Viral infections in pregnancy: Herpes varicella zoster virus

Viral infections in pregnancy
Prepared by:
Ekram Abdullah Nasher

Common viral infections are:
Herpes varicella zoster
virus
Herpes simplex virus
Parvovirus Cytomegalovirus
Rubella virus
HIV

• is DNA virus
• Mode of transmission: by respiratory droplets and by direct contact with vesicle fluid or indirectly via fomites.
• The incubation period : 8-21 days (if receive VZIG become 8-28 days) , is infectious (48 hours before the rash
appears until the vesicles crust over(within 5 days).
• in the UK and Ireland >90% of the antenatal population are seropositive for VZV (IgG) antibody (so primary
infection complicate only 0.3% of pregnancies).
• tropical and subtropical areas women are more likely to be seronegative for VZV
 Herpes varicella zoster virus

 Maternal infection:
 Primary varicella:
• presents with a 1- to 2-day flulike symptoms, which is followed by pruritic vesicular lesions that crust after 3 to 7
days.
• Infection tends to be more severe in adults (mortality(75% of deaths occur in adults).
• There is excess morbidity associated with varicella infection in adults, including:
- Pneumonia(10% increase in later gestation, fatality rate less than 1% but five times higher in pregnancy)
- hepatitis
- encephalitis
• Mortality is predominately due to VZV pneumonia, which is thought to be more severe during adulthood and
particularly in pregnancy (smoking and having more than 100 cutaneous lesions as risk factors)
• Symptoms of VZV pneumonia usually appear 3 to 5 days into the course of illness. Fever, tachypnea, dry cough,
dyspnea, and pleuritic pain are characteristic
• resolution of pneumonitis parallels that of skin lesions but fever and compromised pulmonary function may persist
for weeks
• After primary infection by VZV , the virus remains dormant in sensory nerve root ganglia and when reactivated

 Maternal infection:
 herpes zoster or shingles:
• occur If primary varicella is reactivated years later and characterized by a unilateral dermatomal vesicular eruption
associated with severe pain. Zoster does not appear to be more frequent or severe in pregnant women. Congenital
varicella syndrome rarely develops in cases of maternal herpes zoster .
• Zoster is contagious if blisters are broken, although less so than with primary varicella herpes zoster in non-
exposed sites is considered to be noninfectious but in immunosuppressed patient is considered to be infectious.

 In the pregnant woman at her initial antenatal visit:
Seronegative Women are advised to avoid contact with chickenpox and shingles during pregnancy
and to immediately inform healthcare workers if exposed.
 In the pregnant woman who gives a history of contact with chickenpox or shingles:
A careful history to confirm:
• the significance of the contact( contact in the same room for >15 minutes, face-to-face contact and contact in the
setting of a large open ward).
• the susceptibility of the patient( determined by eliciting a past history of chickenpox or shingles and serological
testing.)
 If pregnant women tested are immune( 80–90%) can be reassured.
 If the pregnant woman is not immune and has had a significant exposure, she should have VZIG as soon as
possible(VZIG is effective when given up to 10 days after contact).
• If another exposure is occurred after 3 weeks from the last dose, a second dose of VZIG is required

 Fetal risks of varicella infection in pregnancy:
• No added risk for miscarriage if chickenpox occurs in the first trimester.
• A small risk 0.91% for fetal varicella syndrome If varicella occur < 28 weeks.
• FVS is characterized by one or more of the following:
1) dermatomal distribution of skin scarring
2) eye defects (microphthalmia, chorioretinitis, cataracts)
3)hypoplasia of the limbs
4) neurological abnormalities (microcephaly, cortical atrophy, dysfunction of bowel and bladder sphincters).
 Neonatal risks of varicella infection in pregnancy
• There is a significant risk of varicella of the newborn If infection occurs at term(1–4 weeks before delivery)
• Route of infection: transplacental, ascending vaginal or direct contact with lesions.
• Severe chickenpox occur if the infant is born within 7 days before or 7 days after the onset of the mother’s rash
because of low transplacentally acquired maternal antibodies.
• · Neonatal ophthalmic examination should be done after birth.
• · Neonatal blood should be sent for VZV IgM antibody after delivery and for VZV IgG after 7 months of age

 Maternal infection:
Maternal varicella is usually diagnosed clinically
Infection may be confirmed by NAAT of vesicular fluid, which is very sensitive(isolated by scraping the vesicle base
during primary infection and performing a Tzanck smear, tissue culture, or direct fluorescent antibody testing)
 infection of the fetus:
1) ultrasound examination:
Microcephaly , hydrocephalus, limb deformity soft-tissue calcification and FGR.
A detailed anatomical sonographic evaluation performed at least 5 weeks after maternal infection may disclose
abnormalities, but the sensitivity is low
2) Amniocentesis: is not routinely advised because the risk of FVS is so low, even when amniotic fluid is positive for
VZV DNA.
- The risk of FVS is low, If amniotic fluid is positive for VZV and ultrasound is normal at 17–21 weeks.
- The risk of FVS is remote, If repeat ultrasound is normal at 23–24 weeks.
- It is not known whether VZIG reduces the risk of FVS.
 Diagnosis:

 Management:
1) Contact their GP immediately.
2) avoid contact with susceptible individuals until the lesions have crusted over.
3) Symptomatic treatment and hygiene advised to prevent secondary bacterial infection.
4) oral acyclovir if they present within 24 hours of the onset of the rash and >20 weeks gestation:
 800 mg five times a day for 7 days.
 Women should be informed of about risk and benefits of treatment with acyclovir.
 there is no increase in the risk of fetal malformation with acyclovir in pregnancy.
5) Indication for immediate referral to a hospital:
 Chest symptoms,
 neurological symptoms,
 hemorrhagic rash or bleeding,
 dense rash
 immunosuppression or taking corticosteroids in the preceding 3 months.
 If the woman smokes cigarettes,
 has chronic lung disease,
 > 20 weeks gestation
6) Assessment and treatment in hospital with a multidisciplinary team: obstetrician or fetal medicine
specialist, virologist and neonatologist.

