Neonatal Teaching: Neonatal Infection Flashcards

1
Q

Perinatal infection

A

Etiology:
1. Bacterial
2. Viral
3. Protozoal
4. Fungal
5. Parasitic

Route of transmission:
1. ***Intrauterine (Bloodborne via placenta)
- Syphilis
- CMV
- Toxoplasma

  1. ***Ascending
    - Bacterial
    - HSV
  2. ***Direct contact
    - HSV
    - HBV
    - HIV
    - HPV

Acute vs Chronic infection:
1. Acute infection
- **Bacterial mostly
- In-utero fetal demise
- **
Perinatal infection
- ***Preterm delivery

  1. Chronic infection
    - **Viral mostly
    - In-utero fetal demise
    - **
    IUGR
    - **Congenital malformations
    - **
    Chronic organ dysfunction
    - ***TORCH syndrome
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2
Q

TORCH syndrome

A
  1. Toxoplasmosis
  2. Others
  3. Rubella
  4. CMV
  5. HSV

Common features (細頭肚大有紅點):
1. **Hepatosplenomegaly
2. **
Microcephaly
3. **Petechiae
4. **
IUGR

Others:
- Varicella
- HIV-1
- Treponema pallidum (Syphilis)
- Coxsackievirus
- Human parvovirus B19
- Mycobacterium tuberculosis
- etc.

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3
Q

Syphilis

A

Maternal syphilis:
- STD
- Incubation period: 10-90 days
- Primary / Secondary / Tertiary

VDRL (Treponemal non-specific test):
- Primary: 80% +
- Secondary: 100% +
- Becomes **non-reactive if treatment effective
- **
False positive in pregnancy

FTA-ABS (Treponemal specific test):
- Primary: 85%
- Secondary: 100%
- Titre ***persists for life

Treatment for maternal syphilis:
- Goal: Reduces chance of **Congenital syphilis
- **
Penicillin

Congenital syphilis:
- Placenta: focal proliferative villitis with necrosis
- Most infants with congenital syphilis are asymptomatic at birth
- “Early” congenital syphilis: first 2 years
- “Late” congenital syphilis: near puberty
- Treatment: Penicillin
- Monitor: Serial VDRL

Clinical features of Congenital Syphilis
1. Skin
- Bullous rash over palm and sole, mucous membrane

  1. Reticuloendothelial system
    - Hepatosplenomegaly + LN
    - Hepatitis, Jaundice
  2. Haematological
    - Anaemia
    - Thrombocytopenia
    - WCC­ ↑↓
  3. Bone
    - Metaphyseal and diaphyseal
    - Osteochondritis
    - Dactylitis
  4. CNS
    - Aseptic meningitis
    - Chorioretinitis
  5. Others
    - Hydrops
    - Rhinitis (purulent / haemorrhagic)
    - Myocarditis
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4
Q

Toxoplasmosis

A
  • Toxoplasma gondii (protozoa)
  • Cats: complete hosts
  • Infection through contaminated water / food
  • Incidence varies 0-90%

Maternal infection:
- Asymptomatic / Mild symptoms
- Diagnosis: Serological: IgM, ↑ IgG

Fetal infection:
- More severe during first half of gestation
- Diagnosis: Cord blood for IgM

Management:
1. **Spiramycin “prophylaxis” once maternal infection documented
2. **
Pyrimethamine + ***Sulfadiazine (for fetal infection) for 1 year

Congenital toxoplasmosis:
1. CNS
- Hydrocephalus
- Intracranial calcifications
- Others

  1. Eyes
    - Chorioretinal scars
    - Chorioretinitis
    - Leucocoria
    - Cataract
    - Nystagmus
    - Optic atrophy
  2. Ears
    - Deafness
  3. Others
    - Anaemia
    - Cholestasis
    - Hydrops
    - Nephrotic syndrome
    - Interstitial pneumonitis

Prognosis:
- Severe symptoms / Untreated —> Mental retardation / Blindness
- Treated —> Lesser degree of damage

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5
Q

Rubella infection

A

Maternal infection:
- Airborne + Direct contact
- Shedding of virus 1 week before rash appears
- 10% of child-bearing age women non-immune
- Time of maternal infection ↑ —> Chance of fetal infection ↑

Congenital infection:
1. Hearing
- ***Sensorineural deafness

  1. CNS
    - ***Microcephaly
    - Meningoencephalitis
    - Mental retardation
  2. CVS
    - PDA
    - Pulmonary stenosis
  3. Eyes
    - Cataracts
    - Retinopathy
    - Cloudy cornea
    - Glaucoma
    - Microphthalmia
  4. Others
    - IUGR
    - DM
    - Anaemia
    - ***Hepatosplenomegaly

Prevention:
- Rubella vaccination
—> Theoretical risk of ***Teratogenicity of life-attenuated vaccine: CI during pregnancy

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6
Q

Hepatitis B

A
  • 10% carrier rate in HK
  • Late morbidity with cirrhosis, chronic hepatitis, HCC

Mode of transmission:
- **Perinatal
- **
Blood / body fluid contact

Mother-to-infant transmission occurs during delivery in most cases through:
1. **Transplacental microhaemorrhages
2. **
Ingestion of contaminated maternal secretions
- Chance of becoming carrier high
- Chance of ***“intrauterine” infection low (5%)
- Breast milk excretion: but not CI

