Infection in Pregnency

8/13/2019 Infection in Pregnency

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Infection in pregnency

23-06-2553


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Case presentation


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Some significant infections inpregnancy TOxoplasmosis

Rubella

CMV

Herpes (vericallar zoster/chiken pox/HSV)

Sypilis

Hepatitis/HIV


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ToxaplasmosisCaused by protozoanToxoplasma gondii

Domestic cat is the definitive host


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Toxaplasmosis A parasitic infection

Incidence 1-5/1,000 of pregnancy

Symptom

malaise, infectious mononucleosis syndrome

Infection rates for exposed fetuses may be as

high as 30-40% throughout pregnancy


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Toxaplasmosis >75% of exposed fetuses unaffected

10% have severe disease

T1 infection risk low (15%) but if infected >60%damage (abort, preterm labour)

T2 intermediate risk of infection and damage

T3 high risk of infection but


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Clinical 12% mortality

Chorioretinitis Hydrocephaly Intracranial calcifications Microcephaly Thrombocytopaenia Anaemia Hydrops

80% of infants with severe infection show ocularand CNS abnormalities Apparently asymptomatic infants at risk for later

development of mental retardation, deafness andocular problem

Classic triad


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Chorioretinitis of congenital toxo


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Diagnosis Maternal

Serum IgM, IgG

Prenatal diagnosis

Cordocentesis, amniocentesis for IgM,Toxoplasmosis PCR

Ultrasound: Random brain calcifications

Cataracts and microcephaly

Polyhydramnios

Placentomegaly

Hepatosplenomegaly


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RubellaSingle-stranded RNA virus


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Rubella Infection in pregnancy Symptom

14-21 days incubation => fever, malaise,upper respiratory

inflammation, lymphadenopathy

Fine pink maculopapular rash

Contact


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Diagnosis(RASH)RASH 1 Titer 2 Titer (1wk) Definite< 3 day < 1:8 Eqaul No

< 1:8 4 fold Yes3-7 day 1:64 increase +/- => IgM

> 7 day 1:64 +/- => IgM


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Diagnosis (Contact)1 Titer 2 Titer (1 month) Definite< 1:8 Eqaul No< 1:8

4 fold

Yes

> 1:8 Eqaul Immune> 1:8 1:64 +/- => IgM


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Typical Serological Events following

acute rubella infection

Note that in reinfection, IgM is usually absent or only present transiently at a low level


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Congenital Rubella SyndromeClassical triad consists of cataracts, heart defects, and sensorineural

deafness. Many other abnormalities had been described and these are

divided into transient, permanent and developmental.

Transient

low birth weight, hepatosplenomegaly, thrombocytopenic purpura

bone lesions, meningoencephalitis, hepatitis, haemolytic anemia

pneumonitis, lymphadenopathy

Permanent Sensorineural deafness, Heart Defects (peripheral pulmonarystenosis, pulmonary valvular stenosis, patent ductusarteriosus, ventricular septal defect) Eye Defects (retinopathy,

cataract, microopthalmia, glaucoma, severe myopia) Other Defects(microcephaly, diabetes mellitis, thyroid disorders, dermatoglypticabnormalities

DevelopmentalSensorineural deafness, Mental retardation, Diabetes Mellitus,(ERS) thyroid disorder


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Blueberry muffin spots representing

extramedullary hematopoesis


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Prevention

Antenatal screening

All pregnant women attending antenatal clinics are

tested for immune status against rubella.

Non-immune women are offered rubella vaccination in

the immediate post partum period.


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Management Immunization

Primary infection (< 16 wk)

Termination(immediate or closely follow-up byu/s)

Prenatal diagnosis (Cordocentesis for IgM)


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CMVInfection in theimmunocompetent host is

generally asymptomatic or maypresent as a mononucleosissyndrome.


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CMV Most common perinatal infection (1-2%)

10% have cytomegalic inclusion disease

Transmitted by infected saliva, breast milk, sexually

and through infected blood

Highly transmitted in first trimester


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Congenital infectionCMV

infection

90%

Asymptomaitc

90%

Normaldevelopment

10%

Late sequelae

10%

symptomatic

Mostlysequelae


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CMVNeed to differentiate between primary & recurrent

CMV

Primary CMV: 40-50% of babies are congenitally

infected(LEADING CAUSE OF CONGENITAL

INFECTION)

Recurrent CMV: 1.5% of babies arecongenitally

infected

Risk mainly in first trimester: termination ofpregnancy should be considered


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CMV How do we tell between primary and recurrent

CMV?