7) Timing and mode of delivery must be individualized.
• Delivery during the viraemia period should be deferred unless indicated.
• maternal risks are bleeding, thrombocytopenia, DIC and hepatitis.
• There is a high risk of varicella infection of the newborn with significant morbidity and mortality.
8) There is no evidence about the optimum method of anesthesia for caesarean section.
• General anesthesia may exacerbate varicella pneumonia.
• Risk of transmitting the varicella virus from skins lesions to the CNS via spinal anesthesia.
• epidural anesthesia is safer than spinal anesthesia
9) Women hospitalized with varicella should be nursed in isolation.
10) Referral to a fetal medicine at 16–20 weeks or 5 weeks after infection for discussion and detailed scan.
 Treatment following onset of maternal rash at term:
• If birth occurs within 7 days before or 7 days after the onset of the maternal rash (Neonate should receive VZIG)
• The infant should be monitored for signs of infection until 28 days after the onset of maternal rash .
• Neonatal infection should be treated with acyclovir following discussion with a neonatologist and virologist.
• VZIG is of no benefit once neonatal chickenpox developed.
• 50% of the neonates exposed to maternal varicella will develop chickenpox despite the administration of VZIG
but mortality rates is lower than 30%.
• Maternal shingles around the time of delivery is not a risk to the neonate because it is protected by
transplacentally acquired maternal antibodies.
 Management

 Varicella prevention
In the non-immune woman preconceptually:
• Determination of the immune status of women planning a pregnancy or receiving treatment for infertility by a past
history of chickenpox(sensitivity97–99%) and serological testing for VZIG antibody.
• vaccination pre pregnancy or postpartum for seronegative women(Two doses of Varivax are given 4 to 8 weeks
apart).
 live attenuated virus vaccine derived from the Oka strain of VZV.
 Vaccination reduce primary infection by 90% and the mortality by 66%.
 Immunity from the vaccine may persist for up to 20 years.
• Vaccinated woman should avoid pregnancy for 3 months and avoid contact with susceptible pregnant women if
post-vaccination rash occur

• Two viral types (HSV-1) and (HSV- 2) are DNA viruses.
• Genital tract infection is due to HSV-2. Infection may be primary or recurrent.
• HSV-1 infection is usually herpes simplex labialis (may also cause genital herpes).
• Neonatal herpes has a high morbidity and mortality commonly acquired at or near the time of delivery.
• Incidence in UK 1 in 60 000 live births annually, in the USA 1 in 15 000 .
• Around 2% of women acquire genital HSV infection in pregnancy, most are asymptomatic or
unrecognized.
 Herpes simplex virus

 Mode of transmission:
Almost all cases of neonatal herpes occur as a result of direct contact with infected maternal
 · Factors influencing transmission include:
• The type of maternal infection (primary or recurrent),
• The presence of Transplacentally acquired HSV antibodies,
• The duration of rupture of membranes before delivery (less or more than 4 hrs.).
• The use of fetal scalp electrodes.
• Mode of delivery.
The fetus becomes affected by virus shed from the cervix or lower genital tract during vaginal delivery
(Transplacental infection is not usual)
The baby may be affected in utero from the contaminated liquor following rupture of the membranes.
Breastfeeding is allowed provided the mother avoids any contact between her lesions, her hands and
the baby.

 Neonatal herpes Classified into three subgroups:
1) disease localized to skin, eye and/mouth: have the best prognosis, Death is unusual, with treatment
neurological morbidity is less than 2%.
2) local central nervous system (CNS) disease (encephalitis alone): present late (between 10 days and 4
weeks postnatally): with treatment mortality is 6% and neurological morbidity 70%.
3) disseminated infection with multiple organ involvement(more common in preterm infants):Have the
worst prognosis , with treatment mortality is 30% and neurological morbidity 17%.
• Disseminated disease and local CNS disease can present with or without localized disease.

 Herpes simplex virus
 Effect on pregnancy:
• - Increased risk of miscarriage is inconclusive.
• - If the primary infection is acquired in the last trimester there is chance of premature labor or IUGR..
• - Disseminated adult herpes: present with encephalitis, hepatitis, disseminated skin lesions or a
combination of these conditions , rare but more commonly reported in pregnancy, particularly in the
immunocompromised Maternal mortality is high.
• · Genital reactivation of HSV may increase the risk of perinatal transmission of both HIV and HSV
 · Recurrent herpes at the time of delivery:
• Has a very low risk of neonatal herpes
• commonly asymptomatic or unrecognized,
• may cause the three subgroups forms of neonatal herpes.

Diagnosis :
• is made by detection of the viral DNA by PCR(Specimens are collected from the base of the
ulcer and vesicular fluid and tested by culture or PCR).
• Testing for IgG and IgM can help to differentiate between primary and recurrent

 Management :
 Primary episode of genital herpes during pregnancy:
• · Women should be referred to a genitourinary physician.
• · Offer oral or intravenous acyclovir(200 mg five times daily or 400 mg three times daily for 5 days).
• · Supportive treatment ( saline bathing and analgesia ).
• · Acyclovir is associated with a reduction in the duration, severity of disease and in duration of viral
shedding.
• · Acyclovir should be used with caution before 20 weeks of gestation.
 Primary genital herpes at the time of delivery:
• · Caesarean section should be recommended to all women presenting with primary episode genital
• herpes lesions at the time of delivery, or within 6 weeks of the expected date of delivery.
• · For women who develop primary genital herpes lesions within 6 weeks of delivery and opt for a
vaginal birth:
 Avoid rupture of membranes and invasive procedures.
 Intrapartum IV acyclovir to the mother and to the neonate.
 The neonatologist should be informed.
• · There is insufficient evidence to recommend the use of daily acyclovir from 36 weeks to reduce the
HSV lesions at term in women with primary genital herpes earlier in the current pregnancy.

 Recurrent episodes of genital herpes during pregnancy:
• Antiviral is rarely indicated for recurrent genital herpes during pregnancy.
• The majority of recurrent genital herpes are short lasting and resolve within 7–10 days without
antiviral.
• Cultures during late gestation to predict viral shedding at term are not indicated.
• A recurrent genital herpes during pregnancy is not an indication for caesarean section.
• Women with recurrent genital herpes and opt for CS if HSV lesions detected at the onset of labour ,
daily acyclovir from 36 weeks of gestation until delivery can be given to reduce the likelihood of HSV
lesions at term.
 Recurrent episodes of genital herpes at the onset of labour:
• Risk of neonatal herpes is small1–3% in women presenting with recurrent genital herpes at the onset
of labour.
• CS is not routinely recommended for women with recurrent genital herpes lesions at the onset of
labour.
• The mode of delivery should be according to the clinical circumstances and the woman’s preferences.
• Women with recurrent genital herpes and PROM should have delivery expedited by the appropriate
means.
 Management :

