Perinatal infection tratment and complication

Perinatal infection

1. Perinatal infection
Dr. Alia kareem

2. Infections during pregnancy or around
delivery can adversely affect fetus, neonate
or causing long term diseases

3. 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.

4. Congenital Infections causing congenital
abnormalities.

—Rubella
—CMV
—chicken pox
—syphilis
—toxoplasmosis

5. •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 maculopapularrash
starting on forehead & spreading on trunk &limbs.

6. Fetal infection
—Malformations of congenital rubella can effect 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.

7. Fetal infection
—Risk of congenital rubella infection depends on gestational age:
80% in 1
st
trimester
25% at end of the 2
nd
trimester.
—the defect caused by rubella is also less severe with more advanced
gestations:
-100% of infant infected at 1
st
11 weeks have a rubella defect.
-16-20 weeks have minimal risk of deafness.
-After 20 weeks ,no documented risks to fetus.

8. Diagnosis of rubella:

vIn the mother:
ØDiagnosis is usually clinical.
Øacute 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.
vIn 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.

9. 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.

10. 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.

11. cytomegalovirus
—Is a DNA herpes virus
—Is transmitted by respiratory droplet, with sexual activity, blood
transfusion &organ transplantation.
—Vertical transmission can occur during pregnancy, delivery& beast
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.

12. Clinical features
vIn mother: asymptomatic or mild flue like illness.
vAbnormalities of congenital Infection can be seen in:
—The fetus on U/S:
( IUGR, microcephaly, ventriculomegaly, periventricular calcification,
intra-abdominal calcification, HSM, hydrops).
—The neonate: ( HSM, thrombocytopenia, jaundice, purpural rash
&anemia).
—Later on as blindness, deafness, developmental delay or mental
retardation, difficulties in learning.

13. diagnosis
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.

14. 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.

15. Chicken pox( varecilla-zoster virus)
—Is caused by varecilla-zoster virus, is a DS-DNA
herpesvirus.
—is transmitted by direct contact, airborntransmission
or in-uterotansmission.
—over 90% of the antenatal population are seropositive
for VZV immunoglobulin (IgG) antibody.
—it is estimated to complicate three in every 1000
pregnancies.

16. Clinical features
—In the mother :
—presents with a 1-to 2-day flulike prodrome, is
followed by pruriticvesicular 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.

17. —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
erythematousskin rash in a dermatomaldistribution
—known as herpes zoster (HZ), or simply zoster or
shingles.

18. In fetus
It depends on gestational age:
ØAt 1
st
28 weeks, there is 1% risk of fetal varicella syndrome
(FVS),which includes one or more of following:
—skin scarring in a dermatomaldistribution;
—eye defects (microphthalmia, chorioretinitis, cataracts);
—hypoplasiaof the limbs;
—Neurological abnormalities (microcephaly, cortical atrophy,
mental restriction and dysfunction of bowel and bladder
sphincters).

19. Atrophy of the lower extremity with bony defects and scarring

20. Ø28-36 weeks ,there is no affect on fetus
ØAt 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.

21. management
Diagnosis:
vIn 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.
vin the fetus:
—U/S findings of FVS.
—PCR on amnionticfluid or fetal blood sampling.

22. vPrevention:
—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.

23. —If contact with chicken pox occurs:
ØAsking about significant of contact(face to face or 15 min at
same room)
ØTesting for immunity by blood test for VZVIgG.
ØIf the pregnant women is not immune ,VZIG is available.
—It is effective when given in the 1
st
10 days of contact.
—It may prevent or attenuated the disease, therefore it should
be advised to notifying the doctor when a rash develops.

24. Managemantof pregnant women with chicken
pox:
vMother: 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 /5t daily, within 24hr of onset of rash & for
7 days.

