Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

O&G > Infections in Pregnancy > Flashcards

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§
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What type of virus is CMV?

A

HHV8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What type of virus is responsible for genital herpes?

A

Type 2 DNA herpes simplex virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is VZV spread?

A

Respiratory droplet transmission

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Outline the epidemiology of perinatal rubella infection

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the required investigations to diagnose maternal rubella infection

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

* USS – foetal anomaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Outline the epidemiology of perinatal parvovirus B19 infection
0.25% of pregnant women | 50% of women are immune
26
During which gestation period is vertical transmission most likely?
Risk period for foetal transmission is between 4-20/40 No transmission before 4/40 Low risk of foetal hydrops after 20/40
27
Outline the clinical features of maternal perinatal and neonatal parvovirus B19 infection
• 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
Describe the investigations required in perinatal parvovirus B19 infection
• 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
Describe the management for perinatal parvovirus B19 infection
* Maternal – symptomatic (mild, self-limiting illness) * Foetus – intrauterine blood transfusion if foetal hydrops Mothers infected are scanned regularly to look for foetal anaemia
30
Outline the prognosis for perinatal parvovirus B19 infection
- Untreated foetal hydrops has 50% mortality, reduced to 18% by intrauterine blood transfusion - Does not cause congenital abnormalities
31
Describe the epidemiology of perinatal Hep B infection and its vertical transmission
Degree of infectivity depends on serology status Women with E antigen (HbeAg +ve) have a high rate of vertical transmission
32
Describe the management plan for perinatal Hep B infection
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
Outline risk factors for vertical transmission of Hep C virus
- High viral loads | - Co-existing HIV infection
34
Outline the clinical presentation of perinatal HCV infection
- Can lead to cirrhosis and hepatocellular carcinoma | - 80% are asymptomatic
35
Describe the management plan for perinatal HCV infection
- 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
Describe the epidemiology, route of transmission and prognosis of perinatal Hep A virus
Transmission: faeco-oral Affects 1:1000 pregnancies (0.1%) Prognosis: - Does not lead to chronicity - 2% mortality
37
Outline the risk factors for vertical transmission of HIV
- High viral load, low CD4 count - Intrapartum: prolonged rupture of membranes (>4h): [elective C-section reduces risk of transmission] - Breastfeeding
38
Describe the clinical presentation of perinatal HIV infection
• Asymptomatic until AIDS progression or febrile seroconversion illness May present with: • Opportunistic infection or AIDS defining illness – PCP, Kaposi sarcoma, oesophageal candidiasis
39
Describe the possible complications of perinatal HIV infection
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
Describe the investigations for perinatal HIV infection
Bloods - Routine HIV testing in antenatal booking visit - Regular viral load, CD4 count - Monitor drug toxicity – FBC, UE, LFT, lactate, blood glucose
41
Generate a management plan for: antenatal HIV infection, intrapartum infection and neonatal infection
• 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
Define Group B Streptococcus infection
Infection caused by the bacterium Streptococcus aglactiae
43
Outline the epidemiology of perinatal GBS
Commensal bacteria of vagina and rectum, carried without symptoms in around 25% of pregnant women
44
Describe the maternal clinical presentation of perinatal GBS and neonatal complications of infection
- Often asymptomatic Neonates - Severe illness: sepsis (collapse, tachypnoea, nasal flaring etc.), pneumonia, meningitis, death - Mortality: 6% in term, 18% preterm
45
Describe the investigations carried out for perinatal GBS
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
Outline risk factors for vertical transmission of GBS
- 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
Describe the treatment strategy for perinatal GBS in the UK
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
Define syphilis infection
Syphilis is a systemic infection caused by the spirochete Treponema pallidum
49
Outline the maternal clinical presentation (primary, secondary, tertiary) of perinatal syphilis
• 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
Describe the complications of maternal syphilis infection
- Miscarriage - Stillbirth - Severe congenital disease - Neonatal mortality
51
Outline the investigations undertaken for maternal syphilis infection
• 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
Describe the management for maternal syphilis infection
* 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
Describe a reaction that may occur after treatment for maternal syphilis
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
Outline complications of maternal TB infection
- Prematurity - IUGR - Miscarriage, small for date uterus, low birth weight, increased neonatal mortality - Congenital TB (rare)
55
Describe the management for maternal TB infection
- 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
Define toxoplasmosis infection
* Infection caused by the protozoon toxoplasma gondii | * A parasite excreted in cat faeces, soil, infected meat
57
Outline risk factors for vertical transmission of toxoplasmosis
Increased risk of vertical transmission with increasing gestational age (5% 1st, 80% 3rd trimester)
58
Describe the complications of perinatal toxoplasmosis infection
Neonatal: - Mental handicap - Convulsions, spasticities - Visual impairment - Congenital toxoplasmosis: hydrocephalus, retinochoroiditis, intracranial calcification, IUGR
59
Describe some investigations undertaken for toxoplasmosis infection
* Bloods – toxoplasmosis IgM (active), IgG (immunity) * USS – foetal anomaly scan * Other – amniocentesis to detect foetal infection
60
Describe the management for perinatal toxoplasmosis
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
Define listeriosis and outline the epidemiology in pregnancy
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
Describe the complications of perinatal listeriosis
- 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
Outline the clinical presentation and investigations undertaken for perinatal listeriosis
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
Describe the management for perinatal listeriosis
• IV antibiotics – penicillin and aminoglycoside e.g. gentamicin Avoidance of high risk foods in pregnancy
65
Outline the complications of perinatal malaria infection
Maternal complications more common (e.g severe anaemia) Foetal: - Growth restriction - Stillbirth - Preterm labour
66
Describe the investigations carried out for perinatal malaria infection
• Gold standard is microscopic examination of thick (detects parasites) and thin (detects species) blood films for parasites
67
Describe the management of perinatal malaria infection
• 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

O&G (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions