Infection in pregnency

23-06-2553

Case presentation

Some significant infections in pregnancy

TO xoplasmosis R ubella C MV H erpes (vericallar zoster/chiken pox/HSV) S ypilis

Hepatitis/HIV

Toxaplasmosis
Caused by protozoan Toxoplasma gondii Domestic cat is the definitive host

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

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 <10% damage

Clinical
12% mortality
Chorioretinitis Hydrocephaly Intracranial calcifications Microcephaly Thrombocytopaenia Anaemia Hydrops Classic triad

80% of infants with severe infection show ocular and CNS abnormalities Apparently asymptomatic infants at risk for later development of mental retardation, deafness and ocular problem

Chorioretinitis of congenital toxo

Diagnosis
Maternal
Serum IgM, IgG

Prenatal diagnosis
Cordocentesis, amniocentesis for IgM, Toxoplasmosis PCR Ultrasound:
Random brain calcifications Cataracts and microcephaly Polyhydramnios Placentomegaly Hepatosplenomegaly

Management
TOP if ultrasound abnormal, prenatal dx In the absence of sonographic anomalies,
aggressive maternal treatment with pyrimethamine and sulfadiazine or Spiramycin may reduce the fetal risk

Rubella
Single-stranded RNA virus

Rubella Infection in pregnancy

Symptom
14-21 days incubation => fever, malaise,upper respiratory inflammation, lymphadenopathy Fine pink maculopapular rash

Contact

Risks of rubella infection during pregnancy

Preconception 0-12 weeks minimal risk 100% risk of fetus being congenitally infected resulting in major congenital abnormalities. Spontaneous abortion occurs in 20% of cases. deafness and retinopathy 15% normal development, slight risk of deafness and retinopathy

13-16 weeks after 16 weeks

Diagnosis(RASH)
RASH 1 Titer 2 Titer (1wk) Definite

< 3 day
3-7 day

< 1:8
< 1:8 <1:8 1:8 1:32 >1:64

Eqaul
4 fold Eqaul Eqaul increase

No
Yes No Immune +/- => IgM No Immune +/- => IgM

> 7 day

<1:8 1:8 1:32 >1:64

Diagnosis (Contact)
1 Titer < 1:8 < 1:8 > 1:8 > 1:8 2 Titer (1 month) Eqaul 4 fold Eqaul 1:64 Definite No Yes Immune +/- => IgM

Typical Serological Events following acute rubella infection

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

Congenital Rubella Syndrome

Classical 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 Sensorineural deafness, Heart Defects (peripheral pulmonary stenosis, pulmonary valvular stenosis, patent ductus arteriosus, ventricular septal defect) Eye Defects (retinopathy, cataract, microopthalmia, glaucoma, severe myopia) Other Defects (microcephaly, diabetes mellitis, thyroid disorders, dermatoglyptic abnormalities

Permanent

Developmental Sensorineural deafness, Mental retardation, Diabetes Mellitus,

(ERS) thyroid disorder

Blueberry muffin spots representing extramedullary hematopoesis

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.

Management
Immunization Primary infection (< 16 wk)
Termination(immediate or closely follow-up by u/s) Prenatal diagnosis (Cordocentesis for IgM)

CMV
Infection in the immunocompetent host is generally asymptomatic or may present as a mononucleosis syndrome.

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

Congenital infection
CMV infection

90% Asymptomaitc

10% symptomatic

90% Normal development

10% Late sequelae

Mostly sequelae

Cytomegalic Inclusion Disease

CNS abnormalities - microcephaly, mental retardation, spasticity, epilepsy, periventricular calcification. Eye - choroidoretinitis and optic atrophy Ear - sensorineural deafness Liver - hepatosplenomegaly and jaundice which is due to hepatitis.

Lung - pneumonitis
Heart - myocarditis Thrombocytopenic purpura, Haemolytic anaemia Late sequelae in individuals asymptomatic at birth - hearing defects and reduced intelligence.

CMV
Need 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 of pregnancy should be considered

CMV
How do we tell between primary and recurrent CMV?
IgM seroconversion IgG avidity testing Isolation of virus from blood Amniocentesis

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 Screening impractical. Vaccination - may become available in the near future.

Herpes
VZV & HSV

Varicella-Zoster Virus
90% of pregnant women already immune, therefore primary infection is rare during pregnancy Primary infection during pregnancy carries a greater risk of severe disease, in particular pneumonia

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 Abort Hypoplasia of limbs DFIU CNS and eye defects Preterm Death in infancy normal IUGR

5 day before and 2 day after 30 % severe congenital vericella syndrome

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

Herpes simplex

Herpes Simplex
Main risk is primary infection during pregnancy
Primary Recurrent = 30-50% infected = 3-5% infected

The baby is usually infected perinatally during passage through the birth canal.
Risk factor
Premature rupturing of the membranes Many lesion Preterm Fetal scalp electrode

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

Diagnosis
History Sign and symptom LAB
Pap smear Tzancks test ELISA

Management
Local treatment Antiviral
Indicated in sever case only (CAT C) For infected neonate (IV acyclovir)

Route of delivery
No lesion, no C/S

Syphilis

Syphilis
Early -> transmittion rate is higher
Primary
Darkfield

Secondary
VDRL, FTA-ABS, TPHA

Late routine serologic screening of pregnant women during the first prenatal visit

Congenital SY
Congenital syphilis results from transplacental infection

T. pallidum septicemia 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

Congenital Syphilis
Fetal:
Stillbirth Neonatal death Hydrops fetalis

Intrauterine death in 25% Perinatal mortality in 25-30% if untreated

Congenital Syphilis
2/3 of affected live-born infants are asymptomatic at birth Clinical symptoms split into early or late (2 years is cut off) 3 major classifications:
Fetal effects Early effects Late effects

Clinical Manifestations
Early congenital (typically 1st 5 weeks):
Cutaneous lesions (palms/soles) HSM Jaundice Anemia Snuffles Periostitis and metaphysial dystrophy Funisitis (umbilical cord vasculitis)

Periostitis of long bones seen in neonatal syphilis

Clinical Manifestations
Late congenital:
Frontal bossing Short maxilla High palatal arch Hutchinson teeth 8th nerve deafness Saddle nose Perioral fissures

Can be prevented with appropriate treatment

Hutchinson teeth late result of congenital syphilis

Adequate treatment
Early Late : Penicillin G 2.4 milliunit IM once : Penicillin G 2.4 milliunit IM once a week x 3 wks Repeat VDRL at 6&12 months

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

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