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Oxford handbook O&G > Chapter 4 - Infectious diseases in pregnancy > Flashcards

Chapter 4 - Infectious diseases in pregnancy Flashcards

1
Q

Describe Rubella-associated congenital defects

A

The virus disrupts mitosis, retarding cellular division and causing vascular
damage.

Severity decreasing with advancing gestation

  • Sensorineural deafness.
  • Cardiac abnormalities including VSD and patent ductus arteriosus (PDA).
  • Eye lesions (congenital cataracts, microphthalmia, and glaucoma).
  • Microcephaly and mental retardation.

**rarely causes defects after 16weeks

Late-developing sequelae include:
• Diabetes.
• Thyroid disorders.
• Progressive panencephalitis.

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2
Q

When can pregnant women have the MMR

A

It is a live attenuated vaccine so contraindicated in pregnancy + avoid pregnancy 12weeks after vaccination

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3
Q

A pregnant woman has been exposed to rubella, what should you advise?

A
  • Need to check vaccine records for confirmation of vaccination or previous antibody confirmation
  • If not, test for IgM + IgG
  • If IgG found reassure + tell to return if rash appears
  • If IgM or neither detected further testing will be needed
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4
Q

Which sign is pathonomonic for measles?

A

Koplick spots in the mouth

Other signs = 4 Cs
Cough, coryza, conjunctivitis + Koplik spots

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5
Q

Maternal complication of measles

A
  • pneumonia
  • acute encephalitis
  • corneal ulcers
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6
Q

Fetal complication of measles

A
  • Death + prematurity
  • no congenital damage
  • Neonatal subacute sclerosing panencephalitis.
    Therefore, administer human normal immunoglobulin
    (HNIG) immediately after birth or exposure is recommended for
    neonates born to mothers in whom the rash appears 6 days before to
    6 days after birth.
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7
Q

Mx of a pregnant woman exposed to measles

A
  • Confirm vaccination
  • Send IgG + IgM
  • If IgG not detected give HNIG
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8
Q

Fetal risks of parvovirus

A

• The virus causes suppression of erythropoiesis sometimes with
thrombocytopenia and direct cardiac toxicity, eventually resulting in cardiac failure and hydrops fetalis.
• There are no congenital defects associated with parvovirus infection.

Mx
- fetal middle cerebral artery monitoring for anaemia +/- In utero transfusion

**10% of fetuses infected at <20wks gestation die.

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9
Q

Symptoms of CMV

A
  • Fever
  • Malaise
  • Lymphadenopathy, mononucleosis
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10
Q

CMV-associated congenital defects

A 
• IUGR.
• Microcephaly.
• Hepatosplenamegaly and thrombocytopenia.
• Jaundice.
• Chorioretinitis.
• Later-developing sequelae include:
- psychomotor retardation in 10%  <6yrs old
- sensorineural hearing loss.

**Although most normal at birth if symptomatic outcome is very bad

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11
Q

Causes of non-vesicular rashes in pregnancy

A
  • Streptococcal infection.
  • Meningococcal infection.
  • Enteroviruses.
  • CMV.
  • Epstein–Barr virus (EBV).
  • Syphilis.
  • Rubella.
  • Measles.
  • Parvovirus B19.
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12
Q

When are people with VZV infectious?

A

Infectious from 2 days before rash until all vesicles are crusted.

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13
Q

Mx of a woman exposed to VZV

A

1) Send VZV IgG

2) If no IgG, give VZIG

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14
Q

Maternal risks of VZV

A
  • Varicella pneumonia.
  • Hepatitis.
  • Encephalitis.
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15
Q

Fetal risks of VZV

A

If <20wks there is a 2% risk of fetal varicella syndrome with congenital defects including:
• Skin scarring.
• Limb hypoplasia.
• Eye lesions (congenital cataracts, microphthalmia, chorioretinitis).
• Neurological abnormalities (mental retardation, microcephaly, cortical
atrophy, and dysfunction of bladder and bowel sphincters).

Neonatal risks:
- Neonatal varicella if mothers contracted it in the
last 4wks of pregnancy.
- Severe infection can be fatal & most likely to occur if the rash appears 5 days before delivery or 2 days after. **These babies should all receive VZIG as soon as possible.