25. —If the woman smokes cigarettes, has chronic lung disease,
is taking corticosteroids or is in the latter half of
pregnancy, a hospital assessment should be considered, even
in the absence of complications.
—Women should be referred immediately to a hospital:
1-if develop any of the following symptoms chest symptoms,
neurological symptoms, hemorrhagic rash or bleeding, a
dense rash with or without mucosal lesions.
2-women with significant immunosuppression should also
be referred.

26. Intrapartum:
—Delivery during the viraemicperiod 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.

27. —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.

28. —Fetus:
ØReferral to a fetal medicine specialist should be
considered at 16–20 weeks or 5 weeks after
infection for discussion and detailed ultrasound
examination.
ØAmniocentesis is not routinely advised because
the risk of FVS is so low, even when amniotic
fluid is positive for VZV DNA.
ØIt is not known whether VZIG reduces the risk of
FVS.

29. vNeonates:
—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.

30. Syphilis
—The causative agent for syphilis is Treponemapallidum.
—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.

31. Clinical presentation
—Maternal syphilis is staged according to clinical features and disease duration:
1.Primary syphilis may present as painless genital ulcer (chancre)
3-6 weeks after infection is acquired
2.Secondary syphilis occur 6w-6m after infection and present as:
-muculopapularrashsor mucoslesions.
-Condylomatalataare flesh-colored papules and nodules found on
the perineum and perianalarea
-Most women with secondary syphilis will also express
constitutional symptoms such as fever, malaise, anorexia,
headache, myalgias, and arthralgias.

32. 3-Latent syphilisdevelops when primary or secondary syphilis
is not treated.
-Early latent syphilisis latent disease acquired within the
preceding 12 months. -late latent syphilisDisease diagnosed
beyond 12 months
-latent syphilis of unknown duration.
4-Tertiary syphilis:
develops 3-10 years after initial stages.
20%of untreated patient will develop CV syphilis &5-10 % will
develop neurosyphilis.

33. Affects on fetus
ØRate of transmission of syphilis to fetus depends on the stage of
diseases.
ØIn 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.
ØBecause of fetal immunocompetenceprior to approximately 18
weeks, the fetus generally does not manifest the immunological
inflammatory response characteristic of clinical disease before this
time.

34. Affect on fetus
Damage to fetus depends on the stage of development
at which infection has taken place and time elapsed
before treatment.
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 2yo.

35. Early Congenital Syphilis
—Hepatosplenomegaly-diffuse
inflammation, scarring
—Jaundice –due to hepatitis
—Generalized lymphadenopathy–
epitrochclearnodes
—Coombs –hemolytic anemia,
thromobocytopenia, leukopenia, leukocytosis
—Mucocutaneous:rhinitis (highly
infectious), “snuffles”, mucous
patches
—Macuolpapularrash
—Desquamation
—Pemphigussyphiliticus(vesicular
bullouseruptions of palms and soles)
—Petechiallesions
—Bony lesions, osteochondritis,
periostitis, pseudoparalysis
—Syphilitcleptomeningitis
—Chorioretinitis,
Early manifestations are varied, with multi-system involvement

36. Papulosquamous Plaques

37. Broken vesicles, desquamation
Infiltration, desquamation and rhinitis

38. Rhinitis (snuffles), mucous patches,
damage to palate(late)
Bullae and vesicular rash on soles
Eroded papularlesions

39. Late Congenital Syphilis
—Interstitial keratitis(inflammatory)
—Nerve deafness
—Clutton’sJoints (synositis, restricted
movement)
—Hutchinson’s triad (teeth,
intersitialkeratitis, 8
th
nerve
deafness)
—Mental retardation
—Frontal bossing
—Saddle nose
—High arched palate
—Generalized paresis of insane
—Saber shine
—Gummata
Results primarily from chronic inflammation of bone, teeth,
and CNS.

