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Microbiology > Viral Infections In Pregnancy > Flashcards

Viral Infections In Pregnancy Flashcards

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1
Q

What are the options for treatment from exposure to virus?

A

Prophylaxis- antivirals, passive immunisation ivig, preventative (active) immunisation
Post infection- treatment

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2
Q

What are the classical infections associated with foetal complications?

A 
Toxoplasmosis
Other- syphilus, parvovirus B19, varicella zoster 
Rubella 
Cytomegalovirus 
Herpes simplex virus 
(Influenza, HIV)
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3
Q

What diseases are women routinely screened for at booking?

A

Syphilus
Hep b surface antigen
HIV
Rubella- igG to determine immune status and need for post natal vaccination (for those who haven’t been vaccinated, can’t use MMR)

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4
Q

Why is antenatal serology done?

A

To determine need for antenatal therapy +/- neonatal vaccination (in case of hepb) to prevent vertical transmission.
Serum stored for 1 year

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5
Q

What other diseases are tests for in some centres?

A

Hep c
Toxoplasma
Varicella igG limited value in UK
CMV igM/igG

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6
Q

What is the clinical course of rubella?

A

Mild illness, during first 16 weeks can cause congenital rubella syndrome
16-20 weeks- minimal risk of deafness only
Beyond 20 weeks- no known risk

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7
Q

What is the classic triad for CRS?

A

Sensineural deafness
eye defects- cataracts, congenital glaucoma, pigmentary retinopathy
Congenital heart disease- pulmonary artery stenosis, PDA
Also: purpura, splenomegaly, microcephaly, mental retardation
UK cases- imported

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8
Q

How do we diagnose rubella?

A

Non specific illness associated with onset of disease: rash, arthralgia 0 to 5, and occipital lymphadenopathy -5 to 15 days

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9
Q

How can rubella be tested?

A

Suspect if unvaccinated
Serology may demonstrate rubella igM or seroconversion to rubella igG
Virus detection- PCR from throat swab or blood, often virus gone from blood when symptoms are there

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10
Q

How do we manage rubella?

A

No specific antiviral or prophylaxis demonstrated to be effective
Termination of pregnancy offered in cases of suspected CRS

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11
Q

How can rubella be prevented?

A

Prevention- universal MMR vaccination, give after delivery but before discharge if antenatal testing indicates susceptibility

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12
Q

What is the commonest infectious cause of developmental delay and congenital abnormalities 4 per 1000 births

A

CMV

Relationship between age of gestation and infection unclear

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13
Q

When is the greatest risk of primary CMV infection (reactivation and reinfection significant)

A

During pregnancy or shortly before conception
Seroprevalence- 30-95% worldwide, lower socio economic, rises with age
Lifelong infection, intermittent shedding via saliva and urine

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14
Q

How do we diagnose CMV?

A

Asymptomatic- mononucleosis like illness, rash, hepatitis

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15
Q

How do we diagnose in utero?

A

Growth restriction, hepatosplenomegaly, ventriculomegaly, cardiac defects, microcephaly, cerebral calcification
Serology: CMV IgM and seroconversion to igG
Virus: saliva, urine, blood, amniotic fluid - not done routinely. Risk
Congenital infection: urine, saliva PCR in first 21 days

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16
Q

What is the treatment for CMV?

A

No specific treatment available to prevent in utero transmission, TOP offered if poor prognosis

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17
Q

What is the avidity testing for CMV?

A

Low avidity- igM and igG may be detected
High avidity- strength of antibody. Affinity of antibody increases over time, B cell undergo maturation. If igG is of high avidity, suggests infection occurred more than 3 months ago

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18
Q

What is the risk of congenital infection in the non immune women for CMV?

A

Moderate at 40%
Vast majority are asymptomatic
Some will develop deafness however
If symptomatic at birth, they will have long term problems

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19
Q

What is the risk of congenital infection in those who have already had the infection ie recurrent infection?

A

Small at 1-2%

Most asymptomatic

20
Q

What is the treatment for CMV?

A

Can’t give to mum- ganciclovir teratogenic
Antiviral treatment of infant may improve outcome
Key is recognition of infection
6 months of oral valganciclovir best for long term outcome
Preventative vaccine in development

21
Q

How does HSV occur in pregnancy?

A

HSV 1- orolabial, 2 is genital, lifelong infection with reactivation and asymptomatic shedding
Disseminated HSV derived rarely in pregnant woman

22
Q

How common is HSV congenitally or neonatal ly?

A

Congenital- very rare, infection occurs in utero, risk of fetal death and growth restriction, towards end of pregnancy
Neonatal- rare, same incidence of HSV 1 and 2

23
Q

What are the 3 manifestations of HSV?

A

SEM: 30%
CNS: 10%
Disseminated: 60%

24
Q

What are the routes of infection in pregnancy?

A

Direct contact during birth, risk increases if primary HSV in 3rd trimester, more viral shedding for longer period of time, maternal antibody may not develop straight away
Ascending infection if PROM
Transmission from orolabial HSV, kissing baby, parents, relatives, staff

25
Q

How is primary HSV diagnosis confirmed?

A

Refer to GUM clinic and obstetrician
Confirm diagnosis and HSV type by lesion swab PCR
Confirm primary infection with type specific HSV igG

26
Q

What is the treatment for primary HSV?

