Download Prevention of rubella infection

Tues. 7th /March
Dr .Rana Al-Khazraji
Perinatal infection
Infections during pregnancy or around delivery can adversely affect fetus,
neonate or pregnant women. It can be divided into four groups:
1) Congenital Infections causing congenital abnormalities.
2) Congenital infection associated with pregnancy loss and preterm labor.
3) Infections acquired around the time of delivery with serious neonatal
consequences.
4) Perinatal infections causing long term disease.
Congenital Infections causing congenital abnormalities:
 Rubella
 CMV (cytomegalovirus)
 chicken pox
 syphilis
 toxoplasmosis
Rubella:
Is a togavirus spread by respiratory droplets or in-utero transmission.
Maternal infection:
 Asymptomatic in 20-50% of cases.
 Febrile rash with conjunctivitis & LAP.
 Typical rash is pink or red maculopapular rash
spreading on trunk &limbs.
Fetal infection:
starting on forehead &
Malformations of congenital rubella can affect all organs, but the eye, ear and
heart seem to be preferentially affected.
Congenital rubella syndrome includes one or more of the following:
 Eye defects—cataracts and congenital glaucoma.
 Heart disease—patent ductus arteriosus and pulmonary artery stenosis.
 Sensorineural deafness—the most common single defect.
 Central nervous system defects—microcephaly, developmental delay,
mental retardation, and meningoencephalitis.
 Neonatal purpura , Hepatosplenomegaly and jaundice.
The risk of congenital rubella infection depends on gestational age:
80% in 1st trimester (reaching 100% if it is at 1st 11ws)
25% at end of the 2nd trimester.
After 20 weeks ,no documented risks to fetus.
Diagnosis of rubella:
 In the mother:
 Diagnosis is usually clinical.
 acute infection can be confirmed by:
1- serological tests by presence of rubella specific IgM.
Presence of rubella-specific IgG anti bodies indicates previous infection or
immunization.
2- by isolation of virus from urine or throat.
 In the fetus: Confirmation of fetal infection is possible in confirmed cases
of maternal rubella by detection of rubella RNA in chorionic villi, amniotic
fluid, or fetal blood.
Prevention of rubella infection:
 Rubella can be prevented by live attenuated vaccine.
 The vaccine is contraindicated in pregnancy due to theoretical risk of
teratogenicity.
 If women is vaccinated , it should be advised to use contraception for three
months.
 Pre-pregnancy counseling should include evidence of immunity and
vaccination should offered to susceptible mother.
 Antenatal screening test to know susceptibility for rubella infection.
 pregnant woman who are screened and antibody is not detected, vaccination
is advised after pregnancy.
Management of rubella infection:
If infection during pregnancy is confirmed the management depends on
gestational age.
 If infection occurred prior to16 weeks gestation, termination of pregnancy
should be offered.
 If infection occurred after 16 weeks , the women should be reassured.
Cytomegalovirus (CMV):
 Is a DNA herpes virus
 Is transmitted by respiratory droplet, sexual activity, blood transfusion &
organ transplantation.
 Vertical transmission can occur during pregnancy, delivery& breast
feeding.
 is the most common perinatal infection in the developed world.
 40% of pregnant women are susceptible.
 Incidence of infection in pregnancy is 1-2%.
 Of those, 30% will transmitted to fetus and 30% of those fetuses are
affected.
Clinical features:
 In mother: asymptomatic or mild flue like illness.
 Abnormalities of congenital Infection can be seen in:
 The fetus on U/S:
( IUGR, microcephaly, ventriculomegaly, periventricular calcification, intraabdominal calcification, HSM, hydrops).
 The neonate: ( HSM, thrombocytopenia, jaundice, purpural rash &anemia).
 Later on as blindness, deafness, developmental delay or mental retardation,
difficulties in learning.
In the mother:
 Serological diagnosis in suspected cases.
 By demonstrating the development of CMV antibodies in seronegative
women .
 Which are initially IgM & then IgG .
 viral culture may be useful, though a minimum of 21 days is required before
culture is reported as negative.
In the fetus
-U/S shows features suspected infection.
-PCR on amniotic fluid can confirmed diagnosis.
Management:
 Prevention : vaccine against CMV still under experimental trial.
 Termination of pregnancy can be offered to women whose fetuses have
evidence of intrauterine CMV infection.
Chicken pox( varecilla-zoster virus):
 Is caused by varecilla-zoster virus, is a DS- DNA herpesvirus.
 is transmitted by direct contact, air born transmission or in-utero tansmission
.
 over 90% of the antenatal population are seropositive for VZV
immunoglobulin (IgG) antibody.
 it is estimated to complicate three in every 1000 pregnancies.
