Obstetric and Perinatal Infections Flashcards

1
Q

Why is the newborn immune system especially susceptible?

A
  1. Cells have a high growth rate
  2. Maternal immunosuppression
  3. Fetal immune system is immature (all immunity is passive via maternal transplacental IgG and IgA in breast milk)
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2
Q

What are the three routes of infection for obstetric / perinatal infection?

A
  1. Congenital - across placenta in utero
  2. Perinatal - acquisition during birth canal passage (in utero)
  3. Postnatal - milk, blood, saliva, contact
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3
Q

What is the leading cause of bacterial meningitis in newborns?

A

Group B Streptococci - Strepococcus agalactiae

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4
Q

What is the morphology of Group B Strep (GBS) and where does it normally live? How does the baby get it?

A

Gram positive diplococci

Normally lives in GI and GU tract of mom

Baby gets it from having a large inoculum inhaled or eaten during birth (oropharyx, gastrointestinal tract)

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5
Q

What are the risk factors for early onset GBS?

A

Heavily colonized mother lacking specific anti-capsule antibody, with pre-term delivery, preterm rupture of membranes, and prolonged labor

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6
Q

What results from early onset GBS?

A

Meningitis, pneumonia, and bacteremia within 7 days of both, which is 60% fatal with sequelae in survivors

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7
Q

What is used for prevention of early onset GBS?

A

“Blind” treatment of sick baby who has risk factors

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8
Q

What is late onset GBS and is it better or worse in prognosis?

A

GBS at 7 weeks to 3 months, better prognosis as horizontal and nosocomial transmission may be implicated. Only 20% fatal, with predominantly meningitis

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9
Q

What is the primary virulence factor of GBS and how does it work?

A

Polysaccharide capsule with sialic acid moiety on terminal sugar, limiting C3b deposition and decreasing phagocytosis

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10
Q

What is the primary GBS virulence factor related to pneumonia? How does it play into meningitis?

A

Beta-hemolysin causes lung epithelial cell injury, can also help with invasion through blood brain barrier

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11
Q

What is intrapartum prophylaxis for GBS?

A

Use of antibiotics to reduce GBS load (as part of normal flora) in mom to prevent risk of infection

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12
Q

What is the second leading causing of neonatal meningitis? What is its morphology?

A

Escherichia coli K1

Gram negative bacillus

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13
Q

What is the prognosis for E. coli meningitis and how is it contracted?

A

Via ruptured amniotic membranes in low BW and pre-term births

Prognosis is poor, mortality as high as 80% with survivors having CNS sequelae.

Most will present with septicemia

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14
Q

What are the two primary virulence factors of E. coli K1?

A
  1. Polysialic capsule - resistance to neutrophil killing and survival in blood and CSF
  2. Invasins - Contribute to crossing of blood-brain-barrier
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15
Q

What is the morphology of Listeria monocytogenes?

A

Gram positive rod

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16
Q

What is the immunity against L. monocytogenes and who is most at risk?

A

Immunity is primarily cell-mediated

At risk: immunosuppressed and pregnant women / neonates

17
Q

What are the routes of infection of newborns for Listeria? Most common way?

A

congenital (transplacental), perinatal (ascending) or postnatal

Most commonly: mother contracts via food-borne transmission, transfers to fetus

18
Q

What are the in utero results of Listeria infection?

A

Spontaneous abortion, premature birth, stillbirth, or death within a short period after birth. Infant will have septicemia develop within hours of a perinatal infection

19
Q

What will Listeria most likely cause if contracted perinatally?

A

Meningitis (3rd leading cause in newborns, beside GBS and E. coli K1)

20
Q

What three virulence factors mediate the lifestyle of Listeria and how?

A

Intracellular lifestyle

  1. Internalins - adhesins aiding in cell invasion
  2. Listeriolysin O - helps Listeria escape from host vacuoles
  3. ActA - recruits host actin filaments to spread to neighboring cell without leaving previous cell (evade humoral immune response)
21
Q

What is one atypical way humans can become infected with T. gondii?

A

Blood transfusion / organ transplantation (if organ contains bradyzoites)

22
Q

When does congenital T. gondii infection affect the baby and when is it worst?

A

Affects the baby when its the mother’s first time being exposed (no immune response)

Worst when the fetal infection happens earlier in pregnancy

23
Q

What do infants born with T. gondii often show? (if not aborted or stillbirthed)

A

Microcephaly, hydrocephaly, psychomotor disturbances, and convulsions (CNS involvement)

24
Q

What is the most common complication of T. gondii infection?

A

Chorioretinitis, with bouts of eye pain and loss of visual acuity

25
Q

What are longterm sequelae of neonatal T. gondii infection?

A

Epilepsy or cognitive impairment years later

26
Q

How is T. gondii detected in utero?

A

Via PCR of amniotic fluid