How can postnatal HSV transmission to the neonate be prevented?
Healthcare workers and family members with active HSV infection, such as orolabial herpes , should
take measures to avoid transmission of the virus to the neonate.
• Breastfeeding is only contraindicated in the event herpetic lesion on the breast

 Parvovirus
• This B19 virus causes erythema infectiosum, or fifth disease.
• It is a small, single stranded DNA virus that replicates in rapidly proliferating cells such as erythroblast precursors .
• This can lead to anemia, which is its primary fetal effect.
• Only individuals with the erythrocyte globoside membrane P antigen are susceptible. In women with severe
hemolytic anemia‒for example,
• sickle-cell disease‒parvovirus infection may cause an aplastic crisis.
• The main mode of parvovirus transmission is respiratory or hand-to-mouth contact, and the infection is common in
spring months.
• The maternal infection rate is highest in women with school-aged children and in day-care workers, but not in
schoolteachers.
• An infected person develops viremia 4 to 14 days after exposure, and an otherwise immunocompetent individual is
no longer infectious at the onset of the rash.

 Parvovirus
 Maternal Infection
• Infection is asymptomatic(20-30%).
• Fever, headache, and flulike symptoms may begin in the last few days of the viremic phase.
• Several days later, a bright red rash with erythroderma affects the face and gives a slapped cheek appearance.
• The rash becomes lacelike and spreads to the trunk and extremities.
• Adults often have milder rashes and develop symmetrical polyarthralgia that may persist several weeks.
• pregnant woman in whom B19 infection was associated with hemophagocytic lymphohistiocytosis.
• No evidence suggests that parvovirus infection is altered by pregnancy.
• With recovery, IgM antibody is generated 7 to 10 days post infection, and production persists for 3 to 4 months.
• Several days after IgM is produced, IgG antibody is detectable and persists for life with natural immunity

 Fetal Infection:
• Transplacental transmission occurs in about 25% of women, with a mean of about 6 week between maternal
infection and fetal symptoms
• The fetus is most vulnerable when it is infected in the second trimester, with the peak risk occurring at 17–24
weeks’.
• The critical period for maternal infection leading to fetal hydrops was estimated to be between 13 and 16
weeks’ gestation, which coincided with the period in which fetal hepatic hemopoiesis is greatest
 the estimated fetal loss rate during pregnancy is about 5–10%. babies that survive to full term are usually born
healthy
Fetal infection has been associated with :
 Abortion
 nonimmune hydrops (it is the most frequent infectious agent of nonimmune hydrops in autopsied fetuses)
 stillbirth .
• Currently, no data support evaluating asymptomatic mothers and stillborn fetuses for parvovirus infection.
 Parvovirus

Diagnosis:
Maternal infection:
• maternal serological testing for specific IgG and IgM antibodies .
• Viral DNA may be detectable by PCR in maternal serum during the prodrome and persist for months to years after
infection.
Fetal infection :
• Detection of B19 viral DNA in amnionic fluid or IgM antibodies in fetal serum obtained by cordocentesis .
• Serial sonography every 2 weeks should be performed in women with recent infection , middle cerebral artery
(MCA) Doppler interrogation can also be used to predict fetal anemia (as Most cases of parvovirus-associated
hydrops develop in the first 10 weeks after infection
 Parvovirus

 Management of suspected parvovirus B19 in a pregnant woman:
• · In adults, parvovirus B19 is often indistinguishable from rubella.
• · Contact the Health Protection Unit (HPU) if rubella or parvovirus B19 infection is suspected at any stage of
pregnancy, irrespective of previous testing or immunization status to rubella.
• · Recommend rest, adequate fluids, and paracetamol for symptoms of viremia and arthropathy if necessary
(although symptoms are usually mild).
• · not usually necessary to stay off work, as the infection is no longer contagious by the time the rash or
arthropathy appears.
• · if the woman has not been fully immunized against rubella, it is important to avoid contact with other pregnant
women as it is difficult to clinically differentiate between parvovirus B19 and rubella.
• · Further screening for rubella is recommended in pregnant women with a rubella-like rash regardless of the
results of previous testing or immunization status because of the possibility of:
 laboratory or documentation error
 failed immunization
 symptomatic rubella reinfection
 parvovirus B19 infection
 Parvovirus
 Management :

 Parvovirus
 Management :
 Management a pregnant woman who has been in possible contact with parvovirus B19:
1) Determine whether the woman has had significant contact with parvovirus B19 or rubella.
• Significant contact means being in the same room for 15 minutes or more, or face-to-face contact, within the
previous 3 W.
• The infectious phase of parvovirus B19 usually occurs before the rash appears, so ask about contact before the
appearance of the rash.
• It is not possible to differentiate between rubella and parvovirus B19 on clinical grounds, For this reason, women
should be managed as they may have rubella infection, except if there has been a local outbreak of parvovirus
B19, or the woman was in contact with a child with classical symptoms of 'slapped cheek' syndrome.
• If the pregnant woman is known to be susceptible to rubella, contact for less than 15 minutes should also be
considered as possible exposure.
2) Contact HPU immediately regarding investigation for parvovirus B19:
3) Screen for rubella if the woman does not fulfil the criteria for immunity to rubella, that is she has:
• Received at least two documented doses of rubella vaccine, or
• Received a documented dose of rubella vaccine and has a previous rubella antibody screening test result which

 Parvovirus
 Management :
 Management a pregnant woman with confirmed parvovirus B19:
1) Refer the woman to an obstetrician within 4 weeks for fetal ultrasound and ongoing management.
2) Advise the woman that the prognosis is partly dependent on the stage of pregnancy that parvovirus B19 is
contracted at, but that the complications of infection can be treated at all stages
• Depending on gestational age, fetal transfusion for hydrops may improve outcome in some cases. Mortality rates
are in those hydropic fetuses without transfusions but with transfusion, 94% of hydrops cases resolve within 6 to 12
weeks, and the overall mortality rate is <10 percent.
• Most fetuses require only one transfusion because hemopoiesis resumes as infection resolves. Concurrent fetal
thrombocytopenia worsens the prognosis
 When should a pregnant woman with suspected parvovirus B19 infection be admitted or
referred?
1) Refer all women with confirmed active parvovirus B19 infection to an obstetrician. The woman should be
seen within 4 weeks of the start of illness or estimated time of seroconversion.
2) Admit those women who develop: - Severe or persistent anaemia, especially if the woman is
immunocompromised
• Symptoms of aplastic anaemia (dyspnoea, lassitude , or confusion), especially if they are known to have an
underlying haemolytic disorder (sickle cell anaemia or thalassaemia).

