Infections in pregnancy Flashcards

1
Q

Number of women of previous CMV exposure?

Incidence of primary CMV in pregnancy?

A

50-70%.

Primary in ~2% of pregnant women

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2
Q

CMV symptoms in mum

A
Asymptomatic in 90%
Non-specific symptoms - viral illness, lymphocytosis
	- Mild febrile symptoms
	- Rhinitis
	- Pharyngitis
	- Myalgia
	- Arthralgia
	- Headache
	- Fatigue 
Pregnancy does not appear to affect clinical severity
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3
Q

Risk factors for CMV

A

Frequent prolonged contact with young children, daycare workers, parents

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4
Q

Diagnosis of CMV

A

IgM and IgG
IgM present after 2 weeks, persists for 3-4 months
IgG present after 2 weeks, lifelong
IgG - low avidity = new infn, high avidity = past
Antibodies bind better (more avid) with time

G like grandma, a.k.a old exposure
M like mum - newer / younger

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5
Q

Risk of MFT for primary CMV

A

For primary infection:
- 30% risk of transmission

–> 10-15% symptomatic congenital CMV
–> 50% risk of sequelae
(death, microcephaly, seizures, developmental delay, hearing loss)

–> 85-90% asymptomatic –> 10-15% risk of sequelae (chorioretinitis, hearing loss)

Sx of congenital CMV if neonate born with Sx - hepatosplenomegaly, jaundice, thrombocytopenia purpura, FGR, microcephaly, pneumonitis, anaemia

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6
Q

Risk of MFT for reactivation / non-primary CMV

A

1% risk of transmission

Less than 1% will be symptomatic –> <10% risk of sequelae

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7
Q

Prenatal diagnosis of fetal CMV

A

Amniocentesis >6-8/52 after presumed maternal infection, >21/40 –> CMV DNA by PCR
Takes 6-8/52 for placental infection and replication, transmission to the fetus, viral replication in the fetal kidney, and excretion into amniotic fluid
Fetal diuresis is not established until 18-20/40
Does not establish which infants will be symptomatic at birth

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8
Q

USS features suggestive of congenital CMV

A
Periventricular calcifications - most characteristic sonographic finding
Cerebral ventriculomegaly
Microcephaly
Echogenic fetal bowel
Hepatosplenomegaly
Hepatic calcifications
FGR
Amniotic fluid abnormalities
Ascites and / or pleural effusion
Hydrops
Placental thickening and enlargement
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9
Q

CMV - counsel women / Prenatal treatment

A

Currently no proven effective therapy for congenital CMV
Refer fetal medicine
No established prognostic factors
Serial 2-4 weekly USS for growth - monitor HC, FGR, structural abnormalities
Consider fetal MRI to assess brain
When USS and MRI are both normal, prognosis is generally good (RANZCOG)
TOP is an option by informed choice if congenital CMV is confirmed in utero, with the knowledge that a positive PCR is not predictive of fetal damage
Antenatal use of CMV immunoglobulin when fetal infection is confirmed may be a consideration with better clinical outcomes for infected babies at 1y in one non-RCT

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10
Q

Neonatal testing if confirmed maternal CMV

A

All babies of mothers diagnosed with primary CMV infection during pregnancy should have CMV testing performed with CMV PCR of saliva, blood or urine. Or CMV IgM. - either + –> congenital CM
Do within first 3/52 of life to distinguish between congenital and postnatal CMV infection

If positive:

  • FBC, LFTs
  • Ophthalmology assessment
  • Head USS and MRI

If infant diagnosed with congenital CMV

  • Discuss / refer to paediatrician
  • Long term follow up of hearing recommended, regardless of infant hearing screen result
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11
Q

CMV prevention

A

Do not share food, drinks or utensils used by children (<3y)
Do not put a child’s dummy / soother in your mouth
Avoid contact with saliva when kissing a child
Thoroughly wash your hands with soap and water for 15-20s 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