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16
Q

Mx of VZV

A

Aciclovir reduces the duration of sx if given within 24hrs of the rash appearing

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17
Q

Maternal risks of HSV

A 
Primary infection:
• Meningitis.
• Sacral radiculopathy—causing urinary retention and constipation.
• Transverse myelitis.
• Disseminated infection.
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18
Q

Fetal risks of HSV

A

Primary infection may lead to miscarriage or preterm labour, but no related congenital defects

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19
Q

Neonatal risks of HSV

A

Usually only if primary infection but transmission rate is 50%

Neonatal herpes appears during the first 2wks of life.
• 25% limited to eyes and mouth only.
• 75% widely disseminated, of which:
• 70% will die
• m any of the survivors will have long-term problems including
mental retardation.

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20
Q

Mx of HSV

A

Aciclovir may decrease severity and duration of the primary attack if given
within 5 days of onset of symptoms.

If labour is within 6wks of primary infection then delivery by CS is recommended provided the membranes have not been ruptured for >4h. With active vesicles from a recurrent
attack, the risk of surgery must be carefully weighed against the very small
risk of neonatal infection.

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21
Q

Dx of maternal malaria

A
  • blood films.
  • Rapid detection tests may miss low parasitaemia.
  • 3 –ve malaria smears 12–24h apart rules out malaria.
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22
Q

Fetal risks of malaria

A
  • Miscarriage or preterm delivery.
  • Stillbirth.
  • Congenital malaria.
  • Low birth weight (s to prematurity or IUGR).
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23
Q

Mx of women with malaria

A
  • Inpatient
  • Quinine and clindamycin for falciparum malaria (IV artesunate for severe).
    • Antipyretics.
    • Screen for anaemia and treat appropriately.
    • Uncomplicated malaria is not a reason for induction of labour.

**Report to HPA

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24
Q

Safest malaria prophylaxis

A

Proguanil and chloroquine are probably the safest drugs for malarial prophylaxis in pregnancy.

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25
Q

Cause + symptoms of toxoplasmosis

A

Cat faeces + eating undercooked meat

–> fever or lymphadenopathy but 80% asymptomatic

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26
Q

Severe complication of fetal toxoplasmosis

A

Cerebral ventriculomegaly but most are unaffected

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27
Q

Severe complication of maternal toxoplasmosis

A

immunocompromised individuals are at risk of chorioretinitis and encephalitis.

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28
Q

Tx of toxoplasmosis

A
  • Spiramycin decrease the
    risk of fetal infection.
  • If vertical transmission occurs = antitoxoplasmosis
    therapy is used.
  • Neonatal follow-up: ophthalmic
    review and cranial radiological studies.
  • Recommend delaying future pregnancies until maternal IgM antibodies have been cleared.
29
Q

Fetal risks of toxoplasmosis

A

Spontaneous miscarriage is common with infection in the first trimester

Defects associated with primary infection include:
• Chorioretinitis.
• Microcephaly and hydrocephalus.
• Intracranial calcification.
• Mental retardation.
30
Q

Cause of hepatitis B + symptoms

A

HBV DNA virus spread by blood, blood products or sexual contact with a <6m incubation period

Present with non-specific GI + jaundice illness

31
Q

+ve HB surface antigen (HBsAg) =

A

Current infection

32
Q

+ve HB E antigen (HBeAg)

A

active viral replication.

33
Q

+ve Anti-HBsAg antibodies

A

Immunity from infection or vaccination

34
Q

Maternal risks of Hep B

A

65% have subclinical disease with full recovery

25% develop acute infection

10% become carriers

<0.5% develop fulminant hepatitis = high mortality

35
Q

Fetal risks of Hep B

A

Miscarriage or Preterm but no known congenital defects

** Transmission during delivery can be fatal and lead to chronic carrier status, cirrhosis and hepatocellular carcinoma especially if HBsAg and HBeAg +ve: 95% risk.

36
Q

Mx of babies born to HBV mothers (acute or chronic)

A

HBV IgG and HBV vaccination within 24h of delivery is up

to 95% effective at preventing neonatal HBV infection.

