infections Flashcards

1
Q
Your patient has a swab confirming HSV
She has never had this before 
She is...  
T1 
or 
T3
A

HSV is a sexually transmitted viral infection affecting 2% of pregnant woman most of which is unrecognised

Risks:
vertical transmission can result in Neonatal herpes, this is a serious viral infection that can affect the skin, Central nervous system or multiple organs
Risk 1-3% if in T1/2
If within 6 weeks of delivery 40% risk transmission

Disseminated HSV in the mother although rare in adults more common in pregnancy especially if immunocompromised

Ix
HSV PCR from viral swabs
If First episode in T3 check IgG serology to confirm primary infection
Tx
Oral aciclovir 400 mg tds for 5 days
Reduces sxs, length of sx and viral shedding
Paracetamol and 2% lignocaine gel

OM
AN
Suppressive treatment from 36 weeks 400 mg tds
If T3 continue aciclovir until delivery 400 mg tds

IP  
First infection After 28 weeks 
Recommended ELLSCS for delivery  
Neonatal transmission 40%  
If refuse LSCS then consider IV aciclovir for mother and baby  
Inform neonates - prophylactic treatment

If early infection of for VB but avoid FBS FSE difficult instrumentals

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2
Q

Your patient has recurrent HSV

Go

A

Sexually transmitted viral infection affecting 2% of pregnant woman most of which is unrecognised
Risks
Low risk of neonatal transmission even if lesions present at time of delivery 0-3%
Tx
Supportive treatment of HSV episodes – saline baths, paracetamol
Don’t need to treat recurrence flares
OM
AN
Suppressive treatment from 36 weeks 400 mg tds to reduce flare at delivery
IP
Examine for lesions
If present - Discuss LSCS vs VB – VB is safe
Avoid prolonged rupture of membranes, FSE FBS
Consider expediting delivery if HSV and PROM / PPROM
Inform neonates

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3
Q

HIV in pregnancy

A

HIV is a viral infection

Vertical transmission this depends on the viral load
If undetectable, formula fed baby with PEP - <2%
Can be up to 40% if higher viral load, breastfed,
Ix
HIV RNA viral load
HIV resistance testing
CD4 lymphocyte subsets
FBC LFT U+E Cr
Screen for syphilis, hep B+C Chlamydia GBS annual smears

Tx
MDT – ID, high risk obstetrics, neonatal team, high risk midwives  
Education 
Written information  
Support groups  
Initiate or continue HAART by 24 weeks  

OM
Discuss plan for reducing MTCT
Conceive on effective HAART
MDT care with infectious disease / MFM
All woman now should be on anti virals pre pregnancy anyway
IP
Depending on treatment and viral load
If undetectable then ok for a vaginal birth
Chose forceps over vaccum
If 50-400 discuss the risks with the patient MOD – IV zidovudine
If viral load over 400 then for LSCS – IV zidovudine
PPROM
Immediate delivery
MDT discussion

PN
Avoid breastfeeding
Dostinex
Contraception advice

Paeds  
Undetetable viral load – zidovudine  
High / unknown viral load / triple anti virals and PCP prophylaxis  
Paeds aware 
Careful FU plan and testing
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4
Q

Rubella non immune

A

Your booking bloods have shown you do not have antibodies against rubella. You are therefore susceptible to acquiring this infection.

Rubella can cause congenital abnormalities if infection occurs before 16 weeks

There is an immunization available but it is unsafe in pregnancy. We recommend you get this before your next pregnancy.

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5
Q

Rubella non immune presents with arthralgia and fevers

A

Rubella is a viral infection that can cause fetal infection and congential abnormalities

Risk is congenital rubella syndrome  
CRS  depends on gestation  
Risk 1-12 weeks 70%  
Risk 12-16 20% 
Risk 17+ -  

Sequelae:
Deafness 70%
Visual impairment 10–25%,
central nervous system dysfunction 10–25%,
cardiovascular defects 10–20%,
IUGR
Risk of fetal infection depends on gestation These can also have delayed manifestations of disease
Ix
If contact with rubella or rubella like illness – fever, erythema, arthralgia
IgG IgM (if previously non immune)
If both + then new maternal infection
Can offer: Prenatal fetal diagnosis/testing to assess for infection
• amnio or CVS for Rubella PCR, rubella culture and fetal IgM
• 6 weeks after known maternal infection / after the 20th week of gestation

Risk maternal contamination, PCR not overly sensitive, false negative IgM
Tx
No treatment avaliable
TOP offered if CRS / fetal infection