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12
Q

HBV in australia

  • prevalence
  • high risk groups
A

1%

Asia and sub-Sahara Africa prevalence as high as 10-15%
Indigenous Australians, Maori, Pacific Islanders, those travelling to endemic areas, people in correctional facilities, sex workers, IVDU

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13
Q

Definition of chronic hep B

A

Persistent detection of Hepatitis B surface antigen for >6 months after initial exposure to the virus
Chronic carriers have 25% chance of dying of liver cirrhosis or liver cancer

Neonates infected at birth - >90% chance of becoming chronic carriers of HBV (c.f. 5% if acquired as adult)

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14
Q

MFT in hep B

A

Usually occurs at labour and delivery through exposure to cervical secretions and maternal blood, but 5% transplacental

Risk of transmission if HBsAg positive:

  • 95% risk if HbeAg positive
  • 2-15% if HbeAg negative
  • Vertical transmission higher if higher viral load
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15
Q

Maternal HBV screening

A
Screening - HbsAg (surface antigen)
If positive screen, then arrange:
- HbeAg
- HbeAb
- HBV-DNA
- LFTs
- Prothrombin time
- Liver ultrasound

Screen household contacts, other children and sexual contacts
- Those non-immune or not already infected should be vaccinated

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16
Q

Management of Hep B in pregnancy

A

Refer to chronic hep B service
Monitoring of ALT

Indications for treatment with Tenofovir in the third trimester (30/40 to 6 weeks PP):

  • Active disease or cirrhosis
  • High viral load (>200,000 IU/ml) in third trimester to reduce risk of neonatal transmission

If receiving anti-viral therapy in pregnancy, monitor closely for several months post-partum for hepatitis flares (ALT every 4 weeks)
Safe to breastfeed on tenofovir

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17
Q

Neonate management with maternal hep B

A

Invasive procedures (e.g. FBS, FSE, Ventouse, or difficult forceps) should be avoided
Neonates given hepatitis B immunoglobulin and HBV vaccine within 24h of birth
- Immunisation 85-95% effective at preventing infection and chronic carrier state
- If immunised can breastfeed
Offer all infants routine HBV vaccination at birth, 6/52, 3/12 and 5/12 as per immunisation schedule
Recommend serology testing >3/12 after completing vaccination course
- HBsAg and HBsAb

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18
Q

Incidence of hep C

Risk factors

A

1% of women of childbearing years
- Up to 80% in high risk groups

IVDU
blood products

Significant risk (80%) of chronic infection 
- With treatment, cure rates of >95%
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19
Q

Diagnosis of hepatitis C

A

Detection of HCV antibody implies persistent infection rather than immunity

If HCV antibody positive, check HCV RNA (PCR test)
LFTs
Screen for HIV (20% have co-infection)

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20
Q

Vertical transmission of hep C

A

Vertical transmission ~5% (1 in 20)

  • Viral load important risk factor, predominantly in women positive for HCV RNA and anti-HCV antibody
  • Higher in those with HIV co-infection

Peripartum infection most common

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21
Q

Hep c management during pregnancy

A

Interferon and ribavirin not recommended in pregnancy or breastfeeding
CS is not recommended as means of reducing perinatal transmission (no evidence to support)
Minimise invasive procedures

Transmission by breast milk is uncommon
OK to breast feed
If cracked or bleeding nipples, advise express and discard milk until open wounds healed

Postpartum - refer for treatment

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22
Q

Neonatal management with maternal HCV

A

Bath baby to remove any maternal body secretions and blood prior to IM injections
All infants of HCV antibody-positive mothers will have detectable levels of maternal HCV antibody for the first few months of life
- Consider diagnosis of vertical transmission when HCV RNA detected in >2 serum samples >3/12 apart in first year of life (via PCR). OR testing of HCV antibodies positive after age 18 months

Immunoglobulin not recommended for infants
Children that contract HCV at birth are usually asymptomatic but at risk of long term liver disease

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23
Q

HSV prevalence, transmission

A

Up to 20% have had genital herpes due to HSV 2
HSV 1 usual cause of oral herpes, but becoming more common as cause of genital herpes

