Viral infections in pregnancy Flashcards
What are the different presentations and potential organisms that cause the following;
- Congenital infections
- Congenital infection:
Manifestations:
- Growth retardation - low birth weight
- Congenital malformations
- Fetal loss - still births
Organisms:
- CMV
- HIV
- Toxoplasma gondii
What are the different presentations and potential organisms that cause the following;
- Perinatal infections:
Manifestations;
- Meningitis
- Septicemia
- Pneumonia
- Preterm labour
Organisms:
- Neisseria gonorrohoea
- Chlanydia trachomatis
- HSV
- Group B strep
- E.coli
What are the different presentations and potential organisms that cause the following;
- Post natal infection
Manifestation:
- Meningitis
- Septicemia
- Conjuctivitus
- Pnuemonitis
Organisms;
- breast milk –> HIV, CMV, HBV
- Umbilicus –> staph aureus, tetanus
- Person to person –> Group B strep, listeria monocytogenes, e.coli
What type of virus is Rubella?
What is the pathogenesis of the rubella virus causing tetraogenicity?
- Decrease in the rate of cell division (structural malformations)
- Decrease in overall number of cells (small babies)
- Interference with development of key organs
- Tissue necrosis due to virus replication
Describe the signs and symptoms of congenital rubella syndrome
- Sensorineural hearing loss – commonest sequelae
- Other neurologic problems
- psychomotor /mental retardation
- Meningoencephalitis
- Microcephaly, intracranial calcifications
- Ophthalmic problems
- cataract, glaucoma
- retinopathy, microphthalmia
- Intrauterine growth retardation
- Congenital heart defects such as patent ductus arteriosus and others
- Hepatosplenomegaly
- Thrombocytopaenic purpura
Describe the timing of the maternal infection with rubella, and the risks to the fetus to developing congenital abnormalities - and what will be affected
- 0-12 weeks
- 13-20 weeks
- >20 weeks
- How is an acute infection with rubella diagnosed?
- How is an immune status screen for rubella done?
- Diagnosis of acute infection
- Rubella IgG
- Seroconversion
- Avidity
- Rubella IgM
- Detection of virus
- Molecular diagnosis (PCR)
- Respiratory secretions, blood, urine, tissues
- Immune status screen:
* Rubella IgG
What should be done if there is a pre-natal diagnosis of Rubella in the mother?
All cases of symptomatic rubella infection in the first gestational trimester should be considered for termination of pregnancy without prenatal diagnosis
How can Rubella be prevented?
Vaccine:
- Highly effective live attenuated vaccine with 95% efficacy
- Universal vaccination of all infants as part of the MMR regimen
- Both universal and selective vaccination policies will work provided that the coverage is high enough
- Antenatal screening
- All pregnant women attending antenatal clinics are tested for immune status against rubella
- Non-immune women are offered rubella vaccination in the immediate post partum period
- What type of infection is CMV?
- How is it transmitted?
- Beta herpes virus that causes latent infection
- Horizontal transmission
- Vertical transmission
- In utero (transplacental)
- During delivery
- Breast feeding
- Define congenital CMV infection
- What can it cause?
- Defined as the detection of CMV from body fluids or tissues within 3 weeks of birth
- Commonest congenital viral infection
- Leading nongenetic cause of neurosensory hearing loss
- Transmission to the foetus may occur following primary or recurrent maternal CMV infection
- May be transmitted to the foetus during all stages of pregnancy
Defined the signs and symptoms of Cytomegalic inclusion disease
- CNS abnormalities - microcephaly, mental retardation, spasticity, epilepsy, periventricular calcification
- Eye - choroidoretinitis and optic atrophy
- Ear - sensorineural deafness
- Liver - hepatosplenomegaly and jaundice which is due to hepatitis.
- Lung - pneumonitis
- Heart - myocarditis
- Thrombocytopenic purpura, Haemolytic anaemia
- Late sequelae in individuals asymptomatic at birth - hearing defects and reduced intelligence.
What is the pathogenesis of congenital CMV?
- Little is known about the molecular mechanisms responsible for the pathogenesis of tissue damage
- No evidence of teratogenecity, damage to the fetus may result from destruction of target cells once they are formed
- CNS is the major target organ for tissue damage in the developing fetus
- Infection of endothelial cells (viral angiitis) may be responsible for perfusion failure in the developing brain with resultant maldevelopment
What are the possible outcomes of maternal CMV infection?