PN
Inform Paeds
Assess for CRS – if concerns will need ongoing assessment opthalmic, hearing and cardiac
Ok to breastfeed

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6
Q

Hep C in pregnancy

A

Explanation
Hepatitis C is an infection that is spread by sharing of bodily fluids – it is often acquire by IVDU
It is an infection that can be cured, but cannot be treated in pregnancy
We need to assess the extent of disease
Untreated hepatitis C can develop into chronic hepatitis and cirrhosis

Risks
Maternal risk
15- 30% of untreated patients with Hepatitis C will develop cirrhosis within 20 years, and 27% of these subsequently develop hepatocellular carcinoma within 10 years.

Fetal risks
Risk of perinatal transmission is 5%
Refer
Gastro for postnatal treatment

Investigation
Hep C RNA to confirm the level for the virus and assess your liver function with LFTs and synthetic function bili albumin and PR
USS liver USS
The degree of risk related to the viral load
Test for Hep B and HIV

Treatment
Cannot treat in pregnancy or breastfeeding as ribovirin is teratogenic

Management
AN
Consider a NIPT for second line screening as it is more sensitive and will Minimise invasive procedures eg amnio and CVS

IP
Try to avoid FSE FBS Prolonged rupture
No evidence that caesarean section reduces transmission
Bath the baby to remove maternal blood from the skin before any IM injections
Care to prevent needle sticks and health care professionals are at a 1-3% risk if this occurs from a woman with Hep C virus PC positive and must undergo adequate occupational health follow up

PP
No evidence that Breast feeding increases transmission

Although consider discarding if breasts care cracked and bleeding

Paeds referral

Infant testing HCV RNA at or after 3 months

Woman or their partners being treated with ribovirin reliable contraception should be used during treatment and for 6 months after completion of treatment

Treatment before the next pregnancy

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7
Q

Hep B

A

The hepatitis B virus is transmitted vertically as a perinatal event, and horizontally through blood products and sexual contact. It is preventable through vaccination and it can be managed although chronic infection cannot be cured.

Risks to mother - Hepatitis with complications of cirrhosis and Hepatocellcular carcinoma 40%

Risks to fetus - Vertical transmission

90% of infected infants become chronic infected

Obstetric medical team / high risk obstetricians / midwives

Refer to a chronic hepatitis clinical service

Written information about NZ services and ongoing management

HBV DNA viral load, Hep B E antigen and antibody, LFTs

(hep B e antigen + risk 80% transmission compared with 30% if neg)

Assess synthetic function Albumin bili and PR

Liver USS if not previously performed

All HBsAg-positive women should have household contacts, other children and sexual partners screened. Those that are non-immune or not already infected should be vaccinated

Gestation and viral load dependent – see below

AN

• Counselled re increased risk of transmission with invasive procedures and discussion around the role of NIPT as a secondary screening tool with increased sensitivity and specificity potentially reducing the need for additional testing.

In those requiring invasive procedures, amniocentesis is probably safer than CVS, and transplacental amniocentesis is best avoided, if possible

•Women with a high viral load in the third trimester (>200,000IU/ml, equivalent to 6 log copies/ml) should be offered tenofivir 30-32 weeks and continued 6 weeks post partum

IP  
Avoid FSE and FBS  
LSCS for obs indication  
 PN  
Baby  
• All infants are offered routine HBV vaccination at birth, 6 weeks, 3 months and 5 months as per the Immunisation schedule.  
• Hep B immunoglobulin at birth (preferably within 12 hours) - other thigh  
Wash baby first 

If immunoprophylaxis is followed then breastfeeding doesn’t increase rates of infection

• Infant Serology at 9 months

Mum
Risk of PN flare – carefully monitored, carefully in touch with chronic hep B services and written information

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8
Q

Syphilis

A

Syphilis is a sexually transmitted infection caused by the spirochete treponema pallidum

It is a systemic infection that has different phases. Primary syphilis can given you a non painful ulcer called a chancre, secondary syphilis you can be unwell with fevers and lymphadenopathy and teritary syphilis can affect your brain and heart.