 Parvovirus
 Management :
 Management available in secondary care for parvovirus B19 infection in pregnancy:
 · In secondary care, pregnant women will be closely monitored using fetal ultrasound:
 The first scan around 4 weeks after the onset of symptoms or estimated time of seroconversion.
 Then every 1–2 weeks until 30 weeks of gestation.
 Fetal hydrops initially presents on ultrasound with the development of ascites and thickening and enlargement of
the fetal heart.
 If an abnormality is found that suggests hydrops fetalis, the woman will be referred to tertiary care.
 Tertiary care may provide:
 Doppler assessment of the middle cerebral artery and parvovirus B19 genome detection in amniotic fluid.
 Fetal blood sampling and intrauterine transfusion of erythrocytes.
 Early delivery of the baby if it is near full term (amniocentesis for lung maturity and treatment with corticosteroids
may be indicated).

 Prevention:
• Currently, no parvovirus vaccine is available, and no evidence suggests that antiviral treatment prevents maternal or
fetal infection.
• Decisions to avoid higher risk work settings are complex and require assessment of exposure risks.
• Pregnant women should be counseled that risks for infection:
 5%for casual, infrequent contact
 20 % for intense, prolonged work exposure such as for teachers
 50 %t for close, frequent interaction such as in the home.
• Workers at day-care centers and schools need not avoid infected children because infectivity is greatest before
clinical illness. Finally, infected children do not require isolation
 Parvovirus

• CMV is a DNA herpesvirus.
• As with other herpesviruses, it becomes latent after a primary infection but can reactivate with renewed viral
shedding.
• Shedding can occur from multiple sites and for prolonged periods of time, This occurs despite high serum levels of
anti-CMV IgG antibody (not prevent reactivation or recurrence) .
• Women can also become infected with a different viral strain.
• The virus is secreted into all body fluids.
• CMV is the most common congenital viral infection, with birth prevalence of 0.48 to 1.3 % in recent decades
Congenital infection may be asymptomatic or symptomatic; symptomatic disease can be severe and life
threatening.
• Both asymptomatic and symptomatic newborns are at risk of developing long-term neurodevelopmental morbidity,
particularly deafness.
 Cytomegalovirus

 Mode of transmission:
 close nonsexual contact (including household and occupational exposure [especially contact with young
children]),.
 sexual exposure
 transfusion, and organ transplant
 CMV has been cultured from multiple body fluids, including urine, saliva, blood, nasopharyngeal secretions,
tears, cervical and vaginal secretions, semen, and breast milk
 Transmission from respiratory droplets or aerosolized droplets is unlikely
 The fetus may become infected by transplacental viremia.
 The neonate is infected at delivery or during breastfeeding.
 Cytomegalovirus
,..

• In the United States demonstrated seropositivity in approximately 58 % of women aged 15 to 44 years .
• The following characteristics are predictive of positive CMV serology:
Lower socioeconomic strata., Contact with children under age 3 years .,Non-Hispanic black or Mexican-
American Age older than 25 to 30 years ,Higher parity, Residence in a developing country.
• Annual rates of maternal seroconversion range from 1 - 7% worldwide .
• Annual rates of seroconversion in different populations were as follows :
●Pregnant women: 2.3 %
●Health care workers : 2.3 %
●Daycare providers: 8.5
•Not shedding CMV: 2.1 %
•Shedding CMV: 24 %
 Seroprevalence:
 Cytomegalovirus

 Primary CMV infection: (Primary infection is strongly suspected if IgM and IgG are positive and IgG has low avidity).
25 % of congenital CMV infections in the United state.
 Clinical findings:
• Mild febrile illness
• Other nonspecific symptoms (rhinitis, pharyngitis, myalgia, arthralgia, headache, fatigue) but is not clinically apparent in 90%.
CMV mononucleosis can be accompanied by dermatologic manifestation in one-third of patients including( macular, papular,
maculopapular, rubelliform, morbilliform, and scarlatiniform eruptions).
• Reinfection or reactivation of virus in women with preexisting antibody generally does not cause maternal clinical illness .
• Hosts with impaired cellular immunity are at risk for severe and disseminated infection.
 Nonprimary infection:
• characterized by presence of maternal anti-CMV antibodies before conception.
• Also called recurrent or secondary infection, may be due to reactivation of latent virus or reinfection with a new strain.
 Cytomegalovirus
 MATERNAL INFECTION:

Maternal viremia can result in transplacental infection (placental cytotrophoblasts are permissive to CMV replication).
 Frequency of perinatal transmission: the rate of transmission appears to increase with advancing gestational age.
•Preconception period (2 months to 3 weeks before the date of conception): 5.2 %
•Periconceptional period (3 weeks before to 3weeks after the date of conception): 16.4 %
•First trimester: 36.5 %
•Second trimester: 40.1 %
•Third trimester: 65 %
 Cytomegalovirus
 Fetal INFECTION:

 Congenital infection:
• Congenital infection may be symptomatic or asymptomatic in newborns. Most congenital infections are asymptomatic in
the neonatal period.
• Both symptomatic and asymptomatic infected newborns are at risk for development of adverse sequelae in early
childhood, but symptomatic newborns are at higher risk ( death 5 versus 0 %, deafness 50 versus 10 %)
• Clinical findings in symptomatic newborns include:
 small for gestational age, microcephaly, ventriculomegaly, chorioretinitis, jaundice, hepatosplenomegaly,
thrombocytopenia, and petechiae.
 These findings are thought to result from the fetal immune response to viral replication in different organs (eg, salivary
gland, lung, liver, kidney, intestine, adrenal gland, placenta, central nervous system) .
 The mortality rate among symptomatic newborns is approximately 5 %, and 50 - 60% of survivors develop serious
long-term neurologic morbidity (eg, progressive hearing and/or visual impairment, motor/cognitive impairment)
• Asymptomatic newborns : Most congenitally infected newborns are initially asymptomatic.
15 - 25 % of these initially asymptomatic newborns go on to develop neurodevelopmental abnormalities, most commonly
hearing loss, within the first three years of life
 Cytomegalovirus