37
Q

Incidence of GBS vaginally

A

20% of women carry it vaginally with no symptoms

38
Q

Recommendations on GBS screening

A

RCOG doesn’t support routine screening however women with previous history of neonatal GBS infection should be given intrapartum prophylactic abx

39
Q

Indications for prophylactic Abx for GBS

A
  • Hx of neonatal GBS infection in previous delivery
  • GBS identified incidentally from the vagina or urine
  • Prematurity
  • PROM
  • Pyrexia in labour
40
Q

Tx for GBS

A

prophylaxis in labour is IV benzylpenicillin started as
soon as possible after onset of labour and at least 2h before delivery (3g
initially then 1.5g every 4h throughout labour). In case of penicillin allergy,
IV clindamycin should be used (900mg every 8h).

41
Q

Neonatal risks of GBS

A

1% of exposed neonates develop neonatal sepsis

  • Early GBS onset <4days from delivery has a mortality of 20% and presents with: Pneumonia, septicaemia and meningitis
  • 50% of survivors have neuro issues: cortical blindness and deafness
42
Q

Epidemiology of Group A strep

A
  • Streptococcus pyogenes.
  • Most common bacterial cause of acute pharyngitis (‘strep throat’).
  • Up to 30% of population are asymptomatic carriers (skin or throat).
  • Easily spread—person to person or droplet.
43
Q

5 Diseases caused by GAS

A
  • Pharyngitis.
  • Impetigo.
  • Cellulitis.
  • Scarlet fever.
  • Rheumatic fever.
  • Toxic shock syndrome.
44
Q

Is GAS sepsis overestimated?

A

Often underestimated and can lead to mortality. Often insidious in a woman appearing well with a sudden collapse with little warning leading to septic shock + DIC + multi-organ failure

45
Q

Fetal risks of GAS

A

No congenital infection or damage would be anticipated .

46
Q

Fetal complications of syphilis

A

The spirochaete can cross the placenta and is associated with preterm
delivery, stillbirth, and congenital syphilis defects, including:
• 8th nerve deafness
• Hutchinson’s teeth
• saddle nose
• sabre shins.

47
Q

Tx of syphilis

A

Treatment with penicillin:
• < 16wks—prevents virtually all congenital infection
• > 16wks—still effective in most cases.

48
Q

Complications of Listeria monocytogenes

A 
Crosses the placenta causing amnionitis, and miscarriage or preterm
labour.
• Neonatal infection may be:
• generalized septicaemia
• pneumonia
• meningitis.
49
Q

Tx of listeria

A

high dose amoxicillin or erythromycin

50
Q

Prevention of listeria

A

Avoiding soft cheese, pate, undercooked meat, and shellfish

51
Q

Sx of listeria

A

Gastroenteritis

52
Q

Risk of EBV to the fetus

A

No specific risk

53
Q

Manifestation of enteroviruses

A

Wide range of manifestations, including meningitis, rash, febrile illness, and myocarditis

54
Q

Fetal risk of enteroviruses

A

Nil known (even hand, foot and mouth has no known adverse consequences to the fetus)

55
Q

What indicates high risk of HIV transmission to the fetus?

A

High viral loads (VL) and low CD4 counts

56
Q

What % of women with HIV receive assisted reproductive tech (ART)

A

> 98%

57
Q

Risk of transmission of HIV during unprotected sex

A

0.03–1% for each act of unprotected intercourse.

58
Q

What recommendations can be made for couples with one having HIV?

A
  • mother is +ve and the partner –ve, self-insemination with
    the partner’s sperm is recommended.
  • Sperm washing or donor sperm if male is +ve and female –ve.
  • IVF should take account of the parents’ viral load, CD4 counts, and any
    AIDS defining illness
59
Q

Tx of HIV in pregnancy

A
  • Start treatment for their own health asap
  • Most evidence for zidovudine +
    lamivudine
  • tenofovir plus emtricitabine or abacavir plus lamivudine
    are acceptable alternatives.
  • The 3rd agent in HAART should be nevirapine if the CD4 count is less
    than 250, or efavirenz, or a boosted PI.
  • If mother isn’t requiring treatment, recommend to start temporary HAART at 14/40 if baseline VL >30k
  • ALL WOMEN ON HAART BY 24 WEEKS
  • Zidovudine monotherapy can be used in women planning a Caesarean
    section who have a baseline VL of <10 000 and a CD4 of >350.
60
Q

When are STI screenings recommended in pregnancy?

