Perinatal infections

Question 1

Complement proteins in infants

Answer 1

no placental transfer, all made by infants
~20 proteins mostly made in the liver
low levels up to 20wks GA
at birth: 2/3 of adult levels
rapidly gain full function by 2 weeks
Lower opsonising capacity, lower chemotaxis, lower lytic activity
–> increased risk for infection with extracellular bugs for 2 weeks

Question 2

Neutrophils in infants

Answer 2

lower BM storage pool
lower level of expression for migration receptors
lower capacity to deform and move
reduced receptors for opsonins
lower respiratory burst upon phagocytosis
gains full function over 2 mo of life
–> lower phagocytic/killing activity, more rapid depletion leading to neutropenia

–> increased risk for infection with extracellular bugs ~2 mo

Question 3

B cells in infants

Answer 3

Premature infant is able to make IgM, but lower levels as term baby
lower IgG and IgA synthesis than adult
complete lack of anti-polysaccharide Ab - full set by 2 y
Overall slightly slower/decreased response
lack response to encapsulated bacteria (e.g. GBS)
–> increased risk for infection with extracellular, esp encapsulated bugs (6 mo, encapsulated 2 y)

Only IgG transported across placenta
all 4 subclasses are transported but at different levels
–> increased risk for infection for extracellular bugs somewhat reduced by passively transferred IgG

Question 4

T cells in infants

Answer 4

term total numbers and CD4/8 greater than adult
TCR repertoire as diverse
naive in phenotype and function - activation threshold is higher
slower to respond
–> increased susceptibility to rapidly spreading intracellular infections (~2y)

Question 5

Symptomatic congenital CMV

Answer 5

0.2-1% newborns infected in Canada
IUGR and prematurity (30-50%)
Thrombocytopenia, petechiae (75)
hepatitis, hepatosplenomegaly, jaundice (60-80)
INtracranial calcifications (50) - most commonly periventricular
Chorioretinitis (15)
N
can’t distinguish it form other congenital infections

Question 6

Placental barrier

Answer 6

physical barrier to most extracellular microbes
Immune-suppressive (tolerance) to intracellular pathogens: HSV, CMV, TB, VZV,EV, Lyme, Toxo, Rubella, LCMV
Specialized tissue: pathogens with placenta/fetal tropism: listeria, malaria

–> increased susceptibility to infections with intracellular/placenta-targeting bugs

Question 7

Skin barrier in infants

Answer 7

stratum corneum develops only >32-34 wk, but rapidly does so within 2 weeks of birth
Premature baby:
- initially decreased physical barrier
- increased physical trauma
- exposure to hospital flora

–> increased susceptibility to infection with skin flora for premature and briefly around birth

Question 8

Mucous membranes in infants

Answer 8

Premature baby:
- increase physical trauma
- altered acid production through continuous feeds and antacids adversely affect gut protection
bottle vs breastfeeding
exposure to hospital flora

overall very little known about ontogeny of mucous mebmranes, but appear fully functional within 1-2 weeks postnatally

Question 9

Pathogen exposure to infants/fetuses

Answer 9

STDs: treponema pallidum, N gonorrhea, C trachomatis, HSV, HIV, etc
Immunosuppressed: intracellular pathogens; HSV, CMV, TB, VZV, EV, Lyme, Toxo, Rubella, LCMV
Placental/fetal tropism: listeria, malaria

Question 10

Congenital syphilis

Answer 10

incidence had decreased significantly in the 90s
but huge increase in Vancouver/Alberta recently
Kills more infants/yr in the world than AIDS
can be prevented with 1 simple test + 1 shot of penicllin

Question 11

Outcome of untreated congenital syphilis

Answer 11

100% affected
intrauterine death - essentially restricted to first trimester acquisition - 25% in primary 1st trimester infection
perinatal mortality ~25%
overt symptoms, 33% at birth, remainder symptomatic by 3 mo

Question 12

Vaginal colonization during pregnancy

Answer 12

increased exposure to e.g. GBS towards end of pregnancy

Question 13

GBS maternal/birth risk factors

Answer 13

Prematurity, GBS bacteruria during pregnancy, GBS + colonization, amnionitis, maternal fever, preterm labour, sustained fetal HR > 160, prolonged labour, APGAR

Question 14

Specific statistics for GBS

Answer 14

2. 3% if mom is GBS carrier

8. 7% if mom has clinical amnionitis (fever, foul-smelling amniotic fluid)

Question 15

GBS neonatal risk factors

Answer 15

low birth weight
male
twins
skin wounds
low APGAR
pre-eclampsia induced neutropenia

Question 16

Prenatal infections

Answer 16

TORCH used often
(Toxoplasmosis, “Other”, RUbella, CMV, HSV)
BUT so many others- order specific tests instead

Question 17

Acute postnatal infection etiology

Answer 17

Usually bacterial
Others: CMV, HepB, HSV, VZV, EV, Parvo
TB rare

Question 18

Early onset infection pathogens

Answer 18

GBS
E coli
Listeria
EV

Question 19

Late onset infection pathogens

Answer 19

GBS, E coli, Listeria, EV (same as early onset) and also:
SA
CoNS
Pseudomonas
Anaerobes
fungus/yeast if on Abx before

Question 20

Perinatal infection specific diagnostic workup

Answer 20

maternal history
CBC, platelets, liver function
placental pathology
lumbar puncture
long bone roentgenogram
CT scan of head
ophthalmologic examination
audiologic evaluation prior to discharge