- May cause congenital infection on 40% –> only 5-10% will have abnormalities at birth. The rest may be asymptomatic at birth but 10% will go on to have abnormalities on follow-up
- CMV can reactivate/re-infect and transmission from person to person. - Low risk of foetal abnormalities, although severe disease may occur
What organ does congential CMV target the most?
CNS involvement
only 0.2-2% have congenital CMV, and of those that are symptomatic (10%) - 75% will have CNS involvement e.g. hearing loss
How is CMV in the mother diagnosed?
Virus Detection (blood, urine, respiratory secretions)
- Cell culture
- Detection of Early Antigen Fluorescent Foci
DEAFF – accelerated cell culture system
- CMV DNA (Polymerase Chain Reaction)
Serology
- CMV IgG seroconversion
- CMV IgG avidity
- CMV IgM
How is diagnosis made of suspected intrauterine infection with CMV:
- Pre-natal
- Post-natal?
- PRE-NATAL
* Detection of CMV DNA in amniotic fluid at 21 weeks gestation - POST-NATAL
- CMV detection within 3 weeks of life
- Positive result beyond that time will NOT make a diagnosis of congenital infection
- Urine/Salivary swab/blood
- Serology
- CMV IgM (low sensitivity)
How is congenital CMV
- Prevented
- Treated?
- Key to prevention is “universal precautions”
- CMV with significant organ disease:
- valganciclovir or ganciclovir for 6/12
- audiology f/u until 6 years of age
- ophthalmology review
What factors influence neonatal trasnmission of an infection?
- Type of maternal infection
- Maternal antibody status (neutralizing Ab)
- Duration of rupture of membranes
- Integrity of mucocutaneous barriers (e.g., use of foetal scalp electrodes)
- Mode of delivery (cesarean section versus vaginal)
What is the risk of neonatal infections based on maternal HSV status?
Nature of maternal infection
- First episode 1 yr –> risk of neonatal infection = 57%
- First episode non 1yr –> risk of neonatal infection = 25%
- Recurrent –> risk of neonatal infection = 2%
When is there the highest risk of neonatal infection with HSV?
Maternal primary HSV infection in the third trimester
- particularly within 6 weeks of delivery
- continuing viral shedding
- birth before development of protective maternal antibodies
- C-section recommended (RCOG)
When are most infections transmitted to the neonate?
- Intrauterine
- Peripartum
- Postpartum
- Peripartum/perinatal - 85% of infections
What is the clinical presentation of an intrauterine infection with HSV?
- Neurological
- Cutaneous
- Opthalmologic
Neurologic involvement
- microcephaly,encephalomalacia, hydranencephaly, and/or intracranial calcification
Cutaneous manifestations
- scarring, active lesions, hypo- and hyperpigmentation
Ophthalmologic findings
- microopthalmia, retinal dysplasia, optic atrophy, and/or chorioretinitis),
What are the signs and symptoms of an infection with HSV in peripartum and postpartum?
Disseminated disease ~ 25%
- DIC
- Pneumonia
- Hepatitis
- CNS involvement (60% to 75%)
Encephalitis (CNS disease) ~ 30%
- Seizures
- Lethargy
- Irritability
- Poor feeding
- Temperature instability
Skin, eyes, and/or mouth (SEM disease) ~ 45%
Describe disseminated disease with HSV in a new born
Poor prognosis even with antiviral treatment
- mortality around 30%
- long-term neurological sequelae in 17%
- Encephalitis in 60-70% of cases
Severe coagulopathy, liver dysfunction, pneumonitis
> 20% will NOT have skin lesions
What are the signs and symptoms of CNS disease with HSV in a new born?
- Local CNS disease often presents late
- between 10 days and 4 weeks postnatally
- with treatment, mortality is around 6% and neurological morbidity 70%
- Seizures (both focal and generalized)
- Lethargy, irritability
- Tremors, poor feeding, temperature instability
- Bulging fontanelle
How can infection with HSV be prevented/outcomes improved?
- Raise awareness of this infection
- Decrease the time to diagnostic consideration
- In the mother
- In the newborn baby
- Early initiation of antiviral therapy
- Prompt collection of specimens for diagnosis
- HSV cultures/PCR of skin vesicles (if present), oropharynx, conjunctivae,urine, blood and cerebrospinal fluid
- Liver transaminase levels (suggest disseminated HSV infection)
What is the antiviral therapy for HSV for a new born?
- High dose acyclovir at 60 mg/kg/day IV in three divided daily doses
- Duration of therapy
- 21 days (minimum) in disseminated or CNS disease
- Repeat LP and CSF PCR testing
- Continue with ACV until PCR negative
- 14 days (minimum) in SEM disease
- Monitor Neutrophil count
- How is VZV spread?