Clinical features:
In the mother :
 presents with a 1- to 2-day flulike prodrome, is followed by pruritic
vesicular lesions that crust over in 3 to 7 days.
 The incubation period is 10 to 21 days.
 Infectious period is from 2 days prior to the onset of the rash until the
lesions are crusted over.
 pneumonia, hepatitis and encephalitis are more common complication
occur in adult.
 Morality rate is 5 times more in pregnant than non pregnant.
 Following the primary infection, the virus remains dormant in sensory nerve
root ganglia
 But can be reactivated to cause a vesicular erythematous skin rash in a
dermatomal distribution
 known as herpes zoster (HZ), or simply zoster or shingles.
In the fetus:
It depends on gestational age:
 At 1st 28 weeks, there is 1% risk of congenital varicella syndrome
(CVS),which includes one or more of following:
 skin scarring in a dermatomal distribution;
 eye defects (microphthalmia, chorioretinitis, cataracts);
 hypoplasia of the limbs;
 Neurological abnormalities (microcephaly, cortical atrophy, mental
restriction and dysfunction of bowel and bladder sphincters).
 28- 36 weeks ,there is no affect on fetus
 At terms , there is significant risk of varicella of neonate.
 Severe chickenpox is most likely to occur if the infant is born within 7 days
of onset of the mother’s rash or if the mother develops the rash up to 7 days
after delivery.
Diagnosis:
 In mother:
 Clinical manifestation is enough to make diagnosis.
 Serological test: measuring IgM& IgG.
 The virus may also be isolated by scraping the vesicle base during primary
infection and performing tissue culture, or direct fluorescent antibody
testing.
 in the fetus:
 U/S findings of CVS.
 PCR on amniotic fluid or fetal blood sampling.
 Prevention:
 Varicella vaccine is a live attenuated vaccine.
 It is contraindicated in pregnancy.
 Pregnancy should be avoided for 3 months after vaccination.
 Advice those susceptible women ( had no history of chicken pox ) to
avoid contact with it.
 If contact with chicken pox occurs:
 Asking about significant of contact (face to face or 15 min at same room)
 Testing for immunity by blood test for VZ IgG.
 If the pregnant women is not immune ,VZIG is available.
 It is effective when given in the 1st 10 days of contact.
 It may prevent or attenuated the disease, therefore it should be advised to
notifying the doctor when a rash develops.
Management of pregnant women with chicken pox:
 Mother: antepartum :
 She should avoid contact with the susceptible individuals until the lesions
have crusted over.
 The pregnant woman with chickenpox should be asked to report
immediately respiratory or other new symptoms to her doctor.
 Symptomatic treatment and hygiene is advised to prevent secondary
bacterial infection of lesions.
 Acyclovir , 800mg /5times daily, within 24hr of onset of rash & for 7 days.
Intrapartum:
 Delivery during the viraemic period may be extremely hazardous:
1- The maternal risks are bleeding, thrombocytopenia, DIC and hepatitis.
2- high risk of varicella infection of the newborn with significant morbidity and
mortality.
 Supportive treatment and intravenous acyclovir is therefore desirable.
 Delaying of elective delivery for 7days after rashes decreases the maternal
complications & allows transfer of protective antibodies from the mother to
the fetus.
 However, delivery maybe required in women to facilitate assisted ventilation
in cases where varicella pneumonia is complicated by respiratory failure.
 Fetus:

Referral to a fetal medicine specialist should be considered at 16–20 weeks
or 5 weeks after infection for discussion and detailed ultrasound
examination.
 Amniocentesis is not routinely advised because the risk of CVS is so low,
even when amniotic fluid is positive for VZV DNA.
 It is not known whether VZIG reduces the risk of CVS.
 Neonates:
 Elective delivery should normally be avoided until 5–7 days after the onset
of maternal rash to allow for the passive transfer of antibodies from mother
to child.
 Neonatal ophthalmic examination should be organized after birth.
 If birth occurs within the 7-day period following the onset of the maternal
rash, or if the mother develops the chickenpox rash within the 7-day period
after birth:
The neonate should be given VZIG.
The infant should be monitored for signs of infection until 28 days.
 Neonatal infection should be treated with acyclovir following discussion
with a neonatologist and virologist.