40. Hutchinson’s teeth –peg shaped upper incisors
Frontal Bossing

41. Saber shins:
Anterior bowing of tibias
Gummata:
Thin atrophic scar

42. Diagnosis
Serologic tests are the principal means for diagnosis:
1)Nontreponemaltest: VDRL, RPR
2)Treponemaltests: TPI, FTA-ABS, MHA-TP
Definitive diagnosis can be made by dark-field microscopy
on specimen from skin lesions, placenta, umbilicus.

43. Diagnosis
Nontreponemal: VDRL, RPR
§ Quantitative results correlate with disease activity,
therefore helpful in screening.
§ Titers rise when disease is active, fall when
treatment is adequat
§ These tests become non-reactive
within a few months of adequate treatment.

44. Non-treponemal testing
§Detects antibodies against a cardiolipin-cholestrol-
lecithin complex, not specific for syphilis.
False Positives:
Only in serum, not in CSF testing
Ø certain viral infection: infectious
mononucleosis,
hepatitis, varicella, measles
Ø lymphoma, TB, malaria, endocarditis,
Ø connective tissue disease
Ø pregnancy (?)
ØVery early or
late diseases
ØHIVpostive
ØReinfection
:False negatives

45. Confirmatory Testing
§TreponemalTests: TPI, FTA-Abs,
MHA-TP
§Detect specific treponemalantibody
§They become positive soon after initial
infection and usually remain positive
for life, even with adequate therapy.
§They do not correlate with disease
activity, and are not quantified.
§Not 100% specific for syphilis: other
spirochetes.

46. .The prenatal diagnosis of congenital syphilis :
ØSonographicevaluation may be suggestive or even
diagnostic.
Øhydropsfetalis, ascites, hepatomegaly, placental
thickening, and hydramniosall suggest infection.
ØPCR is specific for detection of T. pallidumin
amnionicfluid, and treponemalDNA has been found
in 40 percent of pregnancies infected before 20 weeks.

47. management
—Confirm diagnosis
—Testing for other STD
—Contact tracing of sexual partner
—Screening for congenital syphilis in older children.
—Paranteralpencillineis effect in 98% in prevent cong.syphilis.
—In most women with primary syphilis and approximately half with
secondary infection, penicillin treatment causes a Jarisch-Herxheimer
reaction.
—Uterine contractions frequently develop with this reaction, and they may
be accompanied by late fetal heart rate decelerations.
—Women who is not treated during infection, the baby should treated after
delivery.

48. toxoplasmosis
—Is caused by Toxoplasmagondii, it has a complex
life cycle with three forms:
—(1) a tachyzoite, which invades and replicates
intracellularlyduring infection,
—(2) a bradyzoite, which forms tissue cysts during
latent infection, and
—(3) a sporozoite, which is found in oocyststhat
can be environmentally resistant

49. Life cycle of toxoplasmagondi

50. Clinical picture
vIn mother :
—Asymptomatic
—Flue like illness with LAP Infection
—in immunocompromisedwomen,
however, may be severe, with reactivation
involving encephalitis or mass lesions.

51. vIn the fetus:
—In acute infection, transmission and
severity of damage depend on gestational
age.
—In 1
st
trimester, 10% of infection is
transmitted but 85% of those have sever
damage.
—In 3
rd
trimester, 85% of infection is
transmitted but risk of dammagereduces
to10%.

52. —Congenital infection may lead to miscarriage , preterm labour.
—At neonate, anemia, HSM. jaundice
—Severlyinfected infant may have:
—Ventriculomegaly
—Microcephaly
—hydrocephaly
—Chorioretenites
—Cereberalcalcification
—Majority of infected infants may be asymptomatic at birth but
develop sequleelater on in life.

53. diagnosis
—Seriologicaltests
—IgGappear after 2 weeks and persist for life with life long immunity.
—IgGavidity is low in acute infection and andincreases over weeks and months.
—If high-avidity IgGis determined, infection within the preceding 3 to 5 months is excluded
—IgMis appear after 10 day and may persist for years.
§panel of tests Include Sabin Feldman dye test, double-sandwich IgMELISA, IgAand
IgGELISA, IgGavidity test and a differential agglutination test.
§they used to differentiate acute from chronic infection .

