Infections in Pregnancy Flashcards

1
Q

Give 5 general consequences of perinatal infection

A
  • Maternal illness
  • Maternal complications more common in infection (e.g pre-eclampsia with HIV)
  • Preterm labour associated with infection
  • Vertical transmission –> infection in child, teratogenic in child
  • Neurological damage in baby more common with bacterial infection
  • Antibiotic usage: can lead to adverse effects in foetus§
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2
Q

What type of virus is CMV?

A

HHV8

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3
Q

Describe how CMV is spread and its epidemiology in pregnancy

A

Spread: sexual contact, blood-borne, contact with bodily fluids (saliva, urine etc)

Around 50% of women are immune

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4
Q

What are the main complications of perinatal CMV infection?

A
  • Increased risk of miscarriage/still birth
    (Mainly neurological):
  • Congenital CMV IUGR (intrauterine growth restriction)
  • microcephaly, intracerebral calcification, blindness, sensori-neural deafness,
  • Hepatosplenomegaly, skin rash, pneumonitis, mental retardation

Can be asymptomatic at birth, infants may present later with blindness, deafness or developmental delay

Common cause of childhood handicap & deafness

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5
Q

Outline the clinical features of CMV infection in the mother

A
  • Often asymptomatic – fever, malaise, fatigue
  • Often no other signs of infection
  • May have lymphadenopathy
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6
Q

What investigations are indicated for perinatal CMV infection?

A
  • Bloods– CMV IgM or IgG for current infection or immunity
  • USS – foetal anomaly scan (e.g microcephaly, growth restriction)
  • Other – amniocentesis for CMV PCR – 6-9 weeks after primary infection in mother
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7
Q

Outline the management for perinatal CMV infection

A
  • No treatment to prevent foetal transmission, may offer TOP if evidence of CNS damage/congenital CMV
  • Neonatal ganciclovir can attenuate audiological neurodevelopmental problems
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8
Q

What is the prognosis for perinatal CMV infection?

A
  • Rate of transmission to foetus is 40%, 10% of these develop congenital syndrome
  • 90% babies symptomatic at birth will later have neurodevelopmental problems

As most maternal infections do not lead to neonatal sequelae, routine screening with invasive amniocentesis is not undertaken

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9
Q

What type of virus is responsible for genital herpes?

A

Type 2 DNA herpes simplex virus

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10
Q

Describe how HSV is spread, both in primary infection and for vertical transmission

A

Transmitted via physical/sexual contact

Vertical: transplacental, neonatal transmission at delivery

Risk is 41% with primary lesion or 2% with recurrent lesions

Risk is greatest when the woman acquires a new infection (primary genital herpes) within 6 weeks of delivery

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11
Q

Outline the complications of maternal HSV infection

A

Neonatal infection is rare, but has a high mortality

Maternal – disseminated herpes (encephalitis, hepatitis, disseminated skin lesions) rare but more common in
pregnancy

Neonatal – 3 subgroups:
• Localised to the skin, eye and mouth
• Local central nervous system disease (encephalitis alone)
• Disseminated infection with multiple organ involvement

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12
Q

Describe how HSV clinically presents in the mother, and indicated investigations

A
  • Burning sensation, pain, pruritus, dysuria, asymptomatic
  • Clusters of vesicles with erythema, can progress to ulcerated lesions which crust over

Investigations:
- Clinical history and examination

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13
Q

Outline the management for: antenatal HSV infection, delivery with primary infection, delivery with recurrent infection, neonatal infection

A

Antenatal – acyclovir 200mg 5x daily for 5 days in primary infection

Delivery with primary infection:

  • If within 6 weeks of likely delivery, advise C-section
  • If opts for vaginal delivery, give IV acyclovir intrapartum

Delivery with recurrent HSV

  • Does not necessitate C-section, women may opt if lesions detected at onset of labour
  • Can offer daily acyclovir from 36/40 to reduce likelihood of lesions

Neonatal infection: give acyclovir

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14
Q

What type of virus is VZV and what infections does it cause?

