VERTICAL TRANSMISSION

Modes of transmission
1. “Vertical transmission” is a term that refers to
the spread of infections from mother-to-baby.
2. These infections may occur while the foetus is:
1. still in the uterus (transplacental),

2. during labour and delivery, or after delivery or

while breastfeeding.(Perinatal transmission)
 TRANSPLACENTAL
TORCH is an acronym for several of the more common
congenital infections.
1. Toxoplasmosis
2. Other infections (syphilis, hepatitis B, Coxsackie
virus, Epstein-Barr virus,varicella-zoster virus (chicken
pox), and human parvovirus)
3. Rubella
4. Cytomegalovirus (CMV)
5. Herpes simplex virus
6. HIV
7. Listeria monocytogenes,
8. Plasmodium falciparum
 Perinatal infections
Haematogenous or genital route:
1. Gonorrhoea
2. Chlamydia
3. Herpes simplex virus
4. Human Papilloma Virus (genital warts)
5. Group B Streptococci (GBS)
6. human immunodeficiency virus (HIV),
7. herpes zoster virus (HZV),
8. hepatitis B virus (HBV)
Via breastfeeding:HIV
 CONGENITAL RUBELLA

1. RNA virus
2. 90% of infected fetuses will be damaged at
1-11 weeks of gestation,
3. 24% at 15-16 weeks.
 TERATOGENIC EFFECTS

1. Intrauterine growth retardation,

2. Congenital heart disease (patent ductus
arteriosus or pulmonary artery stenosis),
3. Sensorineural hearing loss,
4. Cataracts or glaucoma,
5. Neonatal purpura, and
6. Dermatoglyphic abnormalities.
 SYSTEMIC INVOLVEMENT
1. Adenitis (post auricular common)
2. Hepatitis,
3. Hepatosplenomegaly,
4. Jaundice,
5. Anemia,
6. Decreased platelets with or without petechiae,
7. Myocarditis,
8. Eye lesions (iridocyclitis or retinopathy),
9. Pneumonia.
 Late defects
1. Immunologic dyscrasias,
2. Hearing deficit,
3. Psychomotor retardation,
4. Autism,
5. Brain syndromes such as subacute sclerosing
panencephalitis,
6. Diabetes mellitus, and
7. Thyroid disease.
 DIAGNOSIS

1. ELISA for IgM and IgG antibodies are the

most commonly performed tests.

2. Rubella is difficult to differentiate clinically

from other rash-causing infections such as
measles and parvovirus BE19
 MANAGEMENT

1. There is no specific treatment for rubella.

2. Prevention consists of vaccination of the
susceptible population (especially young
children).
3. Vaccine should not be given to pregnant
women.
 CYTOMEGALOVIRUS
1. DNA virus and a member of the herpesvirus group
(human herpesvirus 5).
2. CMV is the most common cause of congenital
infection.
3. ubiquitous virus transmitted by saliva, tears, semen,
urine, cervical secretions, blood (white blood cells),
and breast milk.
4. may also be transmitted by cervical secretions,
breast milk and blood transfusion.
5. CMV infection acquired during delivery or via breast
milk has no effect on future neurodevelopmental
outcome in full-term infants.
 Risk factors for primary CMV infection during
pregnancy

