Congenital perinatal infections Flashcards

1
Q

by what means does vertical transmission of infections take place?

A

between mother and baby/fetus, either via breastmilk (postnatally) or via transplacentally (prenatally). Note: an ascending infection involves vaginal pathogens producing a fetal infection

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2
Q

what does this child suffer from

A

varicella zoster virus

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3
Q

what is vzv? how is it contracted? how does it present? where is the virus housed in latent infection?

A

herpesviridae family, dsDNA, enveloped virus.

presents as chicken pox or herpes zoster (shingles).

chickenpox is spread by direct contact, respiratory. presents as fever, lethargy and pruritic vesicular rash lasting 2-6 days. (IP 10-21 days),

More severe in adults (but less common)

latent infection in dorsal root ganglion.

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4
Q

what are complications of chickenpox (VZV)?

A
  1. secondary bacterial infection when vesicles lyse.
    - commonly strep pyogenes
    - staph aureus –> bullous varicella
  2. pneumonitis
    - 25x more common in adults (related to smoking)
  3. Acute cerebellar ataxia
    - immunological complication, self limiting ataxia
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5
Q

How does varicella affect the fetus?

A
  • deaths most common in 3rd trimester
  • 1st trimester primary infections may cause deformities (cicatrical scarring, limb hypoplasia, microcephaly, cataracts, mental retardation, GI and genitourinary malformations)
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6
Q

at what point is maternal varicella a great concern for perinatal transmission?

A

when primary infection is contracts -7 to 2 days of delivery before moter has a chance to mount an immune response.(lacks the specific antibody against it)

17-30% chance of transmission

30% chance of mortality

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7
Q

who is a good candidate for prophylactic varicella zoster immunoglobulin tx?

A

received from immune donors, given to non immune people after exposure within 10 days.

Target:

  • premature babies
  • susceptible pregnant women
  • infants whose mothers develop varicella within 7 days of pregnancy or first month of life
  • immunocomporomised

NB: prolongs IP to 30 days

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8
Q

how is acute varicella treated?

A
  • oral acyclovir if <24hrs with rash and no systemic symptoms
  • IV if pneumonitis, neurological symptoms, organ involvement, hemorrhagic rash
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9
Q

T/F there is no vaccine for CMV.

A

FALSE.

vaccine is a live attenuated virus

–>(MMR at 8 months) MMRV at 12 months

2 doses if older than 14 yrs.

For those in high risk occupations:

booster for adults older than >60yrs, 14x more potent than child vaccine (b/c harder to mount a response in adult who has been exposed previously)

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10
Q

what is cmv?

A
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11
Q

how is CMV transmitted?

A

NB: recurrent infections may occur due to reactivation of previous infection or reinfection (b/c no cross protection b/w various strains)

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12
Q

who is at highest risk of developing/contracting CMV?

A

risk increases with age up to childbearing years.

In developed countries its highest in adulthood.

in developING countries it’s highest before age 3.

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13
Q

a fetus contracts CMV, what are the chances this stemmed from the mother contracting a primary infection vs had a reactivation of previous infection?

A

10-30% of cases are a reactivation

…result in 1-3% fetal infection

1% are primary infections

…result in 20-50% fetal infection

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14
Q

how is CMV acquired postpartum? how does it present?

A

via breastmilk.

presents as sepsis like sympoms:

  • hepatomegaly
  • resp distress
  • atypical lymphocytosis
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15
Q

how is CMV best diagnosied?

A

IgG and IgM can give an indication of presence of current or past infection or reactivation of infection. Several confounders such as rheumatoid arthiritis (produces IgM), false positives/negatives, also IgM can remain for up to a year in CMV cases.

PCR of amniotic fluid is very sensitive after 20/40 (95%).

Fetal cord blood analysis for IgM has less sensitivity than PCR also risk of miscarriage.

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16
Q

suppose a mother with CMV has a baby who is normal at birth, what are the consideration to make?

A

considering 90% of neonates can be asymptomatic at birth (with 10-15% having long term sequelae) its important to monitor for development of complications….

  • deafness may be delayed 5 yrs, should undergo serial audiometry
  • chorioretinitis/optic atrophy in 2% of cses, should undergo serial ophtho exams
  • microcephaly and developmental delay. should undergo seial psychomotor assessment
  • pneumonitis at 1-4 months, rare
17
Q

suppose mother with CMV has a symptomatic baby, what are next steps?

A

within 2 weeks urine sample to confirm CMV diagnosis.

cranial ultrasound, and multidisciplinary approahc to development of child (OT, psyiotherapy, speech,etc)

18
Q

tx for neonates with CMV?

A

-oral ganciclovir tx for symptomatic neonates

–>reduced viremia and shedding, reduced rates of sensorimeural deafness

adverse events: carcinogeniticty

19
Q

what is rubella? how is it transmitted? how does it present?

A

aka “ german measles”

transmitted via nasal secretions.

25-50% infections are asymptomatic. Infectious from -7 to +14 days (before symptoms arise).

20
Q

how does rubella present clinically?

A
  • low grade fever
  • lymphadenopathy (posterior cervical, post auricular, occipital)
  • exanthem (maculopapular)
  • polyathralgia/arthritis

-

21
Q

during which congenital period is risk of rubella damage highest?

A

risk of damage highest before 4 weeks (85%)

risk wanes after 16 weeks.

22
Q

what is classical triad of congenital rubella syndrome?

A

Opthalmological - cataracts, glaucoma, retinopathy

Cardiac -PDA, PA stenosis

Auditory - sensorineural deafness

NB: may also see neurological disorders and endocrinopathies (IDDM, thyroid)

23
Q

how can rubella be prevented?

A

rubella vaccine is a live attenuated virus (provides 90% lifelong protection)

NB: women who are seronegative for rubella should be given the vaccine immediatelt post partum. NEVER DURING PREGNANCY.

24
Q

[….] also known as erythrovirus is a ssDNA virus that targets and shortens lifespan of RBC progenitor cells.

A

Parvovirus

25
Q

How does parvovirus present clinically?

A

Erythema infectiousum, characteristic ‘slapped cheek’

26
Q

what are the features of congenital parvovirus?

A

hydrops foetalis (anaemia)

NB: 60-70% of women are immune. foetal loss occurs in 10% of cases before 10 weeks gestation.

27
Q

how is parvovirus diagnosed (ie serology)?

A
28
Q

what is the impact of primary herpes simplex virus if infected during pregnancy? near delivery?

A
29
Q

how should herpes simplex be managed during pregnancy? primary vs recurrent infection

A
30
Q

which STI might present this way?

A

Treponema Pallidum (syphilis)

31
Q

the [….] form/phase/stage of syphilis is most commonly transmitted to fetus. The most common outcome of congenital syphilis infection is […], followed by premature delivery and late/early onset disease.

A

primary.

still birth.

32
Q
A