Freji: Perinatal and Pediatric Infections Flashcards
Cytomegalovirus (CMV)
Structure:
Genome:
Structure: enveloped, dsDNA virus
Cytomegalovirus (CMV)
What happens after primary infection?
How is it spread?
Persists after primary infection: in low-grade chronic or latent states with periodic reactivation
Transmission: spread of infected oropharyngeal secretions, sexual intercourse, blood transfusions or mother to fetus spread (transplacental)
Maternal CMV Infection
What can happen to pregnant women?
Where can they shed CMV from?
Many adults in the population have Abs to CMV, however, pregnant women can have a primary infection
Pregnant women can shed CMV from cervix, urinary tract, throat, and in breast milk post-partum
Primary CMV Infection in Pregnancy
How many are symptomatic?
What symptoms? (4)
Most are asymptomatic (~90%)
Symptomatic cases present with many symptoms, including: o Infectious mononucleosis o Hepatitis o Thrombocytopenia o Myocarditis
Primary CMV Infection in Pregnancy
How often does transmission of CMV to fetus occur in mothers infected for the first time?
Transmission of CMV to fetus occurs ~50% of the time in mothers infected for the first time during pregnancy
Primary CMV Infection in Pregnancy
Diagnosis
Isolate virus from what?
Measure what type of abs?
Rapid diagnosis via what?
Isolate virus from urine, buffy coat or cervical secretions
Measure anti-CMV IgM antibodies (indicates primary infection)
Rapid diagnosis using PCR (can perform on any tissue- urine, blood, CSF etc.)
What percentage of live births have congenital CMV?
~1% of live births: however, only a small amount of these are symptomatic at birth
Congenital CMV
Diagnosis:
Isolation of CMV from urine or saliva within the first 2 weeks of life
Symptomatic Congenital CMV
Mortality Rate:
Common Findings:
Neurological abnormalities:
***Sensorineuronal hearing loss:
Mortality Rate: 15-30%; most survivors have long-term sequelae
Common Findings: petechiae, jaundice, hepato- and splenomegaly, thrombocytopenia, conjugated hyperbilirubinemia
Neurologic abnormalities: microcephaly, seizures, hypotonia, intracranial calcifications
Sensorineuronal hearing loss: most common cause of non-genetic congenital hearing loss
Symptomatic Congenital CMV
Eye abnormalities:
- Most frequent
Dental Defects
Urinary CMV shedding:
Treatment:
Eye abnormalities: chororetinitis most frequently; also optic atrophy, micopthalmia and cloudy cornea
Dental defects
Urinary CMV shedding: continues for months or years
Treatment: Ganciclovir in symptomatic CMV infection
Asymptomatic Congenital CMV
What percent?
Can follow what?
What continues for months or years?
90%
Can follow primary or reactivate CMV infection in the mother
Urinary CMV shedding: continues for months or years
Asymptomatic Congenital CMV
Is there hearing loss?
Mental/behavioral problems?
Antiviral therapy:
Sensorineural hearing loss: found less often than in symptomatic CMV
Mental or behavioral problems: seen in some cases
Antiviral therapy NOT recommended
Perinatal CMV
How is it acquired?
Are most cases symptomatic or asymptomatic?
CMV is acquired during passage through infected birth canal or by ingestions of CMV-positive breast milk
Most cases are asymptomatic
Perinatal CMV
What is the most common clinical illness?
Long term hearing loss?
Most common clinical illness: self-limited infantile pneumonitis (can be severe in premature infants)
No long-term hearing or neurologic deficits
Maternal HSV Infection During Pregnancy
What percentage of infected women will have symptoms?
What happens if infection occurs shortly before delivery?
When can asymptomatic shedding occur?
Only 1/3 of women infected with HSV during pregnancy will have symptoms
If infection occurs shortly before delivery, ~50% of newborns will get infected (not enough Ab to pass on yet)
Asymptomatic shedding: can occur in pregnant women at or near term (most common type of shedding)
Neonatal HSV
What is the usual route of infection?
Risk of vertical Transmission:
Transmission: intrapartum is usual route; can also occur via transplacental spread as well
Risk of Transmission: much higher for mothers with primary HSV infection than those with recurrent infection
Neonatal HSV
Risk Factors: (6)
o Cervical HSV infection
o Multiple genital lesions
o Prematurity
o Prolonged rupture of maternal membranes
o Intrauterine instrumentation
o Low/absent titers of maternal neutralizing Ab (which normally blocks virus action)
Intrauterine HSV
What happens in intrauterine HSV infections?
Hallmarks:
Associated abnormalities:
Mortality rate:
Intrauterine HSV Infections: baby born already sick; only small percentage of neonatal cases
Hallmarks: vesicular rash present at birth/appears shortly after
Associated Abnormalities: microcephly, chorioretinitis, microphthalmia, intracranial calcifications, seizures
High Mortality Rate: ~50%; survivors have long-term complications
Clinical Manifestations of Neonatal HSV
How common is asymptomatic infection?