54. Prenateldignosis
—PCR of amnionicfluid or fetal blood
—Sonographicevidence of intracranial
calcifications, hydrocephaly, liver
calcifications, ascites, placental
thickening, hyperechoicbowel.

55. treatment
—Spiramycinis 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 folinicacid are
used to eradicate parasites in the placenta and fetus.
—Termination of pregnancy is offer if infection occur in 1st
trimester or in U/S evidence of congenital infection.

56. Congenital infection associated with pregnancy
loss and preterm labor.

I.Parvovirus B19
II.Listeriosis

57. Human parvovirus B19(erythema
infectiosum; fifth disease)
—It is SS DNA virus,
—transmitted by respiratory droplet or in utero
transmission
—50% of women at reproductive age are
susceptible to infection.
—It is most common in those who work with
young children like teachers.

58. Clinical presentation
—In adult:
—Asymptomatic
—Flue like illness with rash
In childern:
characteristics malarrash(slapped check syndrome)
Infetus:
§Miscarriage ,stillborn
§Hydropsfetalismay develop within10 weeks after maternal
infection.

59. Hydropsfetalis

60. Hydropsmacerated baby

61. Algorithm for evaluation and management of
human parvovirus B19 infection in pregnancy

62. listeria
•Is caused by Listeriamonocytogenes
•Listeriamonocytogenesis aerobic and facultative anerobic
intracellular gram +vebacillus.
•People with reduced celullarimmunity is more susceptible
e. g pregnant women & elderly people .
•It is food born infection transmitted by ingestion of chilled
food like milk ,soft cheese.
•Transmission to fetus can occur by ascending route through
cervix or can occur tranceplacently.

63. Clinical presentation
vIn mother:
—Asymptomatic
—Flu like ilness
vIn fetus:result in to :
—20% miscarriage or stillbirth.
—50% premature delivery.
vIn the neonate: RDS, sepsis, neurological symptoms.
neonatal mortality is 38%.

64. stillborn fetus due to listeriosis

65. managemant
—Diagnosis depends on clinical suspicion.
—Meconium staining of amniotic fluid in preterm
increases the clinical suspicion.
—Diagnosis is confirmed by culturing the organism
from blood, vaginal swabs or placenta.
—Treatment of infection during pregnancy is by IV
pencillin( ampicilline2g /6hr) .

66. Infections acquired around the time of delivery
with serious neonatal consequences.

I.Herpes simplex
II.Group B streptococcus
III.Chlamydia& gonorrhea

67. herpes
—Iscaused 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.

68. —Neonatal herpes caused by direct contact with
infected maternal secretions during derlivery.
—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%).

69. Clinical presentation
vIn mother :
—Ulcerative lesion on vulva ,vagina or cervix
—Primary infection is associated with systemic infection or
urinary retention.
vIn the fetus: Primary infection may lead to:
•miscaraige,stillbirth or
•IUGR,
•preterm labour.

70. vIn neonate: neonatal herpsemay present in three
forms:
1.Localized: to skin , eye and mouth( mortality
rare , neurological morbidity<2%).
2.Local CNS disease:(mortality 6% ,
neurological morbidity 70%).
3.Disseminated diseases: ( mortality 30% ,
neurological morbidity 17%).

71. Management
ØThe diagnosis :
-Is suggested by clinical presentation.
-Is confirmed by viral culture or PCR on
lesions swab.
ØScreening for other STD.
ØAcyclovir(200mg/5 times daily for 5
days) .

72. 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 FSE or FBS should not
be used.
§Neonatology should be informed .