A

Offer acyclovir, and prophylaxis until delivery to decrease viral shedding and transmission
Caesarean recommended, if presenting within 6 weeks of delivery or a to lesion in labour
Take swabs from neonate and give neonatal IV acyclovir until active infection ruled out

27
Q

What is the management with recurrent HSV?

A

Risk of HSV transmission is low
Women will have igG which may offer protection to neonate
Vaginal delivery can be offered in first instance
Suppressive therapy with oral acyclovir considered from 36 weeks

28
Q

What is the occurrence of VZV?

A

Cause of chickenpox, and shingles
Common childhood exanthem
Seroprevalence in UK born adults for 90%

29
Q

What is the exposure of susceptible pregnant woman for VZV?

A

Maternal varicella- 5x increased morbidity in 2nd and 3rd trimester. Mum can’t take good breaths, could also have pneumonitis
Less than 20 weeks, congenital varicella syndrome, limb hypoplasia, microcephaly, scarring
More than 20 weeks- neonatal zoster, less severe than CVS
7 days before and after birth- neonatal varicella, severe disseminated infection

30
Q

What should be done if their is risk to susceptible pregnant woman, and their unborn child?

A

Determine immune status- reliable history of chickenpox, consider immune
Unknown history- test for VZV igG

31
Q

What is the treatment for prophylaxis VZV?

A

VZIG, prepared from pooled inactivated serum, limited supply, expensive
Effective up to 10 days after contact
May reduce severity of maternal varicella (50% will still get clinical chickenpox, unclear if CVS is prevented)
Reduces likelihood of neonatal varicella, give to neonate
Consider acyclovir if varicella develops despite VZIG

32
Q

When is VZIG also required for neonates?

A

If there is contact less than 7 days and:
Mother susceptible or immunity unknown
Premature or low birth weight

33
Q

What defines ‘contact’ eight VZV?

A

Same room for up to 15 mins, face to face contact
Infectious period- for chickenpox its 2 days before rash and until lesions have crusted over
Shingles- only if contact with exposed lesions

34
Q

What is parvovirus b19?

A

Slapped cheek disease
Erythema infectiousum
Fifth disease common 50-60% seroprevalence in adults
Mild febrile illness with rash, arthropathy, aplastic anaemia, can be asymptomatic

35
Q

How can parvovirus b19 affect pregnancy?

A

Infection in 1st 20 weeks, result in fetal death, fetal anaemia and hydrops fetalis
Reactivation and reinfection occur but no evidence of risk to fetus

36
Q

Why is it Important to manage parvovirus?

A

Maternal parvovirus b19 infection poses risk to fetus even if asymptomatic
Active fetal management may improve outcome

37
Q

How can serology in parvovirus affect management?

A

IgG positive, igM negative- past infection, reassure
IgG negative, igM negative- susceptible, recheck in one month or if illness develops to identify infection, seroconversion to igG
IgM positive- discuss with medical virology, igM can be non specific, and consider referral to fetal medicine

38
Q

How can hep b affect pregnancy?

A

Commonest cause of liver disease worldwide, vertical transmission major route
Early life acquisition- greatly increased risk of chronic carriage, 90%risk at birth
Infection can occur in utero, at birth, or after

39
Q

How can hep b be prevented?

A

Neonatal vaccination plus or minus antenatal antiviral treatment (5-10% risk when treated)
Acute HBV in pregnancy usually not severe and not associated with teratogenicity
Chronic HBV may flare during pregnancy

40
Q

What are the risk factors for HBV?

A

Maternal viral load, very low risk when below 10

41
Q

How is HBV diagnosed?

A

HBsAg- part of routine antenatal screening
Further HBV markers performed if positive to ascertain status
HBV viral load should be measured in HBsAg positive pregnant women

42
Q

How is HBV managed?

A

Refer to hepatologist
HBsAg positive mother, infant should receive accelerated course of HBV vaccine, 1st dose within 12 hours of delivery
HBeAg positive mother, as above and infant should receive HBV immunoglobulin at birth
HBV viral load high, as above and antenatal antiviral therapy- lamivudine, tenofovir for 6-8 weeks before delivery

43
Q

How does influenza affect pregnancy?

A

Pregnant women identified as at high risk of morbidity and mortality in 2009-10 H1N1 influenza pandemic
Pregnancy induced immune suppression, abdo splinting, high Bmi thought to be implicated
Pregnant women offered seasonal influenza vaccine
Pregnant women with influenza like illness during influenza season should be offered empirical antivirals
Diagnostic specimens should be taken

44
Q

What precautions should be taken with vaccination and pregnancy?

A

Women should be vaccinated against preventable diseases prior to conception
Immunisation in pregnant women effective and largely safe
Live attenuated vaccine- not used, no evidence of harm with MMR and varicella
Immunise against diphtheria, tetanus, pertussis, influenza
28-32 weeks- may optimise transplacental transfer of antibodies to fetus
Postpartum, susceptible women immunised against MMR and varicella

45
Q

What happens to the immune system in pregnancy?

A

State of relative immunosuppression
Infections may be more severe
Some specifically teratogenic
Outcome may depend on gestation

Microbiology (15 decks)

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