Transmission - via skin to skin contact when virus is being shed

Once infected, can be reactivated in ganglia of sensory neurons

At the start of pregnancy, seropositive rates of women:

- 50% type 1
- 25% type 2
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24
Q

Mother to child transmission of HSV if active lesions at delivery

A

HSV lesions 34/40 - primary infection, seronegative (due to risk of viral shedding in labour)
- Risk of MFT 25-50%
CS shown to significantly reduce vertical transmission
Maternal and neonatal aciclovir therapy should be considered if there has been ROM for >4h or vaginal birth is unavoidable

Prior to 34/40 (seropositive), risk as for recurrent herpes

Low risk of neonatal herpes associated with vaginal delivery (1-3%)
Risk of MFT is higher in recurrent herpes with shedding of HSV-1 than 2
- 15% HSV-1 vs. <0.01% for HSV-2

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25
Management of HSV in pregnancy
1st episode - treat with valaciclovir 1g BD for 7 days All women with previous HSV, offer suppressive Rx from 36/40 - valaciclovir 500mg BD Avoid invasive procedures in labour Elective CS if primary infection after 34 weeks
26
Neonatal HSV presentation
Skin, eyes or mouth (45%) - presents 10-11 days PP. Normal outcome in 98% with treatment. Encephalitis (30%) - presents 16-19 days PP. Mortality with Rx 6%. High risk of neurological morbidity, even with treatment Disseminated infection (25%) - presents 9-11 days. Mortality 30% with Rx. More common in preterm infants
27
Screening for HIV in pregnancy
``` Need consent HIV antibody - Screen with ELISA - Confirm with Western blot (WB) If negative and recent exposure, repeat after 4/52 Offer concurrent STI screening ```
28
Perinatal transmission of HIV
In undiagnosed and untreated women, 20-30% risk of MTCT With ART, appropriate mode of delivery, formula feeding, baby receiving PEP, incidence of perinatal transmission <2% Risk decreases with decreasing levels of maternal HIV RNA (e.g. <1000 copies/ml) - <1% 2/3 of MTCT occurs during delivery With HAART + breastfeeding, risk ~1-5% in first 6 months
29
Incidence and pathogenesis of listeria in pregnancy
Affects 1 in 10,000 pregnant women Incidence of listeria associated with pregnancy is ~13x higher than in the general population Listeria monocytogenes is a gram positive bacillus - intra-cellular pathogen. Cell-mediated immunity is the primary host defence against Listeria Pregnancy is a state associated with depressed aspects of cell-mediated immunity, in order to protect the fetus from immunological attack by the mother In pregnant women, L. monocytogenes colonises the uterus --> placental immune tolerance mechanisms provided a permissive niche for the proliferation of L. monocytogenes
30
Presentation of listeria in pregnancy
Can present similar to flu, or febrile gastroenteritis - Fever - General malaise - Pharyngitis - Headache - Lymphadenopathy - Back pain - Nausea / vomiting - Diarrhoea Tend to get bacteraemia without CNS invasion in pregnant women 1/3 asymptomatic Incubation period: 11-70 days
31
Diagnosis of listeriosis
Blood cultures Rectovaginal culture - gram stain Placental culture postpartum
32
Management of exposed woman
Fever >38.1 and signs and symptoms consistent with listeriosis and no other cause of illness known, test and treat simultaneously - IV amoxicillin +/- gentamicin for 14 days If asymptomatic despite exposure, no treatment or testing indicated - Consider PO ABs If exposed but afebrile with minor signs or symptoms consistent with minor GI or flu-like illness, test and treat with PO
33
Neonatal listerosis
Fetal and neonatal adverse effects are less common if infection occurs at later gestation or with older gestational age at birth Suspicious clinical findings: - Placental, cord or post-pharyngeal granulomas - Multiple small skin granuloma, papular or pustular skin rash - Mec stained liquor <34/40 - Pneumonitis - Purulent conjunctivitis Can present as early or late onset listeriosis Early - preterm, a/w fulminant disease, high mortality (20-60%), present within 7 days Late - generally term, present after 5 days with meningitis, mortality 10-20% ("cheese at night --> dreams = brain like meningitis)
34
Signs of TB
Mycobacterium tuberculosis TB can cause almost any chest signs Crackles and dullness to percussion over upper lobes Lymphadenopathy Erythema nodosum - red painful lumps on shins Extra pulmonary sites - Extra-pulmonary TB is as common as pulmonary TB in pregnancy
35
Diagnosis of TB
``` CXR: atypical appearances Sputum for acid fast bacilli (Ziehl-Neelsen stain) - Culture can take up to 6 weeks Mantoux test Quantiferon gold ```
36
TB management in pregnancy
Untreated TB represents a greater hazard than the treatment MDT - Respiratory, ID Meds: - Rifampicin ○ Vitamin K to mum at 36/40 and baby after birth - Isoniazide ○ + pyridoxine 50mg od to reduce risk of peripheral neuritis - Pyrazinamide and/or ethambutol Monthly LFTs (because of hepatotoxicity of drugs) Mother non-infectious 2 weeks after treatment
37
Baby management of TB
If mother sputum positive, infant should be treated with isoniazide Medications safe in breastfeeding Baby - BCG vaccine
38
Clinical features of parvovirus B19
Presence of human parvovirus IgG appears to confer lasting immunity 40% of women of child-bearing age are susceptible to infection - If child in home infected --> 50% change of infection - If exposure in community / childcare --> 20-30% of infection 20% asymptomatic - Transient fever - Malaise - Arthralgia - Adults can develop rash, but not as common as in children, slapped check appearance is rare - Mild anaemia Infectious for 3-10 days post exposure, or until rash appears
39
Pathogenesis of parvovirus
Small (20-25nm) single-stranded DNA viruses, require rapidly dividing cells for replication - Mainly the erythroid cell precursors --> interrupts red cell production Hence anaemia
40
MTCT of parvovirus
Transplacental transmission - 15% of cases <15/40, rises to 70% towards term ``` Miscarriage - 9% excess fetal loss rate <20/40 - <1% after 20/40 Fetal haemolytic anaemia - Risk greater if infection in first half of pregnancy - High output cardiac failure - Non-immune hydrops (3%) - accumulation of fluid in the fetal soft tissues and serous cavities - 1/3 resolve spontaneously, 1/3 resolve with treatment, 1/3 IUFD No evidence of teratogenesis ```
41
Management of maternal parvovirus
Confirm maternal infection with + IgG and + IgM (if negative results, retest 2-4 weeks) Serial USS from 4 weeks after onset of illness, every 1-2 weeks for up to 12 weeks If MCA-PSV >1.5 MoM, ascites or hydrops, consider fetal blood sampling ? Need fetal blood transfusion
42
Testing for rubella in pregnancy
General screen with IgG at booking Test for IgG and IgM if contact with rubella or rubella-like illness (fever, erythema, arthralgia) Check serum within 7-10 days of onset of rash, and repeat 2-3 weeks later
43
Maternal reinfection - rubella
Can occur More likely after prolonged or intense exposure More likely with vaccine-induced, rather than natural, immunity Usually subclinical Risk of fetal infection <10%, with risk of fetal injury <5%
44
Risk of fetal infection and CRS with rubella maternal infection
<12/40 --> 80% risk of fetal infection, 85% risk of CRS 12-16/40 --> 55% risk of infection, ~35% risk of CRS 17-30 weeks - 30-40% risk of infection, congenital defects rare >31 weeks 60-100% risk of infection, but little to no risk of congenital rubella
45
Diagnosis of fetal rubella infection
``` Recommended if infection <16/40 Amniocentesis - rubella PCR on amniotic fluid USS features: - FGR - valvular stenosis and VSD - abnormal liver, spleen, bowel - eye defects ```
46
Management of maternal rubella infection
<12/40 - consider TOP After 16/40, risk to fetus is negligible USS surveillance to identify features of congenital rubella syndrome - Fortnightly growth scans - Specialist fetal ECHO If infection prior to estimated conception or after 20 weeks, no documented risk
47
Summary of congenital rubella syndrome