1. prolonged exposure to young children

(daycare workers, multiparous women) and
2. sexual contact
 Terratogenicity
1. During early pregnancy, CMV has a teratogenic potential in
the fetus; 35% fetus affected.
2. More than 85% of infants born with CMV have a subclinical
infection
3. The primary target organs are the CNS, eyes, liver, lungs,
and kidneys.
4. Pathology include focal necrosis, inflammatory response,
formation of enlarged cells with intranuclear inclusions
(cytomegalic cells), and the production of multinucleated
giant cells.
5. A sepsis-like illness has been described in premature
infants.
 Prenatal manifestations
1. Mononucleosis-like illnesses in mother
2. Prenatal ultrasound shows:
1. fetal growth restriction,
2. cerebral periventricular echogenicity or
calcifications,
3. cerebral ventriculomegaly, microcephaly,
polymicrogyria,
4. cerebellar hypoplasia,
5. hepatosplenomegaly,
6. amniotic fluid abnormalities, ascites and/or pleural
effusion, and placental enlargement
 Postnatal presentation
1. Subclinical infection in 85–90% of cases.
2. Sensorineural hearing loss during the first 6 years
3. Low birthweight.
4. Hepatosplenomegaly with jaundice, abnormal liver
function tests (LFTs),
5. Thrombocytopenia
6. microcephaly,
7. intracerebral calcifications
8. Chorioretinitis and visual impairment
9. hemolytic anemia and pneumonitis
10. severely affected infants have a mortality rate of 30%.
 Ophthalmic manifestations
1. chorioretinitis,
2. pigmentary retinitis,
3. macular scarring, optic atrophy, and
4. central cortical defects.
 Diagnosis
1. The gold standard for the diagnosis of
congenital CMV is urine or saliva culture or PCR
obtained before 3 weeks of age
2. (IgM) should not be used to diagnose
congenital CMV because they are less sensitive
3. complete blood count, LFTs, disseminated
intravascular coagulation panel and
cerebrospinal fluid analysis, culture, and PCR.
 Imaging and other studies
1. Ultrasound or CT scans of the head may
demonstrate characteristic periventricular
calcifications.
2. Brain MRI is preferred over other modalities
because it is likely to identify most of the
brain anomalies associated with congenital
CMV.
 Prevention
1. Pregnant mother: frequent hand washing; wearing gloves
for specific child-care tasks; avoiding kissing children
under age 6 on the mouth or cheek; not sharing food,
drinks, or oral utensils
2. administration of CMV hyperimmune globulin (HIG) to
pregnant women
3. administering antiviral therapy to women
4. HIG (100 U/kg) given monthly until delivery
5. CMV vaccine available
 Management
1. No antiviral agent
2. Valganciclovir is a prodrug of ganciclovir that is
suitable for oral administration.
3. Valganciclovir administered orally to young
infants at 16 mg/kg/dose, twice daily, provides
the same systemic ganciclovir exposure as does
intravenous ganciclovir at 6 mg/kg/dose.
 Prognosis
1. Congenital CMV is the leading cause of SNHL
regardless of the seroprevalence in the
population.
2. For symptomatic infants at birth, mortality is up
to 30%,
3. up to 90% will have late complications
(intellectual or developmental impairment,
hearing loss, spasticity).
 GROUP B STREPTOCOCCI
1. Group B streptococci are found in 12-26% of
pregnant women, especially in the urine.
2. Infection has been associated with pre-term delivery
and ascending infection following rupture of
membranes may result in fetal infection
3. Neonatal sepsis with associated mortality of 6%
4. Screening: third trimester vaginal and anal swabs
5. It can be prevented with intrapartum penicillin in
high-risk cases.
 Toxoplasmosis
1. Toxoplasma gondii is a coccidian protozoan that
multiplies only in living cells
2. there are 4 predominant clonal lineages called types I , II
, III , and IV
3. Human infection in older children and adults is usually
acquired orally by eating undercooked or raw meat that
contains cysts or food (e.g., salad greens) or other
material contaminated with oocysts from acutely
infected cats.
4. Rarely, by organ transplantation or transfusion; no sexual
transmission
 Intrauterine Transmission
1. Infection may be transmitted to the fetus
transplacentally or during vaginal delivery.
2. In the first trimester, approximately 17% of