A

Herpes zoster virus

Causes chickenpox and shingles (reactivation of latent infection)

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15
Q

How is VZV spread?

A

Respiratory droplet transmission

Transfer to baby can be transplacental, ascending vaginal or contact after delivery with lesions

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16
Q

Outline both maternal and foetal complications of perinatal VZV infection

A

Maternal – pneumonia risk, encephalitis is rare complication (has 5-10% mortality)
Non-immune pregnant women are more at risk of complications of chicken pox

Foetal:
• Congenital varicella syndrome – skin scarring, limb hypoplasia, muscular atrophy, rudimentary digits, cortical
atrophy, psychomotor retardation, choreoretinitis, cataracts
• Neonatal varicella – severe disseminated haemorrhagic neonatal VZV – purpura fulminans has 30% mortality
if untreated

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17
Q

Describe the clinical presentation of perinatal VZV infection and the indicated investigations

A
  • Prodromal fever, malaise, myalgia (adults > children)
  • Centripetal maculopapular rash mainly in areas not exposed to pressure. Vesicular rash appearing in crops

Investigations:
• Can send vesicular fluid for VZV PCR, electron microscopy (not serology)

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18
Q

When is there greatest risk of neonatal VZV infection?

A
  • Teratogenicity: rare but consequence of early pregnancy infection
  • Maternal infection in 4 weeks preceding delivery
  • If delivery occurs within 5 days after or 2 days before maternal symptoms
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19
Q

Outline the management for perinatal VZV infection (non-immune women with exposure, maternal infection, maternal infection around time of delivery)

A
  • Ask if woman has had chickenpox previously, VZV IgG is marker for immunity

Ig for prevention, aciclovir for treatment

Non-immune women exposed to chickenpox:
- VZ immunoglobulin given ASAP (effective if given up to 10 days after contact)

If infection occurs:

  • Avoid contact with other pregnant women and neonates until the lesions have crusted over
  • Aciclovir within 72hrs of rash appearing (N.B VZIG is ineffective once chickenpox has developed)

Maternal infection around time of delivery:

  • VZIG for neonate
  • Monitor neonate for signs of infection, until 28 days after onset of maternal infection
  • Neonatal infection: give acyclovir

Ideally vaccinated pre-conception if non-immune, can vaccinate post-partum also

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20
Q

Outline the epidemiology of perinatal rubella infection

A

Rare (due to MMR immunisation): 97% of women in the UK are vaccinated

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21
Q

Outline the clinical presentation of maternal rubella infection

A
  • Fever, malaise, coryzal symptoms (cold-like symptoms), arthralgia, rash
  • Lymphadenopathy, maculopapular rash (usually starting behind the ears, spreadingto head and neck, then to rest of body)
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22
Q

Describe the required investigations to diagnose maternal rubella infection

A
  • Bloods – rubella serology IgM (active), IgG (immune)

* USS – foetal anomaly

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23
Q

Outline the complications of perinatal rubella infection, including when the risk to the foetus is greatest

A

• Maternal – miscarriage, pneumonia, arthropathy, encephalitis, ITP

• Foetal – death
- Congenital rubella syndrome: deafness, VSD, PDA, cataracts, CNS defects, IUGR, hepatosplenomegaly, thrombocytopenia, rash

Highest risk of congenital rubella syndrome is in first trimester (90%), then around 5-10% risk 14-16/40, risk after 20/40 is very low

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24
Q

Outline the management and screening options in perinatal rubella infection

A

Non-immune women develops rubella <16/40: TOP is offered

Screening

  • No longer routinely offered in UK (as levels are v low)
  • Screening would identify those in need of vaccination following pregnancy (as live vaccine is contraindicated during pregnancy)
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25
Q

Outline the epidemiology of perinatal parvovirus B19 infection

A

0.25% of pregnant women

50% of women are immune

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26
Q

During which gestation period is vertical transmission most likely?