Ensure all clinical attendants are rubella vaccinated and have specific antibodies detected - Infectious for at least 12 months after birth Isolate in hospital In order of decreasing frequency: - Hearing loss (sensorineural hearing loss, 75%) - Learning disability (10-25%) - Cardiac malformations (10-20%, PDA, pulmonary stenosis, pulmonary artery stenosis) - Ocular defects Can get late manifestations - hearing loss, endocrine disorders, etc.`
48
Strategies to lower risk of early onset GBS infection
Universal prenatal screening for maternal GBS colonisation - Large retrospective cohort study - stronger protective effect (more cases of early onset GBS infection prevented) with this approach, c.f. obstetric risk based prevention strategy Obstetric risk factors alone - Previous infant with EOGBS - GBS bacteriuria this pregnancy - Spontaneous onset of labour <37/40 - ROM >18h - Intrapartum fever >38
49
Intrapartum GBS prophylaxis
Benzylpenicillin first line - Risk of anaphylaxis (1 in 100,000) If penicillin allergy, clindamycin or vancomycin
50
Toxoplasmosis screening
Not routinely recommended Perform serology if symptoms suggestive of acute toxoplasmosis (malaise, fever, lymphadenopathy) ``` Possible recent infection if : - IgM positive - IgG positive or negative Then confirm with: - Repeat IgM and IgG - high +ve IgM - IgA positive - low IgG avidity ``` Seroconversion occurs 2 weeks after exposure
51
Fetal transmission risk of toxoplasmosis
Increases with gestational age at seroconversion - 1st trimester 4-15% - 2nd - 25-44% - 3rd - 30-75% Risk of congenital abnormality is inversely related to the gestation at maternal infection
52
Diagnosis of fetal toxoplasmosis infection
Detection of toxoplasma gondii DNA in amniotic fluid with PCR Consider amniocentesis at 18-20/40 or >4 weeks after infection Ultrasound features: - Hydrocephalus - Intracerebral or hepatic calcification - Splenomegaly - Ascites
53
Antenatal management with confirmed toxoplasmosis infection
Refer MFM Consider Spiramycin if <18/40 and normal USS Spiramycin administered to the mother reduces the risk of fetal infection by 60-70% NPV of PCR is not 100%, therefore do monthly USS even if negative amniocentesis If confirmed fetal infection - TOP can be offered if appropriate - change to different antibiotics (suladizine, pyrimethamine, folinic acid)
54
Screening for syphilis
Initial screen: enzyme immunoassay (EIA) If this is reactive, then further serological tests will automatically be done by the lab for confirmation - TPPA and RPR EIA and TPPA are specific (treponemal) serology (Detect antibodies that bind to proteins derived from T. pallidum) RPR is non-specific (Detect antibodies that bind to antigens that are, or similar to, those expressed by Treponema pallidum or expressed on host tissues during infection)
55
Risk factors for syphilis
Those who originate from a country where syphilis is common - Africa, SE Asia, China , Asia-Pacific (especially Fiji), South America, Eastern Europe Those who have had sex with a person from a country where syphilis is prevalent MSM HIV positive Multiple sexual partners
56
MTCT of syphilis
Can be transmitted transplacentally at any stage of pregnancy Risk of transmission dependent on: - Stage of maternal infection - Duration of fetal exposure Primary - high risk of fetal infection Secondary - moderate Latent - low risk Tertiary - negligible
57
Primary syphilis
Symptomatic and highly infectious Chancre (ulcer at site of inoculation) - Painless, dark red macule or papule --> erosion - Heals within a few weeks even if untreated Generally appears within 2-6 weeks Typically resolves within 4-8 weeks Localised lymphadenopathy Only 30-40% of cases are diagnosed in the primary stage If not treated 1/3 will progress to chronic stages
58
Secondary syphilis
Develops 3 weeks to 3 months after the appearance of primary syphilis (if untreated) Symptomatic and highly infectious 90% develop skin manifestations - Brown sores (about the size of a penny) - Palms of hands and soles of feet Syphilitic roseola - discrete, pink macular eruption favouring the flanks and disappearing after ~2 weeks Condylomata lata - moist, grey, pink or white, raised, wart-like lesions or plaques Mild fever, Headache, Fatigue Alopecia, Oral manifestations (1/3 to 1/2 of patients) Neurological signs and symptoms Signs may come and go over the next 1-2 years 1/3 go on to develop complications of late / tertiary syphilis if untreated
