1. Infections in Pregnancy, Foetus
and Neonates
Dr. Devika Iddawela
Department of Parasitology
Y3S2

2. Objectives
List common infections in pregnancy, and Neonates
Know the principals of diagnosis, management and
prevention of those
Revise information on TORCH screening

3. Fetal and Neonatal infection
Infections occur in the pre, peri and post natal
periods
Baby tends to be susceptible because of
 Immature host defense
 Primary encounter with the organism
 Passive immunity from the maternal
antibodies

4. Modes of transmission
Vertical transmission – transmission that is unique to
a mother/baby relationship.
Note: All neonatal infections where mother is a
source are transmitted vertically
In utero
(congenital)
Ascending
transplacental
Intra partum Genital
Post
partum
mother
Other

5. Viruses
Rubella
Cytomegalovirus
(CMV)
Parvo virus B 19
Varicellar Zoster
Hepatitis B virus
HIV
Maternal infections transmitted to foetus
Spirochetes
Treponema Pallidum
Listeria
monocytogenes
Bacteria
Micobacterium leprae
Group B streptococci
Tissue protozoa
Toxoplasma Gondii

6. Site of infection Phenomenon
Neisseria gonorrhoea Conjunctiva Neonatal conjunctivitis (NC)
Clamydia trachomatisConjunctiva, NC, Pneumonia
respiratory tract
HSV Skin, Eye, mouth Neonatal herpetic
infection
Genital Papilloma virus Res. Tract Laryngeal warts
Group B sreptococci, RT septicemia
gram-negative bacilli
Candida albicans Oral cavity Neonatal oral thrush
Neonatal infections acquired during passage down an
infected birth canal

7. Infections that are more severe in pregnancy
Infection Comment
Malaria CMI,
Choice of treatment
Viral hepatitis - Fulminant liver necrosis
Influenza Increased mortality
Poliomyelitis Paralysis common
UTI Cystitis; pyelonephritis more
common, atony of bladder and
uterine pressure leads to less
effective flushing, empting

8. Reactivation or persistent infections in
Pregnancy
• CMV
• EBV
• HSV

9. Rubella
RNA virus
Clinical features:
 Maculopapuar rash
 Lymphadenopathy
 Fever
Arthropathy
affect anyone of any age and
is generally a mild disease,

10. Risks of rubella infection during pregnancy
Preconception minimal risk
0-12 weeks 100% risk of fetus being congenitally
infected resulting in major
congenital abnormalities.
Spontaneous abortion occurs in 20%
of cases.
13-16 weeks deafness and retinopathy 15%
after 16 weeks normal development, slight risk
of deafness and retinopathy

11. Congenital rubella syndrome
Classical triad
 Cataract
 Heart defects
peripheral pulmonary stenosis,
pulmonary valvular stenosis,
patent ductus arteriosus,
ventricular septal defect)
 Sensorineural deafness

13. Organ involved effect
Brain Small brain, mental retardation
Eye retinopathy, Cataract,
micropthalmia
ear Hearing defects
Sensorineural deafness
Liver, spleen Hepatosplenomegaly
Thrombocytopenic purpura
anaemia
General Low birth weight
Failure to thrive
Increased infant motility

14. Laboratory diagnosis
Acute infection
Raising titres of IgG – ELISA
Presence of Rubella specific IgM -ELISA
The diagnosis of congenitally acquired rubella is made by;
• The presence of rubella IgM in cord blood or serum samples
taken in infancy.
• Detection of rubella antibodies at a time when maternal
antibodies should have disappeared (approx.6 months of age)
•Isolation of rubella virus from infected infants in the first few
months of life.

15. Prevention
Vaccination - Live attenuated vaccine
in childhood or immediately post
partum
avoid pregnancy for 3 months

16. Cytomegalovirus
• DNA virus ,member of the herpesvirus
• primary infection usually asymptomatic. Virus
then becomes latent and is reactivated from time
to time.
• 60% of the population eventually become
infected.
• Virus is generally passed from infected people to
others through direct contact with body fluids, such as
urine, saliva, or breast milk, vaginal secretions, semen

17. •
Foetus can be infected by-
 transplacetal route
Primary maternal infection during first half
of pregnancy ( higher)
Reactivation
May be transmitted to the foetus during all
stages of pregnancy.
 Perinatal infection: Infected maternal
genital tract secretions, breast feeding

18. Defined as the isolation of CMV from the saliva or urine
within 3 weeks of birth.
Commonest congenital viral infection,
affects 0.3 - 1% of all live births.
The second most common cause of mental handicap after
Down's syndrome and is responsible for more cases of
congenital damage than rubella.
Congenital Infection

19. Mental Retardation,
Cerebral Palsy, periventricular calcification
most commonly, hearing impairment
Eye abnormalities –Chorioretinitis
Hepatoslenomegaly, thrombocytopenic purpura
CMV retinitis
Clinical manifestations

