Congenital and Perinatal Infections Flashcards

1
Q

What are the manifestations of congenital infections?

A
  • IUGR
  • Congenital malformation
  • Foetal loss
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2
Q

What are the manifestations of perinatal infections?

A
  • Meningitis
  • Septicaemia
  • Pneumonia
  • Preterm labour
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3
Q

What are the manifestations of postnatal infections?

A
  • Meningitis
  • Septicaemia
  • Conjunctivitis
  • Pneumonitis
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4
Q

Describe parvovirus in pregnancy.

A
  • Risk of adverse outcome for pregnant woman - arthropathy.
  • Risk of intrauterine infection by gestational age:
    • <4 weeks = 0%
    • 5-16 weeks = 15%
    • >16 weeks = 25-70%
    • Increasing risk with increasing gestational age.
  • Risk of adverse foetal outcome:
    • <20 weeks 9% excess fetal loss; 3% hydrops foetalis of which 50% die without treatment.
    • >20 weeks <1%
  • Risk to neonate:
    • None
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5
Q

Describe measles in pregnancy.

A
  • Risk of adverse outcome for pregnant woman - severe measles, including pneumonitis.
  • Risk of intrauterine infection by gestational age:
    • Not known
  • Risk of adverse foetal outcome:
    • Increased foetal loss
    • Premature delivery
  • Risk to neonate:
    • Risk of SSPE with a short-onset latency and fulminant course.
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6
Q

Describe rubella in pregnancy.

A
  • Risk of adverse outcome for pregnant woman - arthritis.
  • Risk of intrauterine infection by gestational age:
    • <11 weks = 90%
    • 11-16 weeks = 55%
    • >16 weeks = 45%
  • Risk of adverse foetal outcome:
    • <11 weeks = 90%
    • 11-16% = 20%
    • 16-20 weeks - minimal risk of deafness only
    • >20 weeks - no increased risks
  • Risk to neonate:
    • None
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7
Q

Describe chickenpox in pregnancy.

A
  • Risk of adverse outcome for pregnant woman - pneumonitis.
  • Risk of intrauterine infection by gestational age:
    • <28 weeks = 5-10%
    • 28-36 weeks = 25%
    • >36 weeks = 50%
  • Risk of adverse foetal outcome:
    • Fetal varicella syndrome risk
      • ​​<13 weeks = 0.4%
      • 13-20 weeks = 2%
    • Neonatal chickenpox risk in 4 days prior to 2 days post-delivery = 20%.
  • Risk to neonate:
    • Severe disseminated haemorrhagic chickenpox.
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8
Q

Describe the presentation of congenital infections.

A
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9
Q

Describe the diagnosis of congenital infections, such as rubella, cytomegalovirus, toxoplasma infection and syphilis.

A
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10
Q

What are the clinical features of cytomegalovirus?

How is it diagnosed?

A
  • Neonatal infection can be severe, or may be asymptomatic, later leading to the development of deafness and/or developmental milestone delay.
  • Postnatal infection usually mild.
  • Immunocompromised patients, especially those with HIV or who have undergone organ transplantation, may develop severe pneumonitis, retinitis or gut infection through reactivation of latent infection from the donor organ.
  • Diagnosis = NAAT
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11
Q

What is caused by congenital cytomegalovirus?

A
  • Foetal death
  • Hearing loss
  • Ocular disease
  • Cerebral damage
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12
Q

Describe the treatment of cytomegalovirus.

A
  • There is no CMV vaccine and pregnant women are not screened.
  • Early treatment with antivial therapy (Ganciclovir) for infants with sensorineural hearing loss or CNS involvement can reduce the adverse impact on sensorineural hearing loss and long-term neurodevelopment.
  • Treatment should be offered if they have:
    • Symptomatic focal organ disease (severe hepatitis, severe bone marrow suppression (anaemia, neutropaenia, thrombocytopaenia), colitis or penumonitis).
      • OR
    • CNS disease (microcephaly, radiological abnormalities on MRI or cranial USS, abnormal CSF parameters or a positive CMV CSF PCR, chorioretinitis, or a sensorineural hearing loss).
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13
Q

Describe the clinicl features of rubella.

A
  • Fever
  • Fine, red maculopapular rash
  • Lymphadenopathy
  • During prodrome - red pinpoint lesions occur in soft-palate.
  • Arthritis (more common in females) and self-limiting encephalitis are complications.
  • Maternal infection may cause foetal death or severe abnormalities such as deafness, CNS deficit, cataract, neonatal purpura and cardiac defects, in up to 60% of cases; the risk being highest in 1st trimester.
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14
Q

Describe the clinical presentation of a neonate infected with rubella.

A
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15
Q

Which protozoan parasite can affect a foetus?

How is it contracted?

A
  • Acute infection with Toxoplasma gondii may result from the consumption of raw or undercooked meat and from contact with the faeces of recently infected cats.
  • Most infected infants are aymptomatic. ~10% have clinical manifestations.
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16
Q

Describe the clinical manifestation of toxoplasmosis.

A
  • The most common manifestations are:
    • Retinopathy, an acute fundal chorioretinitis
    • Cerebral calcification
    • Hydrocephalus
17
Q

What is the treatment for infection by toxoplasmosis gondii?

A
  • Recommended duration of treatment = 12 months.
  • Pyrimethamine and sulfadiazine.
18
Q

Which infections are caused by varicella zoster virus?

A
  • VZV, which has only one serological type, causes the acute primary infection known as chickenpox and its recurrence, which is called shingles.
19
Q

How does shingles develop?

