Infections in pregnancy Flashcards
Number of women of previous CMV exposure?
Incidence of primary CMV in pregnancy?
50-70%.
Primary in ~2% of pregnant women
CMV symptoms in mum
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
Risk factors for CMV
Frequent prolonged contact with young children, daycare workers, parents
Diagnosis of CMV
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
Risk of MFT for primary CMV
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
Risk of MFT for reactivation / non-primary CMV
1% risk of transmission
Less than 1% will be symptomatic –> <10% risk of sequelae
Prenatal diagnosis of fetal CMV
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
USS features suggestive of congenital CMV
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
CMV - counsel women / Prenatal treatment
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
Neonatal testing if confirmed maternal CMV
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
CMV prevention
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
HBV in australia
- prevalence
- high risk groups
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
Definition of chronic hep B
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)
MFT in hep B
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
Maternal HBV screening
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
Management of Hep B in pregnancy
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
Neonate management with maternal hep B
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
Incidence of hep C
Risk factors
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%
Diagnosis of hepatitis C
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)
Vertical transmission of hep C
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
Hep c management during pregnancy
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
Neonatal management with maternal HCV
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
HSV prevalence, transmission
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
Mother to child transmission of HSV if active lesions at delivery
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
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
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
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
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
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
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
Diagnosis of listeriosis
Blood cultures
Rectovaginal culture - gram stain
Placental culture postpartum
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
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)
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
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
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
Baby management of TB
If mother sputum positive, infant should be treated with isoniazide
Medications safe in breastfeeding
Baby - BCG vaccine
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
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
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
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
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
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%
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
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
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
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.`
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
Intrapartum GBS prophylaxis
Benzylpenicillin first line
- Risk of anaphylaxis (1 in 100,000)
If penicillin allergy, clindamycin or vancomycin
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
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
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
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)
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)
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
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
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
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
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)
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
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
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
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
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
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
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
Risk of fetal varicella syndrome
<12/40 - 0.5%
12-28/40 - 1.4%
>28/40 - no cases
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
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
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
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
Risk to pregnancy of influenza
First trimester infection: - Spontaneous miscarriage - Congenital anomalies (maternal hyperthermia) FGR Preterm delivery Subsequent perinatal mortality
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
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
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
Define sepsis
life-threatening organ dysfunction caused by a dysregulated host response to infection
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
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
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
Sepsis 6
- Blood cultures
- FBC and lactate
- Lactate >4 mmol/l is indicative of tissue hypoperfusion - IV fluid challenge (20ml/kg of crystalloid)
- IV antibiotics
- Monitoring of UO
- Oxygen administration
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
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
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
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
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
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
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
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
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
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
