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PATHOLOGY > Viral infections in pregnancy > Flashcards

Viral infections in pregnancy Flashcards

1
Q

complications of viruses in pregnancy

A

Maternal complications (Influenza, VZV, Hep E)
Miscarriage / stillbirth (rubella, measles, Hep E)
Teratogenicity (VZV, Zika)
IUGR / prematurity (rubella / CMV)
Congenital disease (CMV, HSV)
Persistent infection (HIV, Hep B/C)

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2
Q

What viruses do you consider when pregnant woman presents with rash

A

Varicella Zoster virus (chickenpox/ shingles)
Epstein barr virus
Herpes simplex virus
Cytomegalovirus
Parvovirus B19
Enterovirus
Measles
Rubella

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3
Q

Summarise Herpes viruses

A

HSV, VZV, CMV, EBV

DNA viruses
once exposed -> lifetime infection
can reactivate under stress/immunosuppression

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4
Q

transmission, incubation and latency of HSV 1 and 2

A

transmission - close contact

incubation - oropharyngeal/oro-facial 2-12 days; genital - 4-7 days

latency - in nerve cells (dorsal route ganglia) - linked to nerve cells

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5
Q

Sx of HSV 1 and 2

A

asx
painful vesicular rash
lymphadenopathy
fever

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6
Q

Diagnosis of HSV1 and 2

A

Viral detection -lesion swab for PCR
serology - if immunocompromised
IgG develops in 1st 12 wks

seroprevalence is 20-60%

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7
Q

Summarise HSV transmission in pregnancy

A

foetal infection - active infection in genital, have PPROM so that infection can ascend. If have instrumental/PPROM might increase risk

neonatal infection
* direct contact with maternal secretions in delivery
* oral herpes - kissing baby
* non familial transmission

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8
Q

different stages of HSV infection in pregnancy

A

Primary infection = first occurrence of gential HSV. No pre-existing HSV1 or HSV2 antibodies.

Non-primary infection: 1st episode of gential HSV but only has antibodies to the other type

Recurrent: HSV is the same as pre-existing antibodies. Infection may prev have been asymptomatic or symptomatic.

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9
Q

Consequence of HSV infection in pregnancy

A

Vertical transmission
* risk in 3rd trimester with primary genital infection
* if active HSV in final 3wks before delivery - then CS required
* if have regular recurrence - have acyclovir suppression in 6wks to due date

In utero infection
* primary infection only
* miscarriage
* congenital abnormalities - ventriculomegaly, CNS abnormalities
* Preterm
* IUGR

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10
Q

Mx of HSV in pregnancy

A

GUM clinic referral
Acyclovir
HSV anti-body testing, see if exposed before
consider CS 6wks before surgery

if recurrent outbreaks:
* may not treat recurrance
* consider suppressive therapy from 36wks
* Maternal Ab will offer protection - may not prevent transmission
* avoid prolonged ROM/invasive fetal monitoring

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11
Q

Presentation of neonatal HSV

A

Eye disease – initially may just be excessive watering and conjunctival erythema. Periorbital vesicles may present. HSV keratoconjunctivitis may -> cataracts and chorioretinitis -> permenant visual impairement

Present in lots of ways and easily missed – can just be one lesion.

Disseminated – very unlikely to be able to make a difference

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12
Q

Treatment of neonatal HSV

A

Acyclovir

Easy to think staph – so do viral swab and treat with acyclovir if worried until get –ve swab

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13
Q

transmission and incubation of VZV

A

transmission - respiratory (isolate)
70% infection rate if susceptible

infection 7-13 days (mean 14 days)

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14
Q

symptoms of neonatal VZV

A

Symptoms: prodrome of fever, malaise , myalgia
Centripetal maculopapular rash
Vesicular, appears in crops

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15
Q

Maternal varicella

A

10-20% of women of childbearing age are susceptible

10-20% of pregnant women with varicella will have varicella pneumonia (v severe)

Encephalitis is rare but mortality is 5-10%

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16
Q

VZV neonatal transmission

A

antenatal (across the placenta), perinatal or postnatal

0.4% if maternal infection weeks 0-12
2% if weeks12-20

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17
Q

features of congenital varicella syndrome

A

Neurological – intellectual disability, microcephaly, hydrocephalus, seizures, Horner’s syndrome

Occular abnormalities – optic nerve atrophy, cataracts, chorioretinities, micropthalmost, nystagmus

Limb abnormalities – hypoplasia , atrophy, paresis

GI – GORD, atretic or stenotic bowel

low birth weight

skin scarring

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18
Q

management of maternal exposure to VZV

A
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19
Q

Post exposure prophylaxis for maternal VZV

A

oral (or IV if complicated) acyclovir

20
Q

epidemiology, transmission and incubation of CMV

A

Common early childhood infection
2-6% of infants infected by 6 months, 40% by 16yrs.

Transmission: salvia/ resp secretions/ urine

Incubation: 4-8 weeks
Virus persists lifelong

21
Q

Symptoms of CMV

A

asx
macolopapular rash
infectious mononucleosis-like illness

22
Q

Ix for CMV

A

PCR of urine/saliva/amniotic fluid/tissue

serology

23
Q

CMV in pregnancy

A

Primary infection in pregnancy – approx. 30% transmit the virus across the placenta
Reactivation or re-infection with a new strain is more common – approx. 1% will transmit infection

Primary – is infection for 1st time ever – in 30-40% of 2nd trimester??