59
Early / late latent syphilis
Seropositivity but asymptomatic Early latency <2y duration (WHO) Late latency >2y duration (WHO) - People are no longer infectious to sexual contacts, but women may still pass the infection on to the unborn fetus Spontaneous healing (2/3)
60
Tertiary syphilis
Tends to develop 5-20 years from exposure Tuberoserpiginous syphilids Gummas in multiple organs - painless rubbery nodules, mostly seen on the skin, mouth and throat. May form as lesions in the long bones which typically cause bone pain at night Cellular reaction in face of few pathogens Cardiovascular disease - classically chronic inflammation of the aorta resulting in aneurysm formation, aortic valve incompetence, CHF Neurological disease Syphilis reactivates Serious health complications are common
61
Syphilis treatment
Primary, secondary, early latent - 1.8g (2.4 million units) IM Benzathine Penicillin G Late latent, tertiary or unknown - 1.8g (2.4 million units) IM Benzathine Penicillin G once weekly for 3 weeks Benzathine penicillin is the only treatment with proven efficacy in pregnancy for treatment of both mother and baby - Recommended that women who have a penicillin allergy should undergo desensitisation given its efficacy
62
Impact of syphilis on pregnancy
``` Miscarriage Preterm birth Stillbirth (up to 40% of untreated cases) FGR Congenital syphilis ``` USS features a/w infection: - polyhydramnios - hydrops - IUGR - hepatomegaly - placentomegaly - fetal anaemia - lesions of the head
63
Congenital / neonatal syphilis
Can result in stillbirth, neonatal death and long-term disability Infected baby may be contagious until 24h of penicillin treatment has been completed 2/3 asymptomatic at birth, but most will develop symptoms by 5 weeks of age - If symptomatic at birth, 50% will die in the neonatal period If untreated, it leads to physical and neurological impairments affecting the child's bones, teeth, vision and hearing Symptoms of early congenital syphilis - Rash, mucosal lesions, hepatomegaly, nasal discharge, eye lesions
64
Jarisch-Herxheimer reaction
Acute, self-limited (to 48h), febrile reaction Can complicate 45% of syphilis treatment Usually occurs within 24h after Rx for any sphirochetal infection, including syphilis Due to cytokines and fever - not a penicillin allergy Symptoms - Headache, myalgias, rigors, diaphoresis, hypotension, worsening of rash if initially present Can increase the risk of PTL, abnormal CTG Consider fetal monitoring for women who receive treatment after 25/40
65
Management of pregnant women with varicella contact and no PMHx of chickenpox
Consider - type of HZV infection - timing of exposure - closeness and duration of contact If uncertain or no previous history of chickenpox check serology (IgG) - NB part of booking bloods in Australia If non-immune and significant exposure: - VZIG as soon as possible (ideally <96h), can be effective up to 10/7 after contact - Manage as potentially infectious from 8-28 days after exposure if receive VZIG Advise to notify doctor early if develop rash Second dose of VZIG if a further exposure >3 weeks have elapsed since the last dose
66
Treatment of herpes zoster varicella in pregnancy
Symptomatic treatment Hygiene to prevent secondary bacterial infection of lesions Oral aciclovir f present <24h after onset of rash - Reduces the duration of fever and symptoms of infection If severe chickenpox, give IV aciclovir Consider hospital assessment if: - Smoker - Chronic lung disease - Immunosuppressed (e.g. systemic corticosteroids) - Second half of pregnancy Advise her to avoid contact with susceptible individuals (other pregnant women, neonates) until the lesions crust over
67
Risk of fetal varicella syndrome
<12/40 - 0.5% 12-28/40 - 1.4% >28/40 - no cases
68
Diagnosis of fetal infection of varicella