A

Risk period for foetal transmission is between 4-20/40
No transmission before 4/40
Low risk of foetal hydrops after 20/40

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27
Q

Outline the clinical features of maternal perinatal and neonatal parvovirus B19 infection

A

• Rash – commonly ‘slapped cheek’ appearance (erythema
infectiosum)
• Malaise, fever, arthropathy
• May have purpura, erythema multiforme

Neonatal:
Viruses suppresses foetal erythropoiesis –> anaemia, thrombocytopenia
–> cardiac failure –> oedema and foetal hydrops

28
Q

Describe the investigations required in perinatal parvovirus B19 infection

A

• Bloods – parvovirus serology IgM (active infection), IgG (immunity), rubella serology (due to similar presentation)

• USS – foetal anomaly scan 4 weeks after onset of illness, then 1-2 weekly intervals until 30/40
Anaemia detectable via increased blood flow velocity in foetal middle cerebral artery and foetal hydrops

29
Q

Describe the management for perinatal parvovirus B19 infection

A
  • Maternal – symptomatic (mild, self-limiting illness)
  • Foetus – intrauterine blood transfusion if foetal hydrops

Mothers infected are scanned regularly to look for foetal anaemia

30
Q

Outline the prognosis for perinatal parvovirus B19 infection

A
  • Untreated foetal hydrops has 50% mortality, reduced to 18% by intrauterine blood transfusion
  • Does not cause congenital abnormalities
31
Q

Describe the epidemiology of perinatal Hep B infection and its vertical transmission

A

Degree of infectivity depends on serology status

Women with E antigen (HbeAg +ve) have a high rate of vertical transmission

32
Q

Describe the management plan for perinatal Hep B infection

A

For neonates:

  • Hepatitis B immunoglobulin and the vaccine help reduce vertical transmission (given to all positive women)
  • immunoglobulin given immediately after delivery
  • The vaccine is given at birth, 1 month and 6 months

For women:
- Women with high viral load can be treated with antivirals from 32/40 onwards

Part of routine screening in antenatal care

33
Q

Outline risk factors for vertical transmission of Hep C virus

A
  • High viral loads

- Co-existing HIV infection

34
Q

Outline the clinical presentation of perinatal HCV infection

A
  • Can lead to cirrhosis and hepatocellular carcinoma

- 80% are asymptomatic

35
Q

Describe the management plan for perinatal HCV infection

A
  • Detect anti-HCV antibodies
  • Confirm with PCR for the virus
  • In non-pregnant adults, interferon and ribavirin is used to treat hepatitis C (these are CONTRAINDICATED in pregnancy)

Screening is not routine in antenatal care (unlike HBV), but can be offered to high risk groups (HIV positive)

36
Q

Describe the epidemiology, route of transmission and prognosis of perinatal Hep A virus

A

Transmission: faeco-oral
Affects 1:1000 pregnancies (0.1%)

Prognosis:

  • Does not lead to chronicity
  • 2% mortality
37
Q

Outline the risk factors for vertical transmission of HIV

A
  • High viral load, low CD4 count
  • Intrapartum: prolonged rupture of membranes (>4h): [elective C-section reduces risk of transmission]
  • Breastfeeding
38
Q

Describe the clinical presentation of perinatal HIV infection

A

• Asymptomatic until AIDS progression or febrile seroconversion illness

May present with:
• Opportunistic infection or AIDS defining illness – PCP, Kaposi sarcoma, oesophageal candidiasis

39
Q

Describe the possible complications of perinatal HIV infection

A

Increased incidence of:

  • Pre-eclampsia
  • Stillbirth
  • Growth restriction
  • Prematurity

HAART side effects

  • pre-eclampsia
  • obstetric cholestasis, lactic acidosis, glucose intolerance, GDM
  • But NOT teratogenic
40
Q