Toxoplasmosis:
Is caused by Toxoplasma gondii
Clinical picture:
 In mother :
 Asymptomatic
 Flue like illness with LAP Infection
 in immunocompromised women, however, may be severe, with reactivation
involving encephalitis or mass lesions.
 In the fetus:
 In acute infection, transmission and severity of damage depend on
gestational age.
 In 1st trimester, 10% of infection is transmitted but 85% of those have severe
damage.
 In 3rd trimester, 85% of infection is transmitted but risk of damage reduces
to10%.
 Congenital infection may lead to miscarriage , preterm labour.
 At neonate, anemia, HSM, jaundice.
Severely infected infant may have:
 Ventriculomegaly .
 Microcephaly .
 Hydrocephaly.
 Chorioretenitis.
 Cereberal calcification.
Diagnosis:
 Seriological tests,which are used to differentiate acute from chronic
infection
 IgG appear after 2 weeks and persist for life with life long immunity.
 IgG avidity is low in acute infection and increases over weeks and months.
 IgM is appear after 10 day and may persist for years.
Prenatal diagnosis:
 PCR of amniotic fluid or fetal blood
 Sonographic evidence of intracranial calcifications, hydrocephaly, liver
calcifications, ascites , placental thickening, hyperechoic bowel
Treatment:
 Spiramycin is thought to reduce the risk of transmission by 60% ,can start as
soon as maternal infection is confirmed.
 If fetal infection is diagnosed by prenatal testing at or> 18 weeks,
pyrimethamine, sulfonamides, and folinic acid are used to eradicate
parasites in the placenta and fetus.
Syphilis:
 The causative agent for syphilis is Treponema pallidum.
 syphilis is STD.
 The fetus acquires syphilis by several routes:
-transplacental transmission is the most common route.
-neonatal infection may follow after contact with spirochetes through lesions at
delivery or across the membranes.
Effects on fetus:
 Rate of transmission of syphilis to fetus depends on the stage of diseases.
 In pregnant women , early untreated syphilis ( primary and secondary )
with highest spirochete load ,70-100% of infant will be infected and about
25% will be stillborn.
 Because of fetal immunocompetence prior to approximately 18 weeks, the
fetus generally does not manifest the immunological inflammatory response
characteristic of clinical disease before this time.
 Early infection, untreated: miscarriage, stillbirth, hydrops fetalis, neonatal
death, IUGR, premature delivery.
 Survivors:
Early congenital syphilis: clinical manifestations within first 2 years of life
Late congenital syphilis: clinical manifestations after 2y .
Early congenital syphilis:
 Hepatosplenomegaly- diffuse inflammation, scarring
 Jaundice – due to hepatitis
 Generalized lymphadenopathy –
 Coombs – hemolytic anemia, thromobocytopenia, leukopenia, leukocytosis
 maculopapular rash
 Pemphigus syphiliticus (vesicular bullous eruptions of palms and soles)
 Petechial lesions
 Bony lesions, osteochondritis, periostitis, pseudoparalysis
 Syphilitc leptomeningitis
 Chorioretinitis,
Late congenital syphilis:
 Interstitial keratitis (inflammatory)
 Nerve deafness
 Clutton’s Joints (synositis, restricted movement)
 Hutchinson’s triad (teeth, intersitial keratitis, 8th nerve deafness)
 Mental retardation
 Frontal bossing
 Saddle nose
 High arched palate
 Generalized paresis of insane
 Saber shine
 Gummata
Diagnosis:
Definitive diagnosis can be made by dark-field microscopy on specimen from skin
lesions, placenta, umbilicus.
Serologic tests are the principal means for diagnosis:
1) Non-treponemal test: VDRL, RPR
2) Treponemal tests: TPI, FTA-ABS, MHA-TP : they detect specific
treponemal antibody , become positive soon after initial infection and usually
remain positive for life, even with adequate therapy.
The prenatal diagnosis of congenital syphilis :
 Sonographic evaluation may be suggestive or even diagnostic.
 hydrops fetalis, ascites, hepatomegaly, placental thickening, and
hydramnios all suggest infection.
 PCR is specific for detection of T. pallidum in amnionic fluid, and
treponemal DNA has been found in 40 percent of pregnancies infected
before 20 weeks.
Management:
 Confirm diagnosis
 Testing for other STD
 Contact tracing of sexual partner
 Screening for congenital syphilis in older children.
 Parenteral pencilline is effect in 98% in prevent cong.syphilis.
 Women who is not treated during infection, the baby should treated after
delivery.
Herpes:
 Is caused by herpes simplex virus.
 HSV is dS DNA virus.