Refer MFM after maternal primary infn Detailed USS >5/52 after primary infection Repeat USS until delivery Amniocentesis is not routinely advised as the risk of FVS is very low USS features: - Microcephaly - Hydrocephalus - Limb deformities - FGR - Soft tissue calcifications
69
Fetal varicella syndrome
The result of herpes zoster reactivation in utero - does not occur at the time of initial fetal infection Appears to only happen if infection <20/40 ``` Skin scarring Eye defects Limb abnormalities Prematurity / IUGR Mental retardation Poor sphincter control Early death ```
70
Varicella infection of the newborn
If maternal primary infn 7 days prior to birth, or 2 days after - immediate VZIG for baby If 2-28 days after, VZIG
71
Why are pregnant women are more likely to become seriously ill and to die than the general population with influenza
Changes in maternal physiology (cardiac, respiratory) - Lung capacity is reduced (can lead to alveolar collapse) - Oxygen consumption is increased - Blood volume, heart rate and stroke volume are increased - Elevation of the diaphragm to accommodate the uterus, increased intra-abdominal pressure, decreased chest compliance, increased risk of aspiration --> increased risk of respiratory failure and complicate the treatment of respiratory illness Changes in the immune system - Shift away from cell-mediated immunity to prevent harmful immune responses being directed at the growing fetus, which is genetically foreign material to the mother - These changes can leave a pregnant woman more vulnerable to some intracellular pathogens, including viral pathogens
72
Risk to pregnancy of influenza
``` First trimester infection: - Spontaneous miscarriage - Congenital anomalies (maternal hyperthermia) FGR Preterm delivery Subsequent perinatal mortality ```
73
Influenza vaccination in pregnancy
Well established to be safe and effective in pregnancy - Only 5 vaccination doses estimated to prevent one case of maternal or infant respiratory illness Maternal vaccination allows transplacental transfer of IgG - Gives newborn protection for first 6/12 Can be given at any gestation Takes 2/52 to begin to be effective At best, only 60% effective
74
Clinical presentation of group A strep
Typically present within 48 of delivery with fevers, rigours, tachycardia Can present up to 7 days postpartum Rapid onset (key feature), non-specific Confusion, dizziness, collapse Abrupt severe limb or chest pain and lower abdominal pain Foul smelling lochia
75
Group A strep treatment
Start with broad spectrum until cultures back - cefuroxime and metronidazole Group A Strep is sensitive to penicillin - IV benzylpenicillin drug of choice Clindamycin has been shown to suppress the expression of some exoproteins (superantigens) and inhibits bacterial protein synthesis - Given in addition to benzylpenicillin in severe cases If penicillin allergy, given cephalosporins or vancomycin If doesn't respond to initial treatment, look for signs of deep infection
76
Define sepsis
life-threatening organ dysfunction caused by a dysregulated host response to infection
77
Define septic shock
Profound circulatory, cellular and metabolic abnormalities substantially increase mortality Persistence of hypoperfusion (hypotension requiring vasopressors to maintain mean arterial pressure >65mmHg and serum lactate >2 mmol/L) despite adequate fluid replacement therapy
78
Sepsis-related Organ Failure (omqSOFA) screening criteria:
- RR>25 - Any non-alert mental state - SBP <90mmHg Score of >2 having predictive validity for women at increased risk of hospital mortality
79
Surviving sepsis campaign
Empirical ABs within 1h of suspected sepsis Lactate within 6 hours - Recheck if >2 mmol/L Obtain blood culture Begin rapid administration of crystalloid Vasopressors if hypotensive during or after fluid resuscitation to maintain MAP >65 mmHg
80
Sepsis 6
1. Blood cultures 2. FBC and lactate - Lactate >4 mmol/l is indicative of tissue hypoperfusion 3. IV fluid challenge (20ml/kg of crystalloid) 4. IV antibiotics 5. Monitoring of UO 6. Oxygen administration
81
SOMANZ antibiotic guidelines NZ