73. —If recurrent genital lesion present at time of labour:
ØCIS is not routinely recommended.
ØThe mode of delivery should be discussed with the woman
and individualized according to the clinical circumstances
and the woman’s preferences.
ØRupturing of membrane should be avoided.
ØInvasive procedure as FSE or FBS should not be used.
ØNeonatology should be informed .
ØSuppressive daily acyclovir from 36 week may reduce the
possibility of active lesion at delivery.

74. Group B Streptococcus
—Is gram positive coccus.
—Is frequently found as vaginal commensalin about
25% of women.
—It can cause sepsis to neonate.
—It is most frequent cause sever early onset infection
to neonate (6% mortality at term&18% at preterm).
—Transmission to neonate can occur from the time the
membranes are rupture till delivery.

75. Prevention
—Intrapartumantibiotic prophylaxis to women with risk factors .
Risk factors are :
—Intrapartumfever >38 c
—Prolong rupture of membrane > 18 hr
—Prematurity <37 weeks
—Previous infants with GBS
—Incidental detection of GBS in current pregnancy
—GBS bacteruria.

76. —According to this approach:
—3% of women will receive intrapartum
antibiotic.
—with 51%reduction of early onset GBS
neonatal disease.

77. Prophylactic antibiotic
—IV pencilline3g immediately after the
onset of the labour&then 1.5 g/4hr until
delivery.
—Clindamycine900mg /8hr to those who
allergic to pencilline.

78. Chlamydia & gonorrhea
—Are STD.
—Chlamydia trachomatisis the cause of Chlamydia.
—Neisseriagonorrhea is the cause of gonorrhea
—Are transmitted to fetus during delivery.
—Chlamydia may cause conjuctivis& pneumonia
in the neonate.
—gonorrhea may cuaseophthalmianeonatotrum.

79. Perinatalinfections causing long term disease.

—HIV
—Hepatitis B

80. HIV
—Is RNA retrovirus.
—Is transmitted by sexual contact ,blood
&blood products, shared needle.
—vertical transmission which mainly occurs
in the late third trmester,labourdelivery
or breast feading.

81. Clinical presntation
—Infection begins asymptomatic.
—Gradual comprised immunity
—That leading to aquiredimmunedeficiency
syndrome (AIDS)
—Development of AIDS required few
months to as long as 17 years in
untreated pateint.

82. prevention
—screening for HIV had been done
routinely to all pregnant women in UK
—Because antenatal measures had been
used to decreeasethe risk of mother to
child transmission from 30% to < 2%.

83. 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 childernof unknown
HIV tracing
—Advice should be given about safer-sex
practices and the use of condoms

84. 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
Pneumocystiscariniipneumonia(PCP),
depending on their CD4 lymphocyte
count

85. Interventions to prevent
mother to child transmission of
HIV
—Antiretroviral therapy given antenatally(
start at 20-28 weeks)and antepartumto
mother and to neonate for the 1
st
4-6
weeks
—Delivery by elective C/S
—Avoidance of breast feeding

86. infant management
—Cord should be clamped as soon as
possible
—Baby should be bathed immediately after
delivery
—Antiretroviral therapy shuoldbe given to
neonate for 1
st
4-6 weeks
—Testing of neonate for infection by using
PCR at birth ,3 weeks ,6 weeks &6
months.

87. HepititisB
—Is DNA virus
—Is transsmittedbysexualcontact ,blood
&blood products, shared needle.
—vertical transmission which mainly occurs
during delivery8labour delivery
—85% of infected babies will be carries.

88. Managemat
Mother:
—Determingof infectious state for those of
postivehepititisB 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

89. Intervention to prevent transmission of infection to
baby
Intrapartum:
—FSE&FBSshuoldbe avoided
—Use of forceps rather than ventous in IVD
Postpartum
—Passive immunisationwithin 1
st
24 hr shuold
be given to baby
—Active immunization should be given to baby
at birth , one month , six month.
—Provided babies immunised,thereis no
contra indication to breast feeding.

90. Thank you