 There are 2 viral types : HSV-1&HSV-2.
 Orolabial herpes is caused by HSV-1& transmitted by direct contact such as
kissing.
 Genital herpes is caused in most cases by HSV-2 and is sexually transmitted.

Neonatal herpes caused by direct contact with infected maternal secretions
during delivery.
 It is very rarely caused by transplacental transmission.
 Greatest risk of neonatal herpes ( 41%) when maternal primary genital
infection occurs:
at time of delivery or within 6 weeks of delivery.
 Risk of neonatal herpes in recurrent genital herpes is very small (1-3%)
Clinical manifestation:
 In mother :
Ulcerative lesion on vulva ,vagina or cervix
Primary infection is associated with systemic infection or urinary retention.
 In the fetus: Primary infection may lead to:
miscaraige ,stillbirth or
IUGR,
preterm labour.
 In neonate: neonatal herpes may present in three forms:
Localized: to skin , eye and mouth( mortality rare , neurological morbidity<2%).
Local CNS disease:(mortality 6% , neurological morbidity 70%).
Disseminated diseases: ( mortality 30% , neurological morbidity 17%).
Management:
 The diagnosis :
-Is suggested by clinical presentation.
-Is confirmed by viral culture or PCR on lesions swab.
 Screening for other STD.
 Acyclovir(200mg/5 times daily for 5 days) .
If Primary infection is at time of delivery or within 6weeks of delivery:
1 - C/S should be recommended if elapsed time since the rupturing of membrane
is less than 4hr.
2 -in the women who opt vaginal delivery :

Rupturing of membrane should be avoided.

Invasive procedure as FBS should not be used.
Neonatology should be informed.
 If recurrent genital lesion present at time of labour:
 C/S is not routinely recommended.
 The mode of delivery should be discussed with the woman and
individualized according to the clinical circumstances and the woman’s
preferences.
 Rupturing of membrane should be avoided.
 Invasive procedure as FBS should not be used.
 Neonatology should be informed .
 Suppressive daily acyclovir from 36 week may reduce the possibility of
active lesion at delivery.
Perinatal infections causing long term disease.
 HIV
 Hepatitis B
 Hepatitis C
HIV:
Is RNA retrovirus, transmitted by sexual contact ,blood &blood products, shared
needle.Vertical transmission which mainly occurs in the late third trimester ,
delivery or breast feeding.
Prevention:
 screening for HIV had been done routinely to all pregnant women in UK
 Because antenatal measures had been used to decrease the risk of mother to
child transmission from 30% to < 2%.
Antenatal care of women who are HIV positive:
 Management should be by a multidisciplinary team, including an HIV
physician, obstetrician, specialist ,midwife, health advisor and paediatrician
 Screening for other STD
 Contact tracing of sexual contact
 Screening the older childern of unknown HIV tracing
 Advice should be given about safer-sex practices and the use of condoms
Interventions to prevent disease progression in the mother:
 Women who require HIV treatment for their own health should take highly
active anti-retroviral therapy(HAART)
 continue treatment postpartum.
 They may also require prophylaxis against Pneumocystis carinii pneumonia
(PCP), depending on their CD4 lymphocyte count
Interventions to prevent mother to child transmission of HIV:
 Antiretroviral therapy given antenatally ( start at 20-28 weeks)and
antepartum to mother and to neonate for the 1st 4-6 weeks
 Delivery by elective C/S
 Avoidance of breast feeding
Neonatal management:
 Cord should be clamped as soon as possible
 Baby should be bathed immediately after delivery
 Antiretroviral therapy shuold be given to neonate for 1st 4-6 weeks
 Testing of neonate for infection by using PCR at birth ,3 weeks ,6 weeks &6
months.
Hepititis B:
 Is DNA virus
 Is transmitted by sexual contact ,blood &blood products, shared needle.
 vertical transmission which mainly occurs during delivery
 85% of infected babies will be carries.
Management:
Mother:
 Determination of infectious state for those with positive hepititis B
antibodies on antenatal screening.
 Screening for other STD
 Sexual and close household contacts must screened and vaccinated.
 Advice should be given about safer-sex practices and the use of condoms
 Baseline LFT
 Referral to hepatologist
Intervention to prevent transmission of infection to baby:
Intrapartum:
 FBS should be avoided
 Use of forceps rather than ventouse in operative delivery
Postpartum
 Passive immunization within 1st 24 hr should be given to baby
 Active immunization should be given to baby at birth , one month , six
month.
 Provided babies immunised,there is no contraindication to breast feeding.
Thank you