 Cytomegalovirus
• Routine prenatal CMV serological screening is currently not recommended by the Society for Maternal–Fetal
Medicine
 Maternal infection:
• CMV specific IgG testing: for primary infection detection(but CMV IgM does not accurately reflect timing of seroconversion
because IgM antibody levels may be elevated for more than a year, may be found with reactivation disease or reinfection with a
new strain).
• specific CMV IgG avidity testing: for confirming primary CMV infection(High anti-CMV IgG avidity indicates primary maternal
infection >6 months before testing)
 Fetal infection:
• Amniocentesis : Amniocentesis to perform polymerase chain reaction (PCR) for CMV DNA in amniotic fluid is the preferred
diagnostic approach for identifying an infected fetus; viral culture is less desirable because of several limitations( after 21 weeks
of gestation for allowing 6 week between maternal infection and amniocentesis .
• Ultrasound markers and monitoring : In infected fetuses, serial ultrasound examinations at 2-4 week intervals can be useful to
detect development of sonographic abnormalities including:( microcephaly, ventriculomegaly, and cerebral calcifications ,ascites,
hepatomegaly, splenomegaly, and hyperechoic bowel; hydrops; and Oligohydramnios, Fetal growth restriction, Placental enlargement
)
Abnormal sonographic findings seen in combination with positive findings in fetal blood or AF predict 75% risk of symptomatic
congenital infection
 Prenatal Diagnosis:

 Cytomegalovirus
 The management of the immunocompetent pregnant woman with primary or recurrent CMV is limited to symptomatic
treatment.
 If recent primary CMV infection is confirmed, amnionic fluid analysis should be offered, Counseling regarding fetal outcome
depends on the gestational age during which primary infection is documented.
 Despite the high infection rate with primary infection in the first half of pregnancy, most fetuses develop normally, However,
pregnancy termination may be an option for some.
 There is no evidence that antiviral drug treatment of primary infection in pregnant women prevents or mitigates sequelae of
CMV infection in the neonate but Compared with a historical cohort obtained by a meta-analysis, the use of valacyclovir
increased the proportion of asymptomatic neonates from 43 percent without treatment to 82 percent with treatment.
Valacyclovir 8 g daily was initiated at a median of 25.9 weeks of gestation and continued until delivery or termination of
pregnancy.
**intravenous valganciclovir administered for 6 weeks to neonates with symptomatic central nervous system (CNS) disease
prevented hearing deterioration at 6 months and possibly later.
 The timing and route of delivery are determined by standard maternal and fetal indications
 Passive immunization with Hyperimmunoglobulin therapy of pregnant women with primary CMV infection in early
pregnancy is a promising but investigational approach to reducing symptomatic infection in offspring may lower the risk of
congenital CMV infection when given to pregnant women with primary disease
 Management :

 Cytomegalovirus
Prevention of congenital infection relies on avoiding maternal primary infection, especially in early pregnancy.
 The following measures may reduce the risk of transmission:
●Practice good personal hygiene throughout pregnancy, especially hand washing with soap and water after contact with
diapers or oral and nasal secretions wash well for at least 15 to 20 seconds.
●Avoid kissing children under age 6 on the mouth or cheek; instead, kiss them on the head or give them a hug.
●Do not share food, drinks, or oral utensils (e. g, fork, spoon, toothbrush, pacifier) with young children.
●Clean toys, countertops, and other surfaces that come into contact with children's urine or saliva.
●Female childcare employees should be educated concerning CMV
●Pregnant employees working with infants and young children should be informed of their increased risk of acquiring CMV
infection and the possible effects on the unborn child.
●Routine laboratory screening for CMV antibody in female childcare workers is not recommended.
 Prevention :

 Rubella virus
• Is RNA virus a member of the togavirus family, genus Rubivirus cause Rubella or German measles
• humans are the only reservoir for rubella infection.
• The virus is transmitted by direct droplet contact from nasopharyngeal secretions, replicates in the lymph tissue of the upper
respiratory tract, and spreads hematogenously the transmission rate is 80% to susceptible individuals.
• The peak incidence is late winter and spring in endemic areas .
• Congenital infection occurs when maternal viremia allows hematogenous spread of the virus across the placenta
• Rubella and the congenital rubella syndrome (CRS) have largely been eliminated in the United States. The incidence of rubella
has declined from 0.45 per 100,000 in 1990 to 0.1 per 100,000 in 1999 due to rubella vaccine, However, rubella outbreaks
continue to occur in other parts of the world, and CRS remains a concern.

 Rubella virus
• Acquired rubella is generally a mild, self-limited disease (25 to 50 % of cases are asymptomatic) .
• Incubation period: 14 to 21 days .
• Clinical manifestation : mild, prodromal symptoms consisting of low-grade fever, conjunctivitis, coryza, sore throat, cough,
and occasionally headache and malaise which last one to five days before the onset of the rash , Just prior to the onset of the
rash 20 % of infected person will develop discrete rose spots on the soft palate.
• The typical rash of rubella is an erythematous maculopapular eruption, which may be mildly pruritic and evolves into
pinpoint papules similar to scarlet fever which characteristically begins on the face and spreads to the trunk and extremities
within hours and lasts approximately one to three days and resolves first from the face and then from the body.
• Rubella may also be associated with generalized, tender lymphadenopathy, particularly involving suboccipital, postauricular,
and cervical nodes
• Rheumatologic symptoms may develop about one week after the rash and occurring in 60 - 70 % of adult women,
Classically, the hands, knees, wrists, and ankles are affected in a symmetric pattern with pain and morning stiffness for 1-4
weeks , Tenosynovitis and carpal tunnel syndrome may also be associated with rubella.
• Rare complications include: thrombocytopenia associated with purpura or hemorrhage, postinfectious encephalitis,
myocarditis, pericarditis, hepatitis, hemolytic anemia, and hemolytic uremic syndrome and chronic arthritis.
 Maternal Infection:

Maternal-fetal transmission occurs via hematogenous spread and varies with gestational age
 Rate of fetal infection :
 In the first trimester: 81 %
 in the second trimester : 50% at(13 – 14 weeks) , 25 % at late second trimester.
 in the third trimester : 35 % at( 27 - 30 weeks) , 100 % beyond 36 weeks .
• However, the risk of congenital defects after maternal infection is essentially limited to maternal infection in the first 16 weeks
of pregnancy , Little risk of CRS is associated with infection after 20 weeks’ gestation, and intrauterine growth retardation may
be the only sequelae of third trimester infection and there is no evidence that rubella infection immediately prior to
pregnancy increases the risk of congenital infection.
• In general, maternal immunity, either vaccine or naturally derived, is protective against intrauterine rubella infection.
However, there have been CRS cases resulting from maternal reinfection
• Neonates born with congenital rubella may shed the virus for many months
 Rubella virus