A
  • Recovery from chickenpox provides lifelong immunity.
  • The virus remains latent in the posterior root ganglion and in 20% of patients will reactivate with lesions in the related dermatome, causing shingles.
  • Shingles contain VZV and are infectious to non-immune individuals who are at risk of developing chickenpox.
  • It is impossible to contract shingles diretly from chickenpox or other cases of shingles.
20
Q

Describe the clinical features of chickenpox.

A
  • Systemic symptoms are mild
  • Lesions, which appear in crops usually 2-3 days apart, affect all parts of the body including oropharynx and genitourinary tract, and progress through macules and papules to vesicular eruptions whih, following rupture, develop a crust and spontaneously heal.
  • Rash lasts 7-10 days, but complete resolution may take as long again.
  • Haemorrhagic skin lesions that can be life-threatening may occur.
  • VZV pneumonia more common in adults, especially immunocompromised.
  • Postinfectious encephalits, usually minor, but also a rare fatal form.
21
Q

Describe the treatment of chickenpox.

A
  • Aciclovir or valaciclovir may be used for both adult chickenpox and shingles.
  • Zoster immune globulin (ZIG) is given to those in close contact with infection who are at risk of serious disease (neonates, pregnant women and immunocompromised individuals).
22
Q

How should you manage a pregnant woman exposed to chickenpox?

A
  • Perform a general assessment to establish the woman’s risk of chickenpox.
    • Hx of chickenpox
    • Certainty of chickenpox in the contact
    • Level of exposure
  • If no hx. of chickenpox herself (or is uncertain) and has had significant contact, seek specialist advice.
  • Establish gestation.
  • Test for varicella zoster immunoglobulin G (IgG) antibodies.
    • If positive, reassure the woman that she is immune and cannot catch chickenpox.
    • If antibody status is negative, seek immediate specialist advice regarding the need for VZIG prophylaxis.
23
Q

What is the intrauterine effect of a pregnant woman infected with VZV.

A

In the first 20 weeks of pregnancy, there is <2% risk of the foetus developing severe scarring of the skin and possible ocular and neurological damages and digital dysplasia.

24
Q

What is the perinatal effect of VZV in a pregnant woman?

A
  • Within 5 days pre- or post- delivery, when the foetus is unprotected by maternal antibodies and the viral lod is high, ~25% develop a vesicular rash. The illness has a mortality rate as high as 30%.
  • Exposed susceptible mothers can be protected with VZIG and treated with aciclovir.
  • Infants born in the high risk period should also receive zoster immune globulin (ZIG) and are closely monitored and given aciclovir if any signs of infection develop.
25
Q

How do children become infected with HIV?

How is it detected?

A
  • The major route of HIV infection in children is mother-to-child transmission (MTCT), which occurs during pregnancy (intrauterine), at delivery (intrapartum) or through breast-feeding (postpartum).
  • The virus may also be transmitted to children by infected blood products, contaminated needles, or through child sex abuse, but this is uncommon.
  • Antenatally, detection of HIV is actively carried out.
  • If + check viral load, resistance to testing and CD4.
  • Mothers treated with ART to reduce viral load which dramatically reduces the chances of transmission to the baby.
26
Q

Describe early onset sepsis.

A
  • In early-onset sepsis (<48 hours after birth), bacteria have ascended from the birth canal and invaded the amniotic fluid.
  • The foetus is secondarily infected because the foetal lungs are in direct contact with infected amniotic fluid.
  • These infants have pneumonia and secondary bacteraemia / septicaemia.
  • In contrast, congenital viral infections and early-onset infection with Listeria cause foetal infection to be acquired via the placenta following maternal infection.
  • The risk of early-onset infection is increased if there has been prolonged or premature rupture of the amniotic membranes, and when chorioamnionitis is clinically evident such as when the mother has fever during labour.
27
Q

Describe late-onset neonatal sepsis.

A
  • In late-onset infection (<48 hours after birth), the source of infection is often the infant’s evnironment.
  • Gram-positive bacteria (GBS, staphylococcus aureus and enterococcus faecalis) and Gram-negative bacteria (Escherichia coli and Pseudomonas, Klebsiella and Serratia species).
28
Q

Describe the effect of Group B Streptococcal infection in the newborn.

A
  • 10-30% of pregnant women have faecal or vaginal carriage of GBS.
  • The organism causes early- and late- onset sepsis.
    • In early-onset sepsis, the newborn has respiratory distress and pneumonia.
    • Most with early-onset sepsis will have pneumonia only, but it may cause septicaemia and meningitis.
  • The severity of the presentation depends on the duration of the infection in utero.
  • Up to 50% of infants born to mothers who carry GBS are colonised on their mucous membranes or skin.
    • Some of these babies develop late-onset disease, up to 3 months of age.
    • Usually presents with meningitis, or occasionally with focal infection (osteomyelitis or septic arthritis).
29
Q

How can GBS infection be prevented in the newborn?

A
  • Prophylactic intrapartum Abx given IV to the mother can prevent Group B Strep infection in the newborn baby.
30
Q

Describe conjunctivitis in the neonate.

A
  • Sticky eyes are common in the neonatal period, starting on the 3rd or 4th day of life.
  • Purulent discharge with conjunctival injection and swelling of the eyelids <48 hours of life may be due to gonococcal infection.
  • Chlamydia trachomatis eye infection usually presents with a purulent discharge, together with swelling of the eyelids at 1-2 weeks of age, but may also present shortly after birth.
31
Q

Describe Herpes Simplex Virus (HSV) in the neonate.

A
  • Usually transmitted during passage through an infected birth canal or occasionally by ascending infection.
  • The risk to an infant born to a mother with a primary genital infection is high (~40%), while the risk from recurrent maternal infection is <3%.
  • In most infants who develop HSV infection, the condition is unexpected as the mother does not know that she is infected (asymptomatic or non-specific illness).