Can get reinfection with a different strain

Biggest risk to baby is transmission in 3rd trimester

24
Q

Complications from CMV in pregnancy

A

encephalitis
ventriculomegaly
chorioretinitis
hepatosplenomegaly
thrombocytopenia
jaundice
microcephaly

In older children can -> sensorineural deafness and learning disability.
risk for maternal-fetal viral transmission is lower in early vs late pregnancy,
risk for symptomatic disease at birth and long-term sequelae is higher when infection occurs in early pregnancy.
Most congenitally infected newborns are initially asymptomatic.
15 to 25% initially asymptomatic -> neurodevelopmental abnormalities,eg sensorineural hearing loss, within the first 3yrs

Ventriculomegaly/encephalitis in utero – unlikely to develop normally

25
Ix for CMV in pregnancy
Need to know if primary or recurrent Have they seen virus before Have booking bloods – Hep and HIV screen. Add on IgG ab – if no IgG at booking but IgM at present = primary infection. If prev IgG need to think more carefully If primary – more reg fetal monitoring, can do amniocentisis. Guthrie card include CMV. Have urine and saliva test for CMV
26
Mx of CMV in pregnancy
If seroconversion is suspected - (aka infection in pregnancy) - refer to fetal med unit - USS +- amniocentesis No Rx available neonates investigated - urine and saliva CMV PCR in 1st 21 days
27
rubella transmission and incubation
Rubella is a Togavirus - RNA virus AKA german measles transmission - resp - isolate incubation - 12-21 days Replicated in lymph tissue of URT and then spreads hematogenously.
28
Sx of rubella
20-50% are subclinical prodrome - coryza, sore throat, cough, headache (1-5 days pre-rash) fine, macular rash mildy pruritic starts on face -> trunk and limbs in hrs lymphadenopathy - tender, postauricular/cervical/suboccipital
29
rubella in pregnancy
**biggest risk in 1st trimester** Spread is across the placenta During weeks 16-20 only 5-10% of maternal IgG crosses the placenta if <8wks = spont abortion <10wks = 90% incidence of fetal defects 18-28 wks = hearing defects and retinopathy >20wks = risk lower
30
Features of congenital rubella syndrome
manifest in infancy: * microcephaly * cataracts * retinopathy * cardiac - PDA/PS * purpura * hepatosplenomegaly * bone lesions manifest later * panencephalitis * hearing loss (bilateral sensineural hearing loss) * intellectual disability * dm * thyroid dysfunction
31
Features of measles
rash start at hairline/behind ears -> spread cephalocaudally over 3 days conjunctivitis high fever runny nose rash 3-5 days after prodrome sx begin Koplick spots - small, white spots in buccal mucosa
32
summarise measles
paramyxovirus transmission - resp (isolate), conjunctiva incubation - 7-18 days (mean 10)
33
Complication of measles for mother
secondary bacterial infection otitis media/pneumonia/GI encephalitis mortality
34
measles complications for fetus
Fetal loss preterm delivery no congenital abnormalities SSPE - subacute sclerosing panencephalitis – * fatal, progressive degenerative disease of CNS. * 7-10 years after natural infection. * Child may recover from initial infection – long term risk of SSPE
35
What's the rash
Parvovirus B19 - slap cheek syndrome
36
summarise parvovirus in pregnancy
DNA virus 30-60% adults have antibodies transmission - resp, blood products incubation - 6-8days 6 days post exposure – 1 week later. You are infectious before symptoms commence
37
sx of parvovirus
**asx** Erythema infectiosum/ slapped cheek/5ths disease Polyarthropathy Transient aplastic crisis
38
dx of parvovirus
Virus detection serology - IgM detected after 10 days after exposure, before sx
39
Parvovirus in pregnancy
Before 20 weeks - refer to fetal medicine unit, may need intrauterine transfusion * Transmission 33% * 9% risk of infection of fetus * 3% hydrops fetalis if infection) * 1% fetal anomalies * 7% fetal loss >20wks no risk
40
summarise fetal hydrops
Cytotoxic to fetal red blood precursor cells -> anaemia -> accumulation of fluid in soft tissues and serous cavities. -> can rapidly cause fetal death acites, pleural effusion, skin edema, hydopic placenta, pericardial effusion, cardiomegaly, polyhydramnos, oligohydramnos RX: intrauterine transfusion 50% of fetal infections result in interuterine death Can test booking bloods for parvovirus for IgG, and current test for IgM or IgG – has she got immunity. Make sure fetal medicine knew
41
Summarise enterovirus
transmission - resp +- fecal incubation - 2-40days
42
summarise enterovirus
transmission - resp +/- faecal Incubation 2-40days
43
sx of enterovirus
hand foot and mouth disease (enterovirus A) rash encephalitis myocarditis not associated with severe outcomes coxackie has worse risk * perinatal newborn infection in last week of preg * neonate risk of 1. myocarditis 2. fulminant hepatitis 3. encephalitis 4. bleeding 5. multi-organ failure
44
Ix for enterovirus in pregnancy
Swab if lesion isolate
45
Summarise Zika virus
Spread by mosquito, sexual transmission, blood transfusion can cause micocephaly in unborn babies -> abnormally small heads and brains no vaccine incubation - up to 7 days aedes aaegypti mosquito is a major vector for zika 1 in 5 will become ill
46
effect of zika on neonate
Zika infects the placenta and then transmits across the placenta where it targets neuronal progenitor cells. neuronal growth, proliferation, migration, and differentiation are disrupted, thus impairing normal brain development in utero and in infancy **Microcephaly** Craniofacial disproportion and skull abnormality Occular abnormalities - Problem with vision SN hearing loss Contractures / talipes Hypertonia And problem with limbs

PATHOLOGY (94 decks)

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