Risk of transmission to neonate:
- Mother with HBeAg +ve: 80%
- Mother with HBeAg / Anti-HBe -ve: 30%
- Mother with Anti-HBe: 10%

Prevention:
Mother HBsAg negative:
1. HB vaccine at birth, 1 and 6 months old —> 95% seroconvert

Mother HBsAg positive:
1. HB vaccine + ***HBIG at birth
2. HB vaccine at 1 and 6 months old —> 95% protection

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7
Q

HSV infection

A
  • HSV1, 2
  • Primary infection
  • Reactivation:
    1. Gingivostomatitis
    2. Pharyngitis
    3. Genital tract infection

Perinatal HSV infection:
Transmission:
- Mostly acquire during passage through **infected birth canal
- Transplacental transmission **
rare

Chance of Vertical transmission:
- Primary infection: 50%
- Reactivation: 5%

Clinical features:
- Mostly symptomatic within first week
—> **Vesicular skin and mucous membrane eruptions (first 10 days)
—> **
Disseminated disease (9-11 days)
—> ***CNS: meningoencephalitis (15-17 days)
- Intrauterine infection rare
—> Microcephaly, Chorioretinitis, Microphthalmia

Diagnosis:
- Isolation of virus from vesicles / other body fluids

Treatment:
- ***Aciclovir

Prevention:
- ***C-section for women with S/S suggesting genital HSV infection at onset of labour
- Obtain viral cultures from newborn at 24-48 hours of life

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8
Q

CMV infection

A
  • ~80-90% of women at child bearing age are ***seropositive
  • Risk of susceptible women acquire primary CMV infection 1-2% during pregnancy
  • Primary infection during pregnancy —> 40% fetal infection (Mild - Severe)
  • Reactivation / Co-infection with exogenous strain during pregnancy —> Mild fetal infection

Maternal CMV infection:
- Mostly ***asymptomatic
- Diagnosis:
1. CMV-IgM (may persist in blood for up to 8 months)
2. ↑ IgG
3. PCR / CMV Ag

Congenital CMV infection:
- 0.4-1% of livebirths
- 10% **symptomatic at birth —> severe sequelae
- Diagnosis:
1. CMV isolated within first 2 weeks
- Treatment: **
?Ganciclovir

Clinical features:
1. CNS
- **Microcephaly
- **
Hypotonia
- Seizures
- Intracranial calcification
- Porencephalic cysts

  1. Eyes
    - ***Chorioretinitis
    - Optic atrophy
  2. Hearing
    - ***Sensorineural deafness
  3. Reticuloendothelial systems
    - ***Hepatosplenomegaly
    - Cholestasis
  4. Others
    - ***Thrombocytopenia

Perinatal CMV infection:
- Benign
- Acquire CMV during / after delivery

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9
Q

HIV infection

A

Fetal transmission:
1. **In-utero
2. **
Intrapartum (50%)
3. Postpartum: ***Breastfeeding (14%)
- 25% Fetal infection rate

Fetal and Neonatal infection:
- **Asymptomatic at birth
- Median age at presentation: **
17 months
—> 25% develop AIDS by 1 yo
—> 50% by 4 yo
—> 33% AIDS free by 13 yo

Diagnosis:
- DNA-PCR
- Maternal transfer of IgG makes diagnosis difficult (median age of clearance 13 months)

Prevention of perinatal transmission (reduce chance by 50%):
1. Anti-retroviral agent (**Zidovudine)
- Start antenatally
- Intrapartum
- Postnatal for 6 weeks to newborn
2. **
Avoid contamination during labour (prolonged labour, rupture of membrane, invasive monitoring, instrumental delivery)
3. **Septrin prophylaxis since 6 weeks until Dx excluded
4. Avoid **
live vaccine / ***breastfeeding

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10
Q

Acute bacterial infection in Neonates

A

Route:
1. Ascending infection
- Colonised organism from maternal genital tract / urinary tract / GIT
2. Blood borne (via placenta) secondary to maternal sepsis
3. Postnatal infection
- Nosocomial infection
- Community acquired infection

Early Onset: Organisms from mother
Late onset:
1. Organisms from postnatal exposure (including breast milk)
2. Organisms (with long incubation period) from mother
- GBS, Listeria, Enterococcus etc.

Causative organisms:
1. Gram +ve
- GBS
- Other Streptococcus
- Enterococcus
- Staphylococcus
2. Gram -ve
- E. Coli
- Klebsiella
- Haemophilus influenzae
- Pseudomonas
3. Anaerobes
4. Fungus
- Candida

Risk factors:
1. Prolonged rupture of membrane (>18h)
2. Premature labour
3. Chorioamnionitis
4. Maternal fever >38oC
5. GBS colonisation

Clinical features:
Non-specific:
1. Temperature instability
2. Altered conscious state: Irritability / lethargy
3. Tachycardia / Bradycardia
4. Poor perfusion
5. Respiratory distress / Apnea
6. Abdominal distension
7. Hepatosplenomegaly
8. Feeding intolerance / Poor feeding

P/E:
1. Conscious state
2. Perfusion
3. Colour: Pallor / Cyanosis
4. Chest
- Tachypnea (RR ***>60/min)
- Crepitations
5. CVS
- Tachycardia / Bradycardia
6. Abdomen
- Distension (ileus)
- Hepatosplenomegaly
7. CNS
- Bulging anterior fontanelle

Investigations:
1. CