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