20. SEVERE CONGENITAL CMV INFECTION

21. TRANSPLACENTAL TRANSMISSION
PRIMARY MATERNAL INFECTION:
2-6% mothers/yr seroconvert in pregnancy
Transmission 40 – 50 %
Earlier mat. inf. = more severe the fetal inf.
RECURRENT MATERNAL INFECTION:
Transmission 0.5-1.5%
most infants asymptomatic
Infection acquired during delivery or via
breast feeding poses negligible risk

22. DIAGNOSIS OF CONGENITAL CMV INFECTION IN FOETUS
Amniocentesis - viral culture and PCR
Ultrasound
Cerebral
calcification

23. Diagnosis in neonate
a diagnosis can only be made if the virus is detected within
2-3 weeks of life.
 Isolation of CMV from urine, saliva and throat swab of
the neonate
 Presence of CMV IgM
Management
Primary infection – consider termination
Antenatal screening
Vaccination- may become available
in the near future
Treatment for Babies Born with CMV
Ganciclovir, an antiviral drug, may prevent hearing
loss and developmental outcomes in infants
However it has serious side effects
Antibody tests of mother cannot be used to diagnose congenital
CMV

24. Neonatal herpes simplex
Intrauterine (5%), peripartum During delivery (85%), or
postpartum (10%)
Transmission during birth is the commonest
If the lesions are present, cesarean section may
reduce the chance of transmission
Primary infection make more damage than
secondary infection because of large viral load
Premature rupture of membrane is a risk factor
Risk is small from recurrent infections in the
mother due to low viral load & antibodies

25. Clinical presentation
1. skin, eyes, and mouth herpes (SEM)
Most are asymptomatic at birth
3 clinical presentations between birth and 4 weeks patterns of

26. 2.disseminated herpes (DIS) –
Involve the liver, Lung, adrenals
&brain
3. central nervous system
herpes(CNS)- when the brain is
involved prognosis is bad

28. A large number of survivors of HSV
infection have residual disabilities
Acyclovir should be given to all
suspected cases of neonatal HSV
infection

29. Varicella Zoster ( Chicken pox)
Maternal Inf Potential consequences
<20 wks gest Spont abortion
Fetal Varicella Syn - 2%
any stage Fetal death,
herpes zoster 1st yr of life
Near term
5d<delivery
2d>delivery
Cong disseminated varicella
Varicella pneumonia
(can be fatal)

30. Low birth weight
Skin: Cicatricle lesions
in dermatomal distribution
Bone: Limb hypoplasia
equinovarus, calcaneovalgus;
hypoplasia mandible, clavicle, scapula,
digits.
CNS: MR, seizures, cortical atrophy
Eye: chorioretinitis, nystagmus,
microphthalmia, cataract,
corneal opacities, optic atrophy
FETAL VARICELLA SYNDROME - FVS

31. Varicella Zoster immunoglobulin (VZIG) and early anti
viral treatment should be given according to state of
infection
State Rx
Mat exposure VZIG - non-immune mother
Mat infection
(Prevent FVS)
Acyclovir to Rx mother
VZIG to the risk FVS
Mat infection
5d before
or 2d>delivery
Acyclovir to mother
VZIG to neonate
Neonatal varicella
(life-threatening)
IV Acyclovir
(VZIG at birth)

32. Parvovirus B19
Casual agent of 5th disease ( erythema infectiosum)
Spread by the respiratory route. 60 -70% of the
population is infected
Congenital parvovirus infection
Cause hydrops fetalis, haemolytic anaemia, myocarditis,
abortions
Risk of foetal death highest when infection occurs during the
second trimester

33. Spontaneous resolution of anemia and
hydrops often occurs if > 20 wks
Fetus can rapidly deteriorate and should be
monitored
If fetal anemia or hydrops persists determine
fetal hemoglobin level.
If fetal Hgb is <5 g/dL
consider intrauterine blood transfusion

34. Congenital syphilis
Vertical transmission commonly occur after 4
months of pregnancy.
Treatment of mother before 4 months of
pregnancy prevent foetal infection
Clinical features in infants:
Rhinitis
Skin & mucosal lesions
Hepatosplenomegaly
Lymphadenopathy
Abnormalities of bone , teeth and
cartilage( Saddle shaped nose)

36. Congenital syphilis which may not be apparent until
about 2 years of age ( facial and tooth abnormalities
prevented by early detection of maternal infection ( <3 months) &
Treatment of positives with penicillin.