Describe the investigations for perinatal HIV infection

A

Bloods

  • Routine HIV testing in antenatal booking visit
  • Regular viral load, CD4 count
  • Monitor drug toxicity – FBC, UE, LFT, lactate, blood glucose
41
Q

Generate a management plan for: antenatal HIV infection, intrapartum infection and neonatal infection

A

• Antenatal

  • HAART – at least 3 ART if CD4 >350x106/L, aim to suppress to undetectable level (<50 copies/ml)
  • If CD4 and viral load acceptable, start ART rom 28-32 weeks

• Intrapartum

  • If viral load detectable or HAART non-compliance, advise C-section
  • If viral load undetectable, consider vaginal delivery, avoid FBS/FSE or rupture of membranes for more than 4 hours

• Neonatal

  • ART 4-6 weeks
  • PCR testing at birth, 3 weeks, 6 weeks, 6 months
  • HIV antibody test at 18 months
  • Avoid breastfeeding
42
Q

Define Group B Streptococcus infection

A

Infection caused by the bacterium Streptococcus aglactiae

43
Q

Outline the epidemiology of perinatal GBS

A

Commensal bacteria of vagina and rectum, carried without symptoms in around 25% of pregnant women

44
Q

Describe the maternal clinical presentation of perinatal GBS and neonatal complications of infection

A
  • Often asymptomatic

Neonates

  • Severe illness: sepsis (collapse, tachypnoea, nasal flaring etc.), pneumonia, meningitis, death
  • Mortality: 6% in term, 18% preterm
45
Q

Describe the investigations carried out for perinatal GBS

A

Micro
o HVS (high vaginal swab), LVS (low vaginal swab), rectal swab: for MCS
o No national screening programme – no clear benefit, concerns about antibiotic resistance/anaphylaxis

46
Q

Outline risk factors for vertical transmission of GBS

A
  • Positive HVS, LVS, rectal swab or MSU
  • Previously affected baby
  • Pyrexia after labour
  • Prolonged rupture of membranes (GBS is transmitted during labour)
  • Preterm labour
47
Q

Describe the treatment strategy for perinatal GBS in the UK

A

Treatment only used if there are risk factors for vertical transmission or incidental GBS carriage

  • IV benzylpenicillin in labour (use clindamycin if allergic to penicillin)
48
Q

Define syphilis infection

A

Syphilis is a systemic infection caused by the spirochete Treponema pallidum

49
Q

Outline the maternal clinical presentation (primary, secondary, tertiary) of perinatal syphilis

A

• Primary – painless but infectious lesion on skin (chancres), disappear spontaneously after 1 week

• Secondary – 1 to 10 weeks after appearance of the chancre, development of macular-papular skin rash, sore
throat, fever, headache, arthralgia

• Tertiary – 1 to 20 years after initial infection, can develop into neurosyphillis, cardiovascular syphilis, gummatous
syphilis (granulomatous lesion in skin, bone)

50
Q

Describe the complications of maternal syphilis infection

A
  • Miscarriage
  • Stillbirth
  • Severe congenital disease
  • Neonatal mortality
51
Q

Outline the investigations undertaken for maternal syphilis infection

A

• Bloods – RPR and VDRL, can give false positive results (e.g. with EBV, TB, lymphoma, malaria & autoimmune disease)
–> combine with TPHA and FTA-ABS which are more specific based on monoclonal antibodies and immunofluorescence

• Microbiology – microscopy of fluid from primary/secondary lesions (with dark-field illuminations)

52
Q

Describe the management for maternal syphilis infection

A
  • Antibiotics – parenteral penicillin (first choice, gold standard) or oral tetracycline or doxycycline (contraindicated in pregnancy)
  • Follow-up – clinically and serologically at 1, 2, 3, 6 and 12 months then 6-monthly until seronegative
  • Contact tracing, requires full STI screen
53
Q