We need to confirm active disease by performing a trenonemal specific test the EIA

Routine screening in booking bloods for syphilis antibody

Either treponemal test and confirm with non treponemal test (or vice versa)

Trep –Non trep VDRL and RPR

Treponemal specific
EIA / TPPA +

Treponemal specific
EIA / TPPA -

Non trep VDRL / RPR +

Syph
Repeat in 4 weeks
Can have false negative
Non trep VDRL / RPR -
Past / treated infection
Monitor for new infections with the RPR
No syph
Can repeat screening in high risk populations at 28 weeks
Determine stage / Clinical history/Examination / Past test results

Primary -Chancre – high risk fetal infection
Secondary - Systemic illness (fever, rash, lymphadenopathy) - moderate fetal risk
Latent – no symptoms – low fetal risk
Tertiary – cardiovascular, neurological – negligible fetal risk

Woman – late disease
Fetal
IUGR IUFD PTB
Congenital syphilis – can have an immediate or delayed presentation. Classically congential syph presents with hutchinsons triad – hutinsons teeth, interstitial keratitis and 8th nerve deafness

Refer to sexual health

Consider an extended STI panel for screening

If penicillin allergic – refer for desensiting treatment

Treatment if confirmed is IM benzylpenicillin 2.4 million units

1 dose if early infection, 3 doses if late infection

Fetal and maternal Monitoring when treated as 45% risk of Jarisch Herxheimer reaction

Repeat RPR titres monthly in pregnancy

Successful treatment is negative or 4 fold drop in RPR

Retreat if rise

Serial growth scans

Partner testing and treatment

Inform paeds

Send placenta for PCR and histology

Full clinical examination of infant for sequalae for infection and infant serology IgM RPR to be run in parallel to maternal

If positive then FBC U+E LFT XR CSR and treatment if congential syphilis confirmed

If no concern at delivery follow up serology at 3 and 6 months

Ensure adequate documentation for GP, and accessible notes for future pregnancys (as screening will always be positive)

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9
Q

CMV

A

CMV is a common virus that has high prevalence in toddlers and young children. It is excreted in saliva and urine

It affects 0.2-2% of all births

Universal routine serological screening for CMV in pregnancy is not recommended as past infection is not protective.

It may be considered for high risk woman Seropositivity 50%

Transmission
Primary 30%
Secondary 1%
90% children born with CMV are normal
Primary infection 10% risk congenital CMV – half of these ongoing sequelae
10% born healthy may have problems in later childhood

Congenital CMV include IUGR IUFD microcephaly, ventriculomegaly, intracerebral calcifications, microcephaly hepatosplenomegaly, chorioretinitis,

Long term sequelae that may not be evident until later childhood include sensorineural hearing loss, visual impairment cerebral palsy.

Highest risk is in T1 primary infection – 40% risk of fetal transmission and 1/3 of these will have disease
Reactivation has a 1-3% fetal infection risk – similar risk of disease
Suspicion based on serology or USS a referral to MFM
Women with suspected CMV infection
Fetal signs on USS
Flu like illness, malaise, fever, lymphadenopathy
in pregnancy should have
CMV serology testing for IgG and IgM (IgM lasts for ages, confusing)
IgG avidity if both positive.

Diagnosis of primary CMV is based upon:
The new appearance of CMV-specific IgG in a woman who was previously seronegative
The detection of CMV IgM antibody with low IgG avidity.
Low <3 months (primary) High avidity > 3 months (secondary infection)
Can look back at booking bloods if intermediate
If IgM + repeat in 3 weeks for IgG

Dx fetal infection CMV PCR on amnio >8 weeks later and usually > 21 weeks
If positive
USS surveillance +/- MRI to monitor growth and for structural abnormalities

If both normal generally good prognosis

There is currently no effective vaccine to prevent maternal CMV infection, and no proven therapy to prevent or treat fetal infection

Primary prevention - written information for all pregnant woman and those trying to become pregnant

Pregnant women can reduce their risk of being infected with CMV if given the following advice:

Do not share food drinks, or utensils used by children (under the age of 3 years)

Do not put a child’s dummy / soother in your mouth

Avoid contact with saliva when kissing a child (“kiss on the forehead not on the lips”)

Thoroughly wash your hands with soap and water for 15-20 seconds especially after changing nappies or feeding a young child or wiping a young child’s nose or saliva

Clean toys, countertops and other surfaces that come into contact with children’s urine or saliva

PN

All babies of mothers diagnosed with primary CMV infection during pregnancy, should have CMV testing performed with a CMV PCR of saliva or urine with the first 3 weeks of life.

If an infant is diagnosed with congenital CMV, discussion with a paediatrician with experience in infectious diseases is recommended for further assessment and management.

If abnormal newborn screening should test for CMV

Encourage breast feeding

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10
Q

Rubella

A
Rubella is a viral infection that can cause fetal infection and congential abnormalities  
Risk is congenital rubella syndrome  
CRS  depends on gestation  
Risk 1-12 weeks 70%  
Risk 12-16 20% 
Risk 17+ -  

Sequelae:
Deafness (sensory neural hearing loss, 60–75%)
Visual impairment (10–25%, cataracts, micropthalmos, retinopathy, glaucoma, strabismus, cloudy cornea),

central nervous system dysfunction (10–25%, mental retardation, developmental delay, microcephaly),

cardiovascular defects (10–20%, patent ductus, pulmonary artery stenosis, pulmonary stenosis), IUGR

Risk of fetal infection depends on gestation These can also have delayed manifestations of disease

If contact with rubella or rubella like illness – fever, erythema, arthralgia

IgG IgM (if previously non immune)

If both + then new maternal infection

Prenatal fetal diagnosis/testing to assess for infection

  • Rubella PCR, rubella culture and fetal IgM can be performed following chorionic villus sampling (CVS) or amniocentesis.
  • 6 weeks after known maternal infection / after the 20th week of gestation

Risk maternal contamination, PCR not overly sensitive, false negative IgM

TOP offered if CRS

PN
Inform Paeds
Assess for CRS – if concerns will need ongoing assessment opthalmic, hearing and cardiac
Ok to breastfeed

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11
Q

Parvovirus

A

History points:
Timing of contact
Type of contact (home/ childcare worker/ community)

Parvovirus is a common childhood virus that is transmitted from person to person by respiratory droplets. 50% of pregnant women are already immune. If you are infected, there is a 50% risk that it will be transmitted to your baby through the placenta. It is usually asymptomatic but can result in a mild infection in immune competent adults. There is a higher risk of getting parvovirus if you work with children. The highest risk is if you are exposed at home.

If you have been exposed we will test your serum IgG and IgM to determine whether you are immune, susceptible or have had a recent infection.

If IgG negative and IgM positive, we will retest 2-4 weeks after the exposure or if symptoms occur – if the IgG becomes positive this confirms a recent infection.

The incidence of acute parvovirus in pregnancy is 3-4%, affecting 1:400 pregnancies. Of the women affected in pregnancy, 86% will have a normal outcome.

If you are not immune, the incubation period is up to 3 weeks. You are infectious until the rash develops and should avoid contact with pregnant women, young children and immune compromised people.

Risks to mother:
General unwellness – fever, malaise, arthralgias, rash
Aplastic crises in women with sickle cell anaemia
Mirror syndrome if fetal hydrops

Risks to fetus:
Fetal loss if <20/40 (10%)
9-20/40: Fetal anaemia, high output cardiac failure, non-immune hydrops (3%) – onset 2-17 weeks after maternal infection
32% spontaneous resolution
33% death without IUT (within 4-5 days of abnormal USS)
27% resolution after IUT
6% death after IUT
NOT teratogenic – no fetal abnormalities

MFM if confirmed infection in pregnancy
MFM monitoring will include
Fortnightly scans from 4/52 after infection for signs of anaemia
Growth, hydrops, MCA-PSV
There is no intervention to prevent fetal infection or damage
Amniocentesis for the diagnosis of asymptomatic fetal infection is not recommended
Termination is not routinely recommended because of the low risk of fetal damage, may be offered for hydropic infants
1-2 weekly USS for signs of fetal anaemia (MCA-PSV and fetal hydrops)
If present:
Refer to MFM when MCA-PSV >1.5MoM
– a fetus who is mildly hydropic may be profoundly anaemic
Consider blood sampling/ IUT
Cordocentesis for Hb, hct ,platelets
If hydrops occurs and resolved, monitoring for anaemia should continue

IUT: O negative, CMV negative, irradiated, warmed packed RBC

Intrapartum:
Vaginal delivery not contraindicated
Level 3 NICU
Hb, platelets, hct day 1 +/- further transfusion
There are no specific investigations needed for normal infants.

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12
Q

toxoplasmosis

A

Toxoplasmosis is a parasitic infection which carries an increasing risk to the fetus with increasing gestational age at infection. It can be transmitted via uncooked meats and cat faeces. It can be transmitted to the fetus transplacentally.

Most infants are asymptomatic at birth.

The risk of transmission is 10% first trimester, 45% second trimester and 90% third trimester.

The risk of fetal damage if infected is 90% first trimester, 20% second trimester and 10% third trimester.

We first need to confirm whether you have been infected or not, then we will confirm whether your baby has congenital infection.

