce recurrent HSV among pregnant patients with frequent recurrences,61 but this treatment is currently experimental.42VARICELLAVaricella-zoster virus (VZV) is a herpesvirus that causes varicella (chickenpox) and herpes zoster (shingles).
It most commonly occurs in children: 90% of VZV cases occur in persons less than 15 years of age. Infection develops after respiratory inhalation of or direct contact with varicella lesions.
VZV has an incubation period of 11 to 21 days (mean, 15 days), which is followed by a transient asymptomatic primary viremia.62 During the primary viremia, VZV spreads from the lymph nodes to internal organs. After replication in these organs, a secondary viremia occurs, and by day 14, virus in the skin produces an exanthem.63 Fever, malaise, intensely pruritic vesicles, and a rash then develop. The rate of varicella complications for adults is 9- to 25-fold higher than that for children. Although only 2% of varicella cases occur among adults older than age 20, adults constitute one quarter of all VZV-related deaths.
Smokers are particularly susceptible to pneumonia secondary to varicella.65Virus-specific IgM antibodies develop in the first 5 days of infection and peak between 2 and 3 weeks. Approximately 95% of American women66 and 84% of women from the subtropics have antibody to varicella; subclinical infection is rare.
Varicella pneumonia in pregnancy requires blood gases, supportive therapy, respiratory support in some cases, and intravenous acyclovir.
Early administration of acyclovir reduces the mortality from VZV pneumonia in adults from 7% to 0%,72 and acyclovir given to pregnant women reduces the mortality from 40% to 14%.71Varicella also can cause serious infection and death in term neonates who acquire varicella in utero and are born before they have had a chance to receive antibody passively from the mother. Term infants are susceptible to varicella when the mother develops a rash 4 days before delivery to 2 days after delivery. Infants born to mothers who develop a rash 3 or more days after delivery have not been exposed to the in utero maternal viremia.Spontaneous abortion68, 76 and preterm delivery68, 69 secondary to VZV appear to be uncommon. It is unusual for varicella in the first 20 weeks of pregnancy to cause stigmata of intrauterine infection. In fact, the frequency of stigmata from congenital varicella is too small for reliable estimates. The abnormalities associated with congenital VZV infection include skin lesions (vesicles and cicatricial lesions), hypoplastic limbs from viral infection of the ganglion nerve supply to these muscles, hydrocephalus, chorioretinitis, and optic atrophy.After primary varicella infection, VZV enters the dorsal root ganglia to produce latent infection.
Reactivation of the virus produces herpes zoster, which is characterized by a unilateral painful vesicular rash in the skin innervated by that dorsal root. The cervical, thoracic, and lumbar areas are affected most commonly, but facial nerve involvement with palsy can occur. A fourfold rise in IgG titer can be documented in two sera specimens drawn 7 to 10 days apart. VZIG is expensive and in limited supply, so before deciding to administer VZIG, it should be determined whether the patient is likely to be susceptible, whether exposure is likely to result in infection, and whether an increased rate of complication is to be expected.A history of chickenpox is reliable, and patients with such a history should be considered immune.
Even without having a known history of chickenpox, most adults older than age 15 (85% to 95%) are immune. Thus, a history or age is usually sufficient to establish immunity, but serologic testing can be used in unusual circumstances.Neonatal varicella infection is likely to occur after exposure to household contacts, playmates, or hospital contact75 as well as to the mother during the contagious period. Candidates for VZIG include newborns of mothers who acquired varicella 5 days before to 2 days after delivery, premature infants less than 28-weeks' gestation with postnatal exposure regardless of maternal history (who may not yet have had antibody passed from the mother), pregnant women, and given the high complication rate, perhaps all susceptible adults.VZIG reduces the rate of clinical infection and the severity of complications when infection ensues. It should be given to pregnant women to prevent maternal complications, rather than to prevent congenital infection, because it is not known whether VZIG effectively prevents neonatal infection.75 Newborns born to mothers in whom varicella developed within 5 days of delivery should receive VZIG, even if VZIG was administered to the mother.
VZIG should be given within 48 to 72 hours of exposure; it may not be effective when given after 96 hours from exposure. It is spread by the inhalation of droplets from respiratory secretions or from direct contact. Rubella enters the respiratory tract and disseminates to regional lymph nodes, where it replicates.
Viremia occurs 7 to 9 days after exposure; it is during the viremia stage that the placenta can become infected. The infection is most contagious when the rash is erupting, but nasopharyngeal viral shedding continues to occur for 2 weeks.
The rash is preceded by malaise, fever, headache, conjunctivitis, and postauricular and posterior cervical lymphadenopathy.
The rash typically appears on the face and trunk and moves peripherally to the extremities within a 1- to 2-day period.
One quarter to one half of all rubella infections are subclinical, and the rash can mimic other viral syndromes.The rash appears as immunity develops and the virus disappears from the bloodstream, suggesting an immune-mediated mechanism.
The most important determinant of the severity of rubella infection is the age at which it is acquired. Infections in children and adults are usually mild or subclinical, and only rarely do complications such as arthritis, encephalitis, hepatitis, or hemorrhagic complications occur in these persons.
Arthralgias occur in 25% of vaccine recipients, but frank arthritis in only 1%.87 Immunosuppressed and pregnant patients should not be vaccinated against rubella.
The live virus in the vaccine can cross the placenta and potentially infect the fetus if administered to a pregnant woman; however, congenital rubella has not occurred after vaccination for rubella to date. Defects consistent with congenital rubella were not found in more than 700 women vaccinated in the 3 months before and after conception, although 9 of 143 term infants born to vaccinated mothers had serologic evidence of rubella infection.87 Of 307 maternal exposures to rubella vaccine either before conception or during the first trimester, there were no cases of illness or defects consistent with congenital rubella.
In the United States during the last rubella epidemic (1964 to 1965), more than 11,000 cases of fetal death resulted from either miscarriage or therapeutic abortion, and approximately 20,000 infants were born with congenital rubella syndrome (CRS).91 Of those with CRS, 2100 died as neonates, and nearly 12,000 infants were born deaf. Of adult survivors of CRS, 40% have been noted to have insulin-dependent diabetes mellitus.93The effects of rubella infection on the fetus vary with maternal age and parity as well as the gestational age at the time of infection. The incidence of CRS increases as maternal age and parity increase.Sorry, this link is malformed.



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