- What are the complications of a VZV infection while pregnant (mother and fetus)
- DNA virus, Herpes family, Spread by respiratory droplets and direct contactcand highly contagious
- Varicella in pregnant women is associated with a risk of VZV transmission to the foetus or newborn
- Risk to mother: pneumonia/encephalitis
- Intrauterine VZV infection might result in
- Congenital varicella syndrome
- Neonatal varicella
- Herpes Zoster during infancy or early childhood
How can congenital varicella syndrome manifest itself in the newborn?
Can be manifested by
- Low birth weight
- Cutaneous scarring
- Limb hypoplasia
- Microcephaly
- Cortical atrophy
- Chorioretinitis
- Cataracts
Describe the risk of causing congenital varicella zoster syndrome
- Maternal infection during 0-12 weeks’ gestation 0.4% risk
- Maternal infection during 13-20 weeks’ gestation Highest risk (2%)
- Rare cases involving birth defects consistent with congenital varicella syndrome have been reported after maternal varicella beyond 20 weeks’ gestation (with the latest occurring at 28 weeks)
- Zoster during pregnancy does not pose risk to the foetus
- Describe varicella neonatal infection
- How does the infection manifest itself?
Newborn is vulnerable when maternal infection occurs within 7 days prior to delivery or 7 days post-partum
- No time for passive transfer of VZV antibodies
Manifestations of infection may include
- Mild course of infection
- Disseminated skin lesions
- Visceral infection
- Pneumonia
How can infection with varicella be prevented?
- Live virus vaccine available (give preconception)
- Avoidance of exposure in pregnancy if susceptible
- Varicella-zoster immune globulin (given with 10 days of exposure)
- Antiviral chemotherapy if exposed (aciclovir from day 7 to 14 post exposure)
Measles paramyxovirus RNA:
- Transmission
- Incubation
- Symptoms
- Complications
- Transmission: respiratory, conjuctiva
- Incubation: 7-18 days (typically 10 days)
- Symptoms:
- prodrome 2-4 days- fever, malaise, congestion, conjuctivitis, koplik’s spots
- Rash classically starts behind ears & on forehead then spreads
- Complications
- Opportunistic bacterial infections
- Otitis media
- Pneumonia, bronchitis
- Opportunistic bacterial infections
- Encephalitis
- SSPE
Human parvovirus
- Type of virus
- Incubation
- Clinical presentation
- DNA virus, Family Parvoviridae, genus Erythrovirus
- Transmission is by respiratory droplets and by blood
- Incubation period is 4 to 20 days
- Clinical presentation
- Erythema infectiosum (fifth disease)
- Transient aplastic crisis
- Arthralgia
- Non-immune hydrops foetalis
What is the pathophysiology of Parvovirus?
- Unique tropism for rapidly dividing erythrocyte precursors
- Virus requires the P blood antigen receptor (globoside) to enter the cell
- Suppression of erythrogenesis
- No reticulocytes are available to replace aging or damaged erythrocytes as they are cleared by the reticuloendothelial system
Virus crosses the placenta and destroys red cell precursors
Foetal anaemia –> high output congestive heart failure –> hydrops fetalis
Virus also directly infects and injures myocardial cells
Parvovirus B19 in pregnancy
- What can happen if there is a maternal infection before 20/40?
- After 20/40 weeks?
Maternal infection before 20/40
- Transplacental transmission estimated at 33%
- 9% risk of infection overall
- 3% risk of hydrops fetalis if infection from 9-20/40
- Risk of foetal anomalies less than 1%
Maternal infection after 20/40
- No documented risk
- How is maternal diagnosis of Parvovirus made?
- How is fetal infection diagnosis made?
Maternal Infection
- Parvovirus DNA amplification from blood, respiratory samples
- Serology
- Parvovirus IgG seroconversion
- Parvovirus IgM
Foetal Infection
- Foetal blood and amniotic fluid for serology and PCR
How is congenital parvovirus infection treated?
Intrauterine transfusion
Some cases resolve spontaneously
If infant survives the hydropic state, long-term prognosis is usually favorable
Zika virus is usually asymptomatic. What are the consequences of Zika virus in pregnancy?
- Miscarriage/stillbirth/microcephaly
- Congenital Zika syndrome is described by 5 features:
- Severe microcephaly + skull deformity
- Decreased brain tissue, seizures
- Retinopathy, deafness
- Talipes
- Hypertonia
Associated with travel to Caribbean/Central/South America