IgM seroconversion

IgG avidity testing

Isolation of virus from blood

Amniocentesis


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Management

Primary Infection - consider termination of pregnancy. 40% chance of the fetus being infected.

10% chance that congenitally infected baby will be

symptomatic at birth or develop sequelae later in life.

Recurrent Infection - termination not recommended

as risk of transmission to the fetus is much lower.

Antenatal Screeningimpractical.

Vaccination - may become available in the near future.


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Varicella-Zoster Virus

90% of pregnant women already immune, thereforeprimary infection is rare during pregnancy

Primary infection during pregnancy carries a greater riskof severe disease, in particular pneumonia


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Varicella-Zoster Virus

First 20 weeks of Pregnancy (high risk = 13-20 wk)

up to 2-5% chance of transmission to the fetus,

recognised congenital varicella syndrome;

Scarring of skin

Hypoplasia of limbs

CNS and eye defects

Death in infancy normal

5 day before and 2 day after

30 % severe congenital vericella syndrome

Abort

DFIU

Preterm IUGR


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Management Primary contact

VZIG in 96 hr

Chicken pox

Risk management

Acyclovir if maternal sever symptom

In perinatal : VZIG for naonatal Herpes zoster Low risk


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Herpes simplex


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Herpes Simplex

Main risk is primary infection during pregnancy Primary = 30-50% infected

Recurrent = 3-5% infected

The baby is usually infected perinatally duringpassage through the birth canal.

Risk factor

Premature rupturing of the membranes

Many lesion

Preterm

Fetal scalp electrode


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Affect to pregnancy Abortion risk 3 times

Congenital & Perinatal infection Vesicular skin lesions, atypical pustules, bullous lesions

Seizures (herpes encephalitis): wk 2 or 3

Unexplained sepsis

Low platelets, elevated LFTs, DIC

Late respiratory distress Corneal ulcers or keratitis


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Management Local treatment

Antiviral

Indicated in sever case only (CAT C)

For infected neonate (IV acyclovir) Route of delivery

No lesion, no C/S


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Syphilis


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Syphilis Early -> transmittion rate is higher

Primary

Darkfield

Secondary VDRL, FTA-ABS, TPHA

Late

routine serologic screening of pregnant womenduring the first prenatal visit


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Congenital SY Congenital syphilis results from transplacental infection

T. pallidumsepticemia in the developing fetus and

widespread dissemination

Abortion, neonatal mortality, and late mental or physical

problems resulting from scars from the active disease and

progression of the active disease state

Severity Congenital SY

mostly appear after 16 wk

Maternal severity of symptom

Maternal adequacy of treatment


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Congenital Syphilis

Fetal:

Stillbirth

Neonatal death

Hydrops fetalis

Intrauterine death in 25%

Perinatal mortality in 25-30% if untreated


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Congenital Syphilis 2/3 of affected live-born infants are asymptomatic atbirth

Clinical symptoms split into early or late (2 years iscut off)

3 major classifications: Fetal effects

Early effects Late effects


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Clinical Manifestations Early congenital (typically 1st5 weeks): Cutaneous lesions (palms/soles)

HSM Jaundice

Anemia

Snuffles

Periostitisand metaphysial dystrophy Funisitis (umbilical cord vasculitis)


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Periostitis of long bones seen

in neonatal syphilis


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Clinical Manifestations

Late congenital:

Frontal bossing

Short maxilla

High palatal arch

Hutchinson teeth

8thnerve deafness

Saddle nose

Perioral fissures

Can be prevented with appropriate treatment


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Hutchinson teethlate result of

congenital syphilis


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Congenital SY Confirmed if T. pallidum identified in skin lesions,placenta, umbilical cord, or at autopsy

Presumptive diagnosis if any of: 1) Inadequate treatment

2) reactive treponemal test plus

Physical examination

Long bone x-ray (osteitis) CSF VDRL/CSF infection

RPR/VDRL >4 times maternal test

IgM positive


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Inconclusion TORCHS screening

Do not use TORCH titer as routine

Good maternal/prenatal history

Remember most infections of concern are mild

illnesses often unrecognized

Thorough exam of infant

Directed labs/studies based on most likely diagnosis


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Infection in Pregnency

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