 Rubella virus
 Manifestations of CRI during the neonatal period may include:
●Fetal growth restriction
●Meningoencephalitis, large anterior fontanelle , Microcephaly(27%) and intellectual disability (13 %)
● Cardiac defects:1/2 of children infected during the first two months of gestation have congenital heart disease, PDA and
branch pulmonary artery stenosis are the most common lesions, Other including PVS, AVS, VSD, FT, and COA.
●Hearing loss
●Cloudy cornea, cataract , infantile glaucoma, retinopathy("Salt and pepper“) : one-quarter of infants infantile. Cataracts and
infantile glaucoma usually become apparent during the early weeks of life. retinopathy
●Interstitial pneumonia
●Hepatosplenomegaly, jaundice, hepatitis, diarrhea
●Radiolucent bone lesions (in the long bones)
●Petechiae and purpura ("blueberry muffin lesions")
● Osteopathy
● Hemolytic anemia, thrombocytopenia

 Rubella virus
 Delayed manifestations of CRI : occur in 20% of children with symptomatic CRI. Some of the late manifestations may
relate to subtle damage that is present but not detected in early life. Late manifestations include :
●Hearing loss: Permanent hearing loss is the most common one(80%)
●Endocrine disorders : as diabetes mellites
●Eye problems
●Vascular effects
●Progressive panencephalitis: rare
●Immune defects

 Rubella virus
 Diagnosis:
 Maternal cute rubella infection is diagnosed by:
●A fourfold rise in IgG titer between acute and convalescent serum specimens: Serum should be obtained within 7 - 10 days after
the onset of the rash and repeated 2- 3 weeks later
●The presence of rubella specific IgM: If is detected in a pregnant woman in the absence of a history of rubella-like illness or
contact, further investigation is required as it likely falsely positive (RF or other antibodies cross react with assay )Use of rubella
specific avidity assay may be useful in these situations.
●A positive rubella culture: Rubella virus may be isolated from nasal(from the pharynx 1 week before to 2 weeks after the rash),
blood, throat, urine, or cerebrospinal fluid (CSF) specimens
 Fetal cute rubella infection is diagnosed by:
● Rubella specific PCR on CVS samples : superior to standard serologic testing on fetal blood (CVS sampling ideally done at 10 to
12 weeks’ gestation)
● A reverse transcription-nested PCR assay : it detects rubella virus in (CVS) samples and AF samples of affected pregnancies.
● Ultrasound diagnosis would be extremely difficult given the nature of the malformations seen with CRS, although, the workup
of any fetus with intrauterine growth restriction should include evaluation for congenital viral infections including rubella

 Rubella virus
 Management :
• There is no specific treatment for rubella but supportive measures are reserved for patients with complications :
 acetaminophen for symptomatic relief.
 Glucocorticoids : for encephalopathy
 platelet transfusion: thrombocytopenia
• The prognosis for pregnant women with rubella is generally excellent.
• However, because of the potentially devastating effects on the fetus, women should be counseled about maternal-fetal
transmission and offered pregnancy termination, especially prior to 16 weeks’ gestation.
• There is no definitively beneficial in utero treatment available for exposed or affected fetuses.
• Postexposure passive immunization with polyclonal immunoglobulin may be of benefit if given within 5 days of
exposure but its use controversial
• There are no data to suggest that IgG has a beneficial effect on the fetal response to disease. Thus, the Centers for Disease
Control and Prevention (CDC) recommends limiting the use of immune globulin to women with known rubella exposure
who decline pregnancy termination

 Rubella virus
• Vaccination is recommended for all children at 12 to 15 months and 4 to 6 years in conjunction with measles and
mumps (MMR). All other persons should be vaccinated unless immunity is documented by serology.
• Rubella vaccination should be avoided 1 month before or during pregnancy because the vaccine contains attenuated
live virus
• Vaccination of all susceptible hospital personnel who might be exposed to patients with rubella or who might have
contact with pregnant women is important.
• A small percentage of individuals will have side effects, such as arthritis, arthralgia, rash, adenopathy, or fever
• pregnancy should be prevented within three months by contraceptive measure but if it is occur is not an indication
for pregnancy termination.
• Contraindications to rubella vaccination include : febrile illness, immunodeficiency disorder, history of anaphylaxis
to neomycin, and pregnancy.
• Postpartum vaccination should be performed in all women known to be susceptible.
• Breastfeeding is not contraindicated.
 Prevention:

 HIV
• Is a retrovirus containing reverse transcriptase which allows the virus to transcribe its RNA genome into DNA, which then
integrates into host cell DNA.
• Human immunodeficiency virus (HIV) causes an incurable infection that leads ultimately to a terminal disease called
acquired immunodeficiency syndrome (AIDS).
• Worldwide 25–30% of infected patients are women and 90% of them are 20–49 years of age.
• The prevalence of HIV infection in women giving birth in England in 2008 was 0.2%.
• In most Asian countries the infection rate is less than 0.5%.
• HIV preferentially targets lymphocytes expressing CD4 molecules (CD4 lymphocytes).
• When CD4 lymphocytes fall below a critical level, increase the risk of opportunistic infections and malignancies.

• The main modes of transmission of HIV are:
(i) Sexual contact (homosexual or heterosexual)
(ii) transplacental (iii) exposure to infected blood or tissue fluids and (iv) through breast milk
• Stages of infection:
 Primary infection 3–6 weeks
 Acute syndrome (1 week–3 months)
 Immune response to HIV (1–2 weeks)
 Clinical latency—about 10 years
 AIDS.
 HIV

 Risks of mother-to-child transmission:
 in untreated women:
• · 15%-20% in non-breastfeeding women in Europe and 25%-40% in breastfeeding African populations, Transplacental
transmission occurs: 20% before 36 weeks
• · In the absence of breastfeeding, >80% of transmissions occur perinatally, around time of delivery.
• · there is a linear correlation between maternal viral load and the risk of transmission but transmissions are rare when
plasma viraemia < 50 copies/ml at the time of delivery.
Obstetric factors associated with transmission are:
1. mode of delivery 2. duration of membrane rupture 3. delivery before 32 weeks of gestation.
• · Breastfeeding doubles the risk of mother-to-child transmission from around 14% to 28%.
 in treated women:
• Maternal anti-retroviral therapy reduces the risk of vertical transmission by 70%
• · The decline in CD4 lymphocyte count in pregnancy is due to haemodilution, resolves in the postpartum period
• · HAART are associated with increased risk of obstetric complications:
1. gestational diabetes. 2. pre-eclampsia. 3. preterm .
 HIV