Three Presentations:
Asymptomatic Infection: very rare
- Skin/Eyes/Mucous Membranes (SEM)
- Localized CNS Involvement (Encephalitis)
- Disseminated Disease
Neonatal HSV
Skin/Eyes/Mucous Membranes (SEM)
Cutanteous lesions:
Eye disease:
Mouth:
Neurological abnormalities:
Cutaneous Lesions: discrete vesicles, large bullae, or denuded skin (10-11 days old)
Eye Disease: keratoconjunctivitis and chorioretinitis
Mouth: ulcerative lesions
Neurological Abnormalities: can develop in some, although CNS involvement was not evident during acute illness
Neonatal HSV
Localized CNS Involvement (Encephalitis)
Symptoms: What makes it difficult to diagnose? CSF: Mortality: - What do survivors have?
Symptoms: focal or generalized seizures, lethargy, or apnea
Skin lesions often absent: makes it hard to diagnose
CSF: mononuclear pleocystosis and elevated protein
Mortality Rate: fairly high; survivors have long-term sequelae (a small number have a CNS relapse within one month of completing therapy)
Neonatal HSV
Disseminated Disease
Presents similar to:
Usual age at presentation:
How often is the CNS involved?
Presentation: similar to sepsis patient (around age 9-11 days)
CNS involvement: only in about 2/3 of cases
Neonatal HSV
Disseminated Disease
Other infected organs:
Mortality:
Other severely infected organs: adrenal glands, GI tract, liver, pancreas, heart, and kidneys
High mortality rate: over 50% even with therapy; majority of survivors have severe neurologic impairment
HSV
Treatment:
Treatment: acyclovir (almost always) or vidarabine
HSV
Prevention
If there are signs at the onset of labor:
Late in pregnancy for women with frequent genital recurrences:
C-section for women with signs and symptoms suggestive of genital HSV at onset of labor (as long as membrane rupture is not greater than 4-6 hours)
Oral acyclovir or valcyclovir given late in pregnancy for women with frequent genital recurrences (in practice, many more than just this receive this therapy)
HSV
Diagnosis
What does PCR detect?
Isolate virus from vesicular lesions or CSF
PCR: detects HSV DNA in CSF, blood and skin lesions (very sensitive and test of choice)
Varicella
General:
Highly communicable and usually benign disease of childhood
95% of women have Abs to VZV
Varicella
Typical Illness: (3)
Rash:
Typical Illness: fever, malaise, pruritic rash
Truncal rash characterized by crops of maculopapules that evolve in to vesicles, which eventually crust over (presence of lesion in various stages of evolution)
Varicella
Complications:
What population is more likely to have complications?
Complications: bacterial superinfection (most common), pneumonia, arthritis, encephalitis, bleeding diathesis
Adults are more likely to have complications
Zoster (General)
Rash:
Pain in adults vs children
Rash: unilateral, usually follows distribution of one or more sensory nerve roots (shingles)
- Follows same evolutionary pattern as varicella
Painful in adults; not so much in kids
Varicella Zoster
Diagnosis:
How is the laboratory confirmation possible?
Diagnosis: usually done clinically with laboratory confirmation rarely being needed
Laboratory confirmation possible via:
o Recovery of virus from vesicle fluid or detection of VZV Ags from base of fresh vesicles
o PCR detecting VZV DNA (most common now)
Fetal Varicella Syndrome
Cause:
When does it occur?
Cause: occurs after maternal chicken pox during the first 20 weeks of pregnancy (although risk of transmission is small)
Fetal Varicella Syndrome
Clinical Findings: (6)
o Cutaneous scars, denuded skin
o Limb hypoplasia: usually unilateral; most commonly leg
o Shingles during infancy
o CNS abnormalities: microcephaly, seizures, focal brain calcifications
o Ocular abnormalities
o Autonomic dysfunction: dysphagia, loss of urinary or bowel sphincter control
Neonatal Varicella Syndrome
Cause:
Most often due to maternal chickenpox during the last 3 weeks of pregnancy (no Abs transferred to help)
Neonatal Varicella Syndrome
How many days of maternal varicella before delivery for severe infection?
Mortality:
How many days of maternal varicella before delivery for mild infection?
Maternal infection within 5 days of delivery and 2 days after delivery: may be mild but can become severe (fever, hemorrhagic rash, generalized visceral involvement)
- Mortality high for severe infection: ~30%; usually due to pneumonia
Infection 5-21 days before delivery: illness usually mild
Neonatal Varicella Syndrome
Treatment:
Prevention:
Treatment: acyclovir
Prevention: infants born to mothers who develop varicella 5 days before or 2 days after delivery should receive 125 units of varicella zoster immune globulin ASAP