A

At presentation + 3rd Trimester

61
Q

HAART monitoring in pregnancy

A

In women who commence HAART in pregnancy a VL should be performed 2–4wks after commencing HAART, at least once every
trimester, at 36wks, and at delivery.
• In women commencing HAART in pregnancy LFTs should be performed at initiation of HAART and at each antenatal visit.

62
Q

When can vaginal delivery be safe in a woman with HIV

A
  • Untreated women with a CD4 count 350 and a viral load of <50 + zidovudine monotherapy or HAART (including
    Trizivir ® ) and can aim for a vaginal delivery.
  • Vaginal delivery is recommended for women on HAART with an HIV
    viral load <50 at 36wks.

• In women in whom a vaginal delivery has been recommended and
labour has commenced, obstetric management should follow the same
guidelines as for the uninfected population.

• Vaginal birth after Caesarean (VBAC) should be offered to women
with a viral load <50.

63
Q

When should CS be recommended in women with HIV

A

• Delivery by CS is recommended for women taking zidovudine
monotherapy, irrespective of plasma viral load at the time of delivery
and for women with viral load >400 regardless of ART.

• Where the indication for CS is the prevention of MTCT, CS should be
undertaken at between 38 and 39wks gestation.

64
Q

Mx of ROM in HIV

A

• In the presence of ROM >34wks delivery should take place immediately, by either CS or induction of labour (IOL) according to
viral load.

• When PPROM occurs at <34wks:

  • steroids
  • virological control
  • MDT discussion about the timing and mode of delivery.
65
Q

When is Intrapartum IV zidovudine (ZDV) infusion recommended?

A
  • women with a viral load of >10 000 who present in labour, or with ruptured membranes, or who are admitted for planned CS
  • untreated women presenting in labour or with ruptured membranes + unknown current viral load
66
Q

Mx of women presenting in labour/with ROM/without HIV documentation

A

HIV diagnostic point of care test (POCT)

  • If >28weeks start HAART
  • If VL >100k start a 3 or 4 drug regimen including raltegravir
  • if in labour give stat nevirapine and commence fixed-dose zidovudine with
    lamivudine and raltegravir.
  • intravenous zidovudine be infused for the duration of labour and delivery.
67
Q

Can women stop HAART after delivery?

A
  • If AIDs defining illness or CD4 <350 continue HAART
  • HAART continued in all women who commenced cART for MTCT with a CD4 count of between 350 and 500 during pregnancy
    who are co-infected with hepatitis B virus (HBV) or hepatitis C virus
    (HCV).
  • When stopping NNRTI-based HAART post-partum the NNRTI washout period should be covered by 2wks PI-based therapy.
  • All mothers and children require long-term follow-up.
68
Q

Neonatal Mx of delivery form HIV +ve mum

A
  • PEP within 4hours for 4 weeks
  • Zidovudine monotherapy is:
    • maternal viral load is <50 HIV RNA copies/mL at 36wks gestation/delivery
    • mother delivered by CS whilst on zidovudine.
  • Neonates <72h old should initiate 3-drug therapy immediately if:
    • their mothers are HIV +ve and untreated
    • maternal viral load at 36wks gestation/delivery is not <50 HIV RNA copies/mL.
  • Primary pneumocystis pneumonia (PCP) prophylaxis, with co-trimoxazole, should be initiated from age 4wks in:
    • all HIV infected infants
    • infants with an initial +ve molecular diagnostic test result
    • infants whose mother’s viral load at 36wks was >1000 or unknown (and continued until HIV infection has been excluded
69
Q

Recommendations on flying whilst pregnant

A
  • Most airlines will allow flying up to 36wks
    • 32wks with multiple pregnancy
    •>28wks many will request medical certification of fitness to fly.
  • The risk of venous thromboembolism (VTE) significantly increases with
    flights of >8h.
    • avoid dehydration (and alcohol!)
    • take regular short walks around the plane
    • use graduated compression hosiery.

**Consider low dose aspirin.

** Women with other risk factors for deep vein thrombosis (DVT)
(such as factor V Leiden carriers) may require low molecular weight
heparin for flights of >5h

Oxford handbook O&G (7 decks)

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