 Effects on pregnancy:
• Increased incidence of abortion, prematurity, preeclampsia, IUGR and perinatal mortality in HIV seropositivm
mothers still remains inconclusive.
• Maternal mortality and morbidity are not increased by pregnancy.
 Clinical presentation:
• Initial presentation may be fever, malaise, headache, sore throat, lymphadenopathy and maculopapular rash.
Primary illness may be followed by an asymptomatic period.
• Progression of the disease may lead to multiple opportunistic infections (OI) with candida, tuberculosis,
pneumocystis and others.
• Patient may present with neoplasms such as cervical carcinoma, lymphomas (Hodgkin’s and non-Hodgkin’s) and
Kaposi’s sarcoma.
• There may be associated constitutional symptoms like weight loss, lymphadenopathy or protracted diarrhea.
• CD4 count < 200 cells/mm3 is diagnostic of AIDS. The median time from infection to AIDS is about 10 years.
 HIV

• detecting HIV viral RNA in blood by PCR testing (HIV RNA PCR)
• detecting antibodies to HIV by enzyme immunoassay (EIA) extremely sensitive (99.5%), inexpensive but less
specific.
• An initial positive EIA test must be confirmed with a second, more specific test Western blot or HIV RNA PCR.
• This is then confirmed by Western blot, immunofluorescence assay (IFA) or HIV RNA PCR.
• The western blot detects specific viral antigens P24 (Capsid), GP41 (envelope) and GP 120/160 (envelope) has
False positive rate less than 1 in 10,000.
 HIV
 Diagnosis:

 Antenatal HIV screening:
• · screening for HIV, syphilis, hepatitis B and rubella in every pregnancy at booking is recommended.
• · If woman declines HIV test, this should be documented with reasons behind and screening offered again at 28 weeks.
• · If a woman tests HIV negative at booking but at high risk of acquiring HIV, offer a repeat HIV test.
• · Midwives and doctors reviewing women should ensure that the HIV result is clearly documented.
• · Fourth-generation assays are recommended as the first-line HIV test for antenatal screening:
 In this type of assay p24 antigen is detectable during seroconversion.
 have a high sensitivity (> 99.9%) and specificity (> 99.5%).
• · if a woman books at 26 weeks or later, request the result issued within 24 hours.
• · Rapid HIV tests with results within 20 minutes are recommended with unknown HIV status in labour.
• Most of rapid-test test for antibody (not p24 antigen), so test is likely to be negative during seroconversion.
 HIV

 HIV
 Anti-HIV drugs are grouped into :
(A) Nucleoside reverse transcriptase inhibitors (NRTIs : Zidovudine , Didanosine, Lamivudine, Abacavir).
(B) Non-nucleoside reverse transcriptase inhibitors (NNRTIs : Nevirapine , Efavirenz).
(C) Protease inhibitors (PI : Indinavir, Saquinavir, Ritonavir).
(D) Entry inhibitors: Enfuvirtide.
• Triple chemotherapy is preferred as a first line defense and to be started any time between 14 weeks and 28 weeks and then
continued throughout pregnancy, labor and postpartum period.
• WHO recommends first line ART regimen to include: Zidovudine (ZDV), + Lamivudine (3 TC), + Nevirapine (NVP) or ZDV + 3 TC +
EFV (Efavirenz).

 Antenatal care of women who are HIV positive:
• multidisciplinary team approach: HIV physician, obstetrician, specialist midwife, health advisor and paediatrician.
• Social circumstances for newly diagnosed HIV positive.
• Reassure women that confidentiality will be maintained.
• Encourage and support women to disclose their HIV status to their partner.
• Avoid inadvertent disclosure to a woman’s partner or family, as they may be unaware of her HIV diagnosis.
• Advice about safer-sex practices and the use of condoms, to prevent HIV and STIs transmission.
• There is a risk of super infection associated with unprotected sex if both woman and partner are HIV positive.
• Women with children of unknown HIV status should have them tested for HIV.
• If women refuse interventions to reduce the risk of mother-to-child transmission, a pre-birth planning meeting should be hel
with social services to discuss safeguarding issues.
• There should be a named respondent to notify all HIV positive pregnancies to the National Study of HIV in Pregnancy and
Childhood.
 HIV

 HIV
 Antenatal care of pregnant women who are HIV positive:
• Screening at booking for:
1. syphilis, hepatitis B and rubella like general population+ hepatitis C, varicella zoster, measles and toxoplasma.
2. gestational diabetes for women on HAART.
3. genital infections and again at 28 weeks. Any infection should be treated even if asymptomatic
• · Screening for aneuploidy like general population.
• · Dating and anomaly scans.
• · Hepatitis B and pneumococcal vaccination is recommended .Influenza vaccination is also safe in
• pregnancy .
• · Varicella zoster and measles, mumps and rubella vaccines are contraindicated in pregnancy.
• · Monitoring of plasma viral load and drug toxicities directed by the HIV physicians.
• · A plan of therapy and mode of delivery should be made at 36 weeks following detailed discussion.

 Interventions to prevent disease progression in the mother:
• Women who require HIV treatment for their own health should take :
1. HAART and continue postpartum.
2. prophylaxis for Pneumocystis carinii pneumonia (PCP), depending on CD4 lymphocyte count.
• Women already taking HAART and/or PCP prophylaxis before pregnancy should not discontinued
 Interventions to prevent mother to child transmission of HIV
• 1) Transmission rates < 2% are associated with: effective HAART, appropriate management of delivery, avoidance of
breastfeeding.
• 2) Women require HIV treatment for their health, HAART should be continued through pregnancy and postpartum.
• 3) Women do not require treatment for their health, start HAART between 20-28 weeks and stop at delivery.
• 4) women do not require treatment for their health with viral load <10 000 copies/ml and booked for elective CS, an
acceptable alternative is zidovudine (ZDV) monotherapy initiated 20-28 weeks, 250 mg orally twice daily and intravenously at
delivery.
 HIV

 Management of antenatal complications
• HIV complications should be considered as a cause of acute illness in pregnant women with unknown HIV status.
• In these circumstances, a rapid HIV test should be considered.
 Pregnant women with advanced HIV are at increased risk of opportunistic infections, particularly PCP with fever, dry cough
shortness of breath and hypoxia.
• ·HAART regimens are associated with GIT disturbances, skin rashes, hepatotoxicity and Lactic Acidosis
• Symptoms suggestive of pre-eclampsia, cholestasis or signs of liver dysfunction may indicate drug toxicity.
 HIV
5) Delivery by elective CS at 38 weeks to prevent labour and/or ruptured membranes for:
 Women on HAART with viral load > 50 copies/ml
 Women on ZDV monotherapy.
 Women with HIV and hepatitis C virus co-infection.
6) planned vaginal delivery can be offered if women on HAART with viral load of < 50 copies/ml.
7) Delivery by elective CS for obstetric indications or maternal request at 39+ weeks if viral load < 50 copies/ml..