fetuses are infected, in the third trimester,
approximately 65% of fetuses are infected.
3. Most often, maternal infection is asymptomatic
or without specific symptoms or signs.
4. Congenital infection may present as a mild or
severe neonatal disease
 Manifestations
1. Hydrops fetalis
2. Perinatal death to small size for gestational age,
3. prematurity,
4. peripheral retinal scars,
5. persistent jaundice, mild thrombocytopenia, CSF
pleocytosis,
6. The characteristic triad is chorioretinitis,
hydrocephalus, and cerebral calcifications.
 CNS
• Neurologic signs such as convulsions, setting-sun
sign with downward gaze, and hydrocephalus
with increased head circumference may be
associated with cerebral damage or
inflammation obstructing the aqueduct of
Sylvius.
• If affected infants are treated and shunted
promptly, signs and symptoms may resolve, and
development may be normal.
 Skin
• Rashes and jaundice
• Petechiae secondary to thrombocytopenia,
but
• Ecchymoses and large hemorrhages may also
occur.
 Endocrine
1. Endocrine abnormalities may occur
secondary to hypothalamic or pituitary
involvement
2. Mmyxedema, persistent hypernatremia with
vasopressin-sensitive diabetes insipidus,
sexual precocity, and partial anterior
hypopituitarism.
 Neurologic manifestations
1. Toxoplasmosis should be considered in neurologic
disease in <1 yr old, especially with retinal lesions
2. Hydrocephalus may be the sole clinical neurologic
manifestation
3. Later, focal motor seizures, petit and grand mal
seizures, muscular twitching, opisthotonos, and
hypsarrhythmia can occur.
4. Microcephaly usually reflects severe brain damage
5. Intellectual impairment
6. Calcifications occur throughout the brain
7. CSF abnormalities
 Eyes
1. chorioretinal lesions may have severe visual
impairment
2. Focal necrotizing retinitis
3. Retinal detachment
4. erythema of the external eye
5. strabismus, nystagmus and microphthalmia.
 Ears
1. Sensorineural hearing loss, both mild and
severe, may occur.
2. It is not known whether this is a static or
progressive disorder.
3. Treatment in the 1st yr of life is associated
with decreased frequency of hearing loss.
 Diagnosis
1. Isolation of T. gondii from blood or body fluids
2. Tachyzoites in sections or preparations of tissues and
body fluids, amniotic fluid, or placenta;
3. Identification of cysts in the placenta or tissues of a
fetus or newborn; and characteristic lymph node
histologic features.
4. Serologic tests are very useful for diagnosis.
5. Polymerase chain reaction (PCR) is useful to identify T.
gondii DNA in CSF and amniotic fluid, urine and blood.
 Prenatal diagnosis
1. Fetal ultrasound examination, performed
every 2 wk during gestation, beginning at
diagnosis of acute acquired infection in a
pregnant woman.
2. PCR analysis of amniotic fluid are used for
prenatal diagnosis.
 Maternal Treatment
1. Pyrimethamine and sulfadiazine act synergistically
against Toxoplasma.
2. Use of pyrimethamine is contraindicated during the first
trimester of pregnancy.
3. Spiramycin should be used to attempt to prevent
vertical transmission of infection.
4. All patients treated with pyrimethamine should have
leukocyte counts twice weekly.
5. Folinic acid, as calcium leucovorin , should always be
administered concomitantly
 Infant treatment
1. Infants should be treated for 1 yr
2. Pyrimethamine (2 mg/kg/day PO bid for 2 days, then
beginning on the 3rd day, 1 mg/kg/day for 2 or 6 mo,
and then 1 mg/kg given on Monday, Wednesday, and
Friday),
3. sulfadiazine (100 mg/kg/day PO bid), and leucovorin (5-
10 mg PO given on Monday, Wednesday, and Friday, or
more often depending on neutrophil count).
4. Prednisone (1 mg/kg/day PO bid) has been used in
addition when active chorioretinitis
 Syphilis
1. Syphilis remains endemic in many other parts of the
world (Africa, South East Asia and ex-USSR)
2. Transplacental transmission occurs in 90% of
untreated women
3. Hutchinson's triad (abnormal teeth, interstitial
keratitis and sensorineural deafness) arise later in
untreated children.
4. Maternal infection is usually detected by antenatal
screening using a non-treponemal test (e.g. VDRL) but
there is a risk of false-positive results
5. Treatment is with parenteral benzylpenicillin