Describe a reaction that may occur after treatment for maternal syphilis

A

Jarish-Herxheimer reaction:

  • This presents with worsening of symptoms and fever for 12-24 hours after starting treatment
  • Associated with uterine contractions & foetal distress
  • Women may be admitted at the time of treatment for monitoring
54
Q

Outline complications of maternal TB infection

A
  • Prematurity
  • IUGR
  • Miscarriage, small for date uterus, low birth weight, increased neonatal mortality
  • Congenital TB (rare)
55
Q

Describe the management for maternal TB infection

A
  • First-line drug treatment: isoniazid, rifampin, and ethambutol (EMB) daily for 2 months, followed by I and R daily, or twice weekly for 7 months (for a total of 9 months of treatment)
  • Streptomycin should not be used (harmful to foetus)
  • Pyrazinamide is not recommended
56
Q

Define toxoplasmosis infection

A
  • Infection caused by the protozoon toxoplasma gondii

* A parasite excreted in cat faeces, soil, infected meat

57
Q

Outline risk factors for vertical transmission of toxoplasmosis

A

Increased risk of vertical transmission with increasing gestational age (5% 1st, 80% 3rd trimester)

58
Q

Describe the complications of perinatal toxoplasmosis infection

A

Neonatal:

  • Mental handicap
  • Convulsions, spasticities
  • Visual impairment
  • Congenital toxoplasmosis: hydrocephalus, retinochoroiditis, intracranial calcification, IUGR
59
Q

Describe some investigations undertaken for toxoplasmosis infection

A
  • Bloods – toxoplasmosis IgM (active), IgG (immunity)
  • USS – foetal anomaly scan
  • Other – amniocentesis to detect foetal infection
60
Q

Describe the management for perinatal toxoplasmosis

A

Health education (washing hands after contact with soil, cat litter etc.)
• Antibiotics – spiramycin (reduces risk of vertical transmission)
• Foetal infection: termination should be offered

61
Q

Define listeriosis and outline the epidemiology in pregnancy

A

Infection caused by the gram-positive bacillus bacterium Listeria monocytogenes
Transmission is faecal-oral route (eating soft cheese, pate,
unpasteurised dairy products, unwashed salads)

1 per 20 000 pregnancies (very rare)

62
Q

Describe the complications of perinatal listeriosis

A
  • Potentially fatal infection of foetus (particularly if maternal bacteraemia occurs)

Prognosis
- Poor with septicaemia, meningitis or neonatal infection with mortality of 50%, 70% and 80% mortality respectively

63
Q

Outline the clinical presentation and investigations undertaken for perinatal listeriosis

A

Presentation:

  • None specific
  • Diarrhoea, vomiting, malaise, fever, sore throat, myalgia
  • Often asymptomatic

Investigations:
Microbiology – blood culture, amniotic fluid culture, placental culture (serological not reliable)

64
Q

Describe the management for perinatal listeriosis

A

• IV antibiotics – penicillin and aminoglycoside e.g. gentamicin

Avoidance of high risk foods in pregnancy

65
Q

Outline the complications of perinatal malaria infection

A

Maternal complications more common (e.g severe anaemia)

Foetal:

  • Growth restriction
  • Stillbirth
  • Preterm labour
66
Q

Describe the investigations carried out for perinatal malaria infection

A

• Gold standard is microscopic examination of thick (detects parasites) and thin (detects species) blood films for parasites

67
Q

Describe the management of perinatal malaria infection

A

• Treated in pregnancy as an emergency – IV artesunate 2.4mg/kg at 0,2,24 hrs then daily for severe
falciparum malaria

• Oral quinine 600mg TDS and PO clindamycin 450mg TDS for 7 days for uncomplicated falciparum or mixed
(e.g. falciparum and vivax)

N.B 75% of malaria caused by plasmodium falciparum, others are vivax, malariae, ovale and rarely knowlesi