 Management of preterm delivery and PPROM:
1) initial assessment for threatened preterm labour is like the general population.
2) multidisciplinary team should be involved for clear plan and choice of anti-retroviral therapy.
3) Screening for genital infections and any infection should be treated even if asymptomatic.
4) Apply the usual indications for steroids.
5) Women should be counselled about the increased risk of preterm delivery with HAART.
6) Administering anti-retroviral therapy to the mother < 32 weeks of gestation just before and during delivery will provide
prophylaxis to the neonate.
7) If PPROM after 34 weeks, delivery should be expedited. Augmentation may be considered if the viral load < 50 copies/ml.
and start broad-spectrum intravenous antibiotics.
8) If PPROM occurs before 34 weeks, oral erythromycin should be started with expectant management yf there is no Evidence
of chorioamnionitis and fetal distress.
 HIV

Management of delivery:
1) A maternal sample for plasma viral load and CD4 count taken at delivery.
2) Women on HAART should have their medications before delivery and, if indicated, after delivery.
3) Elective caesarean section:
 If IV ZDV is indicated, start infusion 4 hrs. before CS Loading dose 2 mg/kg/hr, maintenance dose 1 mg/kg/hr continue
until the umbilical cord has been clamped.
 Haemostasis as much as possible and avoid rupturing the membranes until delivery of head through the incision.
 Peripartum antibiotics.
 Take a maternal sample for viral load and CD4 lymphocyte count at delivery.
4) Planned vaginal delivery:
 plan of care for delivery should be reviewed and recent viral load results should be confirmed as < 50 copies/ml.
 HAART should be prescribed and administered throughout labour.
 Invasive procedures such as fetal blood sampling are contraindicated.
 HIV

 Management of delivery:
 Amniotomy should be avoided till delivery is imminent.
 Amniotomy and oxytocin may considered for augmentation of labour.
 If instrumental delivery is indicated, low-cavity forceps are preferable.
5) PROM:
 delivery should be expedited. If the viral load <50 copies/ml, augmentation may be considered.
 Broad-spectrum intravenous antibiotics if there is evidence of infection.
6) Prolonged pregnancy:
 For women on HAART and viral load > 50 copies/ml, IOL for prolonged pregnancy should be individualized.
 There is no contraindication to membrane sweep.
7) VBAC: can be considered for women on HAART with viral load < 50 copies/ml.
8) HIV diagnosed in labour:
 multidisciplinary team should be involved for clear plan and choice of anti-retroviral therapy.
 Delivery should be by caesarean section and, where possible should be timed with antiretroviral administration.
 HIV

 Postpartum management of women who are HIV positive:
1) Advice about formula feeding.
2) Oral cabergoline to suppress lactation.
3) Women taking HAART should have their medication administered.
4) Guidance about contraception should be given in the immediate postpartum period.
 There are many interactions between hormonal contraception and HAART.
5) MMR and varicella zoster immunization, according to the CD4 lymphocyte count.
 Management of the neonate:
1) All neonates should be treated with anti-retroviral therapy within 4 hours of birth.
2) ZDV monotherapy is accepted
3) If neonates at high risk of HIV infection consider HAART and prophylaxis against PCP Infants should be tested at 1 day, 6
weeks and 12 weeks of age.
If tests are negative and the baby is not breastfed, the child is not HIV-infected.
A confirmatory HIV test is performed at 18 months of age.
 HIV

 Prepregnancy management:
1) Couples who are serodiscordant :
 choosing to have intercourse should be advised to use condoms.
 The female is HIV negative should be advised that assisted conception with either donor insemination or sperm washing is
significantly safer than timed unprotected intercourse.
2) Couples should be advised to delay conception until:
 plasma viraemia is suppressed,
 prophylaxis for PCP is no longer required
 any opportunistic infections have been treated.
3) Folate supplementation should be administered in accordance with national guidelines.
4) annual cervical cytology, because of the association of HIV, immunosuppression and cervical neoplasia.
 Post exposure prophylaxis: with triple therapy for 4 weeks, reduces the risk of seroconversion by more than 80%. (ZDV
200 mg tid + Lamivudin 150 mg bid + Indinavir 800 mg tid).
 HIV

• This RNA virus of the Flavivirdae family has recently been recognized as the first major mosquito-borne teratogen
Although Zika virus is primarily transmitted by mosquito bite, sexual transmission is also possible, and the virus may
be detected in body fluids for months following acute infection
 Maternal–Fetal Infection:
• In adults Zika infection may be asymptomatic or cause mild symptoms of rash, fever, headache, arthralgia, and
• conjunctivitis lasting a few days.
• Virus is typically detectable in blood around the time of symptom onset and may persist days to months in pregnant
women
• Serum IgM antibodies typically become detectable within the first two weeks after symptom onset and remain a
median of four months The fetus can be severely infected whether or not the mother is symptomatic.
• Among live births, the rate of fetal birth defects ranges from 5% among women with possible Zika infection—to 15%
among pregnant women with laboratory-confirmed infection in the first trimester
• In the most severely affected fetuses, a congenital Zika syndrome has been described that includes microcephaly,
lissencephaly ,ventriculomegaly, intracranial calcifications, ocular abnormalities, and congenital contractures
Zika Virus:

 Diagnosis:
• detection of Zika virus RNA in blood or urine or by serological testing.
• Detection of Zika virus RNA by PCR confirms infection.
• Serological assays for Zika IgM antibodies may cross react with other flaviviruses. Thus, a positive assay result is
followed by another assay containing virus-specific neutralizing antibodies
 Management:
• Currently, no specific treatment or vaccine is available for Zika infection, although several vaccine candidates are in
development Prophylaxis includes protective netting and insect spray to control the vector mosquito and avoidance of
sexual contact with partners recently exposed

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