Maternal:
Flu like illness
Disseminated disease
Encephalitis

Fetal 
Hepatosplenomegaly 
Intracranial calcifications 
Micro/ hydrocephaly 
Hydrops 
Neonatal 
Chorioretinitis 
Sensory neural deafness 
Seizures 
Developmental delay 
If this is confirmed to be a primary infection in pregnancy, we will refer you to MFM for detailed scanning for anomalies +/- invasive testing 

Serology
IgG and IgM (both appear within 1-2 weeks)
If both negative: susceptible, repeat in 2/52
Positive IgM – do IgG avidity and IgA (if low avidity and positive IgA this indicates recent infection)
If low positive IgM, IgA negative, or high IgG avidity <16 weeks then is past infection
But if >16 weeks and high avidity cannot rule out infection early in pregnancy

Fetal infection can be diagnosed with:
Tertiary USS for fetal anomalies
Amniocentesis for PCR 4/52 after infection or at least 18-20/40 gestation
Refer to MFM
Identify risk
Commence antibiotic therapy at diagnosis
<18/40 – spiramycin (to prevent vertical transmission until diagnosis), doesn’t cross placenta, treats MOTHER only

> 18/40 Pyrimethamine + sulfadiazine + folinic acid (treats fetus, potential teratogen in 1st trimester), crosses placenta, treats MOTHER AND FETUS

Once diagnosis confirmed, can alternate spiramycin with PSF (after 18/40)
Efficacy of regimes is not confirmed in randomised trials
Intrauterine diagnosis
USS +/- fetal MRI
T gondii PCR
Toxoplasma amniocentesis for PCR at 18-20/40 or >4 weeks post maternal infection
If positive (with or without abnormal USS)
Consider TOP or
Continue to treat mother
If negative but maternal infection confirmed – continue to treat mother
Serial USS for growth and abnormalities
Postnatal investigation and diagnosis of infant at risk
Recurrence is unlikely as antibodies provide long term protection (unless severely immunosuppressed)
MDT: obstetrics, midwifery, MFM +/- paediatrics
Written information
MFM: serial growth scans

Postpartum 
Placental histology  
Neonate 
IgG/ IgM/ IgA serology 
Full examination 
Hearing test 
Ophthalmology review 
Head USS +/- MRI 
Treatment: pyrimethamine, sulfadiazine, folinic acid
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13
Q

HIV

A

HIV is a viral infection
Vertical transmission this depends on the viral load
If undetectable, formula fed baby with PEP - <2%
Can be up to 40% if higher viral load, breastfed,
HIV RNA viral load
HIV resistance testing
CD4 lymphocyte subsets
FBC LFT U+E Cr

Test partner
Screen for syphilis, hep B+C Chlamydia GBS
MDT – ID, high risk obstetrics, neonatal team, high risk midwives
Education
Written information
Support groups

Initiate or continue HAART by 24 weeks
Discuss plan for reducing MTCT
Conceive on effective HAART
MDT care with infectious disease / MFM
All woman now should be on anti virals pre pregnancy anyway
Vaccination for pneumococcus and meningogocccal
Cotrimox if PCP prophylaxis is CD4 count less then 200

IP
Document and inform staff performing intrapartum care of HIV status and ward appropraite PPE
Depending on treatment and viral load
If undetectable then ok for a vaginal birth
Chose forceps over vaccum
If 50-400 discuss the risks with the patient MOD – IV zidovudine
If viral load over 400 then for LSCS – IV zidovudine
PPROM
Immediate delivery
MDT discussion
Active management of third stage

PN  
Avoid breastfeeding  
Dostinex  
Contraception advice 
Annual smears 
Advise prepregnancy consult in the future  
Paeds  
Inform paeds  
Undetetable viral load – zidovudine  
High / unknown viral load / triple anti virals and PCP prophylaxis  
Wash baby before IM injections  
Careful FU plan and testing
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14
Q

Varicella

A

Varicella exposure

If no hx or hx of immunisation

Fetal Varicella Syndrome
<12 weeks à 0.4%
12-20 weeks à 2%
>20 weeks à isolated case reports only

Sequelae of FVS
Skin scars (dermatomal distribution) 78%
Eye abnormalities (microphthalmia, chorioretinitis, cataracts) 60%
Limb abnormalities 68%
Prematurity, low birthweight 50%
Cortical atrophy, mental retardation (microcephaly) 46%
Poor sphincter control 32%
Early death (in first months of life) 29%

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