Cefuroxime 1.5g IV q8h + gentamicin 4-7mg/kg (first dose) IV + metronidazole 500mg IV q12h Severe penicillin allergy: Clindamycin 600mg IV q8h gentamicin 4-7mg/kg (first dose) IV Risk of GAS: Add clindamycin 600mg IV q8h
82
Timing of pertussis vaccination
Ideal timing: 20-32/40 - Antibody levels peak ~2/52 after vaccination - Active transport of maternal antibody to the fetus occurs predominantly from 30/40 - Vaccine can be given any time during the third trimester up to delivery Booster immunisation recommended as a single dose in each pregnancy Including pregnancies that are closely spaced to provide maximal protection to every infant
83
Pertussis in newborns
Infants <3/12 are at highest risk of morbidity and mortality from pertussis >50% contract disease from family members, mostly from mother
84
Justify food safety advice for listeria
Predominantly foodborne illness, with sporadic and outbreak-related cases Listeria can be found in soil and water Wash vegetables Advise pregnant women to avoid high risk foods - Unpasteurised dairy products (soft, ripened cheese), seafood, rice salad, sushi Do not re-heat leftover food - listeria can grow at low temperatures, including refrigeration temperatures <5 degrees Celsius Pasteurization kills listeria
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Malaria | - impact on pregnancy
Potentially life-threatening condition in pregnancy that requires urgent treatment In pregnancy, malaria parasites sequester in the placenta where infection is often extremely heavy ``` Implications on pregnancy Fever - Associated with miscarriage and PTL Severe anaemia, may develop rapidly Hypoglycaemia Pulmonary oedema - Results in high mortality (~50%) Jaundice Renal failure Coagulopathy Acidosis Shock ``` Fetal effects: - FHR abnormalities - PTB - Fetal distress - Low birthweight
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What is zika and what are the clinical features
Transmitted by Aedes mosquitoes Most people are asymptomatic - 1 in 5 infected develop symptoms Mild, short-lived illness for 2-7 days Diagnosis: PCR for Zika virus in blood during symptomatic period
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Prevention of Zika
Vector prevention Avoid travel if possible - South and Central America - Pacific and Caribbean Couples should take precautions to prevent mosquito bites and use condoms consistently and correctly when having sex in that country Postpone pregnancy until 3 months after return
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Zika implications on pregnancy
Zika crosses the placenta Probable association with congenital microcephaly - Causal relationship has not been proven No evidence of transmission via breast milk Uncertain when highest risk ? 1st trimester USS findings: - Microcephaly - Intracranial calcifications - Occular lesions - Ventriculomegaly - Cerebral atrophy - IUGR - Placental insufficiency - IUFD
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Management is suspect zika
Baseline fetal USS (anatomy scan) Consider investigations for other travel-associated infections No specific antiviral treatment If positive (or inconclusive): - Serial fetal growth USS (4 weekly) from 24/40 - Refer MFM - Fetal MRI and amniocentesis for ZIKV PCR may be considered (amnio doesn't correlate with outcomes, won't change management) Abstain from sex for rest of pregnancy - can be detected in semen for 180 days Following livebirth: - Send placenta - If congenital infection confirmed, baby should be followed up into childhood
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Impact on COVID on pregnancy
No evidence that pregnant women are more likely to get coronavirus - Changes in immune system in pregnancy can be associated with more severe symptoms Pregnant women, when compared to non-pregnant women of reproductive age, with COVID-19 have higher rates of: - ICU admission - Invasive ventilation - Death Slightly higher rates of preterm birth and CS compared with national averages Breastfeeding advised Vertical transmission rare RANZCOG - vaccine recommended for pregnant and breastfeeding women