Perinatal infections CMV HSV Syphillis Rubella Toxoplasmosis Flashcards
What public health intervention should be taken to combat congenital CMV infection? Justify your answer.
- All women should receive advice on CMV during routine antenatal care
- Avoid kissing small children on the mouth
- Wash hands regularly, and especially after wiping the nose, mouth or toileting young children
- Wash surfaces with antibacterial after contact with urine/saliva of small children
- Do not share food or drink utensils
- Don’t put dummies into the mouth
- There is no evidence for routine serological screening during scheduled antenatal care
Justification
- Children under 3 years old are particularly likely to excrete virus, and at a higher titre than adults
- This risk is increased if they go to day care
- They excrete virus in urine and saliva
- Both primary and secondary infections (reinfection), or reactivation, can result in transmission to the fetus and potentially cause congenital CMV
- Though transmission to the fetus is less in secondary infection or reactivation as compared to primary infection (1-3% vs 30-40%), the rate of seropositivity (and hence latent phase of infection) in the the Australian population is 40-60%, and the largest burden of congenial CMV is attributed to secondary infection/reactivation
- Consequently any public health approach needs to target all women, regardless of their existing CMV serological status
Describe the transmission of CMV, and the risk for congenital CMV.
Primary CMV: 30-40%
Reactivation: 1-3% transmission risk
1st trimester infection: neurodisability risk higher
2nd/3rd: acute visceral disease more likely
- The mother often contracts CMV from other children (particularly under 3 years, or attending day care); it can be transmitted in their urine or saliva
- Adults transmit CMV from the cervix, semen and other bodily fluids
- It can be contracted from direct contact with infected fluid, or via fomites
- Transmission to the fetus is across the placenta, or can be during or after delivery
- The highest risk of transmission to the fetus is during primary infection in the first trimester, when the risk is 30-40%; roughly 1/3 will develop symptoms of congenital CMV (10% overall)
- The risk of transmission to the fetus in secondary infection or reactivation is 1-3%; however, once infected, the risk of morbidity and mortality is comparable to during primary infection
- 90% foetuses will have no signs/symptoms of congenital CMV at birth; however 10-15% of these may develop longer term sequelae in early childhood (SNHL, chorioretinitis most common)
A woman who is 24 weeks pregnant presents acutely with flu-like symptoms, a fever, and cervical lymphadenopathy. Describe your approach to screening and diagnosing possible congenital CMV in this case.
- History
- Examination
- Serological testing (CMV IgM, IgG …+/- IgG specific avidity)
- USS findings +/- MRI
- Amniocentesis and CMV nucleic acid PCR- 6-8 weeks after infection
Outline the interpretation of different CMV serological results
IgM -, IgG - = no previous CMV, still susceptible
IgM -, IgG + = Previous CMV infection, no current infection
IgM +, IgG - = false positive IgM, or possible early primary infection; repeat test in 2 weeks
IgM +, IgG +, low IgG avidity = Primary infection within last 3 months
IgM +, IgG +, intermediate IgG avidity = Possible primary infection within last 3 months - manage as acute primary infection
IgM +, IgG +, high IgG avidity = Infection > 3months, reinfection or reactivation
Retrospective assessment of booking bloods can also be helpful to determine a primary infection, by demonstrating seroconversion within the pregnancy
What investigations can be used to diagnosis congenital CMV?
Maternal Serology
USS for fetal anomaly +/- MRI fetal intracranial lesion
Amniocentesis
- Ideally after 21wks gestation and >8 weeks after acute infection for best sensitivity (80-100%) and specificity (-high false negative <21 wks gestation)
Neonate:
CMV serology
CMV PCR testing on saliva or urine within first 3 wks of birth
USS +/- MRI of head
What is the management for babies affected by congenital CMV?
Antenatal:
- Refer to MFM specialist
- Serial US for growth monitoring
- MRI to assess for congenital abnormality, particularly intracranial and neurological defects
- If US and MRI are normal, there is a very good prognosis
After birth:
- Newborn hearing assessment
- Ophthalmology and head USS +/- MRI after birth
- Referral to paediatric with specialist interest in congenital CMV
- 3-6 monthly review for first 2 years of life, including hearing and neurodevelopment assessment
- Treatment dependent on level and site of organ involvement
- IV ganciclovir for 6 weeks or oral valganciclovir for up to 6 months has demonstrated some benefits in improving hearing and neurological outcomes at 6 and 12 months
- Breast feeding should be encouraged, there is no evidence that transmission after birth has any significant sequelae
What are the findings and sequelae associated with congenital CMV infection?
- SGA
- polyhydramnios or oligohydramnios
- microcephaly
- Intracerebral calcification
- ascites/hydrops
- chorioretinitis
- hepatosplenomegaly
- anaemia/thrombocytopenia
- still birth and neonatal death
Long term sequelae:
- sensorineural hearing loss (not always present at birth)
- cerebral palsy
- developmental delay
- visual impairment
- Poor school performance
What 3 infections can be transmitted in utero and cause congenital defects?
- CMV
- Rubella
- VZV (chicken pox)
What is the prevalence of CMV congenital infection?
- 0.2 - 2.2% pregnancies (roughly 1 in 200 pregnancies)
- It is the commonest of congenital infections
What causes toxoplasmosis and how is it transmitted?
- Toxoplasmosis Gondii (a protozoan parasite)
- Common gut parasite in cats (can be in any animal); after ingesting infected food cats excrete oocysts in their faeces for several weeks - kittens tend to shed highest numbers due to primary infection
- Transmission to humans is food borne (contaminated, undercooked food or poor food hygiene during preparation); zoonoses via cat faeces; congenital vertical transmission
What is the presentation of toxoplasmosis in adults?
- In the adult most are asymptomatic; 10% get flu-like illness, fever, cervical lymphadenopathy, chorioretinitis
- After acute infection it remains in the body in an inactive state, which can be reactivated during times of immune suppression
- Severe presentations are common in the immune compromised and can be reactivated during immune suppression; pneumonitis, myocarditis and encephalitis
What are the sequelae of congenital toxoplasmosis?
- Can cause miscarriage, stillbirth and neonatal death
- Majority of babies born with toxoplasmosis are asymptomatic
- 10% of affected babies are born with chorioretinitis and blindness
- 20% have generalised disease: hepatosplenomegaly, anaemia, thrombocytopenia, jaundice, SN hearing loss, microcephaly (rare), spasticity, mental retardation and seizures
In congenital toxoplasmosis, what are the risks to the fetus in each trimester?
If the mother is immune (20-35% reproductive population), the risks of transmission and significant sequelae are low.
First trimester
- Low risk MTFT (4-15%)
- High risk of morbidity/mortality
Second trimester
- Intermediate risk MTFT (25-40%)
- Intermediate risk of morbidity/mortality
Third trimester
- High risk MTFT (30-75%)
- Low risk of morbidity/mortality; majority born without symptoms
How is toxoplasmosis diagnosed in pregnancy?
- Maternal serology
- USS +/- MRI - poor sensitivity and specificity
- Amniocentesis and T.Gondii PCR (>4 weeks after acute infection)
Once confirmed, what are the management options for toxoplasmosis infection during pregnancy?
Antenatal:
- Fetal USS +/-MRI
- Amniocentesis and toxoplasma PCR from 4 weeks after expsoure
- spiramycin if <18 weeks gestation
- Pyrimethamine and sulfadiazine from ≥18 weeks gestation ( with folinic acid)
Postnatal:
- Full examination after birth, with ophthalmology and hearing review, head USS +/-MRI, fetal serology IgA/IgM, T.Gondii PCR
- If any of the above are abnormal, the infant should be treated with 12 months of pyrimethamine and sulfadiazine with folinic acid; they will require ongoing monitoring of vision, hearing and neurodevelopment delay through early childhood
Which 3 congenital infections are most strongly associated with SGA?
CMV, rubella, syphilis
What are the sequelae of congenital syphilis?
Saddle nose, interstitial keratitis, Hutchinsons incisors, sensorineural deafness, CN palsies, learning difficulties, Cluttons joint (arthritis typically affecting the knees)
How does gestation affect the risk of birth defects with congenital rubella syndrome?
The greatest risk is within the first 16 weeks gestation. Between 16-20 wks low risk of deafness only. After 20 wks the risk of congenital abnormality is minimal.