37. • During Pregnancy 30%
• Intrapartum 70%
• Breast feeding
excess risk to uninfected = 12 –
14%
Human immunodeficiency virus
Vertical HIV transmission can occur
in utero, during delivery and
during breastfeeding

38. Risk Increased, if:
Prolonged labor
Preterm delivery
Invasive procedures
Chorioamnionitis
Advanced maternal disease, low CD4
Risk Reduced, if:
Antiviral Rx
Elective CS before labor/ROM
INTRAPARTUM RISK FACTORS

39. Clinical problems :appear sooner in infected
baby than in adult AIDS (e.g. at aged 6
month)
with:
- hepatosplenomegaly - failure to thrive -
encephalopathy - recurrent fever -
respiratory diseases (interstitial lymphocytic
pneumonitis) –
septicemia (salmonella) - pneumocystis
- lymphadenopathy.
Death is usually from respiratory failure or
overwhelming infection( 20% at 18 months

40. Hepatitis B
Vertical transmission specially in the third trimester
In acute infection and in chronic infection
Screening: Routine HBsAg (performed in 1st
trimester)
.
Prevention: HBIG (Hepatitis B immune
globulin) and HBV vaccine should be given
to baby at birth.
If non-immune mother exposed in
pregnancy give HBIG and HBV vaccine.
Complications: may cause Hepatitis ,Cirrhosis and/or
liver cancer (as an adult at age of 30- 40 years)·

41. Gonorrhea
Infection through birth canal
Can lead to
Conjunctivitis ( ophthalmia neonatorum)
Arthritis
Meningitis

42. Group B Streptococci ( GBS)
 5 -20% of ladies carry GBS in vagina
 Infection is through birth canal
 Is associated with PROM
 Can lead to neonatal meningitis, pneumonia,
sepsis
 Intrapartum prophylaxis is indicated for carriers

43. Urinary tract Infection
Dilatation of ureters and pelvis
Reduction of bladder tone
Pressure from the gravid uterus
Due to :
Bacteriology – similar to non pregnant women
Asymptomatic bacteriurea unless treated a significant proportion
would develop pyelonephritis and this in turn is associated with
adverse pregnancy outcomes
Treatment – antibiotics should be given with care

44. Maternal parasitaemia and subsequent
placentitis
Maternal infection in early pregnancy –
Foetal damage
Transmission
Congenital toxoplasmosis
Due to Primary maternal infection

45. CF ranges from death in utero to an infected but
clinically unaffected child
Sever congenital toxoplasmosis -10% of all
congenital infected infants ( Classical triad)
Hydrocephalus
Cerebral calcification
Retinochoroiditis
Skin rash, hepatitis, pneumonia, myocarditis and myositis
May be present
Can develop ocular disease in later life
Sever congenital eye manifestations: Microphthalmia,
cataract, strabismus and nystagmus

46. Hydrocephalus
Intracranial caicification Retinochoroiditis

47. TOXO – PRENATAL DIAGNOSIS
• Amniotic Fluid - PCR parasite particles
• AF and fetal blood –
specific IgM, IgA, IgG
• Blood / placental tissue
inoculation into mice
• Fetal HUS - calcifications / hydrocephalus
• Isolation of parasite
placenta, amniotic fluid, fetal blood

48. Amniocentesis
• Done around 16th week of pregnancy
• A long needle is inserted into the Amniotic sac and
amniotic fluid is drawn.

49. Diagnosis of acute infection in pregnant mothers
Detection of Toxoplasma specific IgG and IgM
Acute infection:IgG – raising titer
IgM, Detection of Low avidity IgG or IgA is more
specific

50. Treatment
Immunocompetent patients : Does not need
treatment
Except when the illness is prolong or unusually
severe
Pyrimethamine and Sulfadiazine
+ Vitamin supplement folinic acid to prevent bone
marrow toxicity
Spiramycin – pregnant mothers

51. Congenital infection;
All infected infants are given specific
therapy until the age of 1 year irrespective
of the severity of the disease
Ocular disease:
Quiescent lesions recognized >1year _ observation
Active inflammation: Sulphadiazine and pyrimethamine
Toxoplasmosis in AIDS
Treatment with Sulphadiazine and pyrimethamine for 6
weeks

52. Pregnant women:
Spiramycin is given throughout the confinement to
reduce the transplacental passage of parasite.
If foetal infection is confirmed by amniocentesis
Pyrimethamine and Sulfadiazine
+ Vitamin supplement folinic acid alternate with
Spiramycin

53. Prenatal Management of Congenital
Toxoplasmosis
– Identified acute maternal Toxo infection
– Test amniotic fluid for parasite particles
– confirmed foetal CNS involvement (ultrasound)
•spiromycin for acute infection in
affected mother
•add pyrimethamine /sulfadiazine if fetus
is affected
–reduced congenital symptoms by 70%
»2 of 15 children infected in utero
had chorioretinitis
(

54. TORCH infections
T = Toxoplasmosis
O = Other ( Congenital syphilis, HIV, etc)
R = Rubella
C = Cytomegalovirus (CMV)
H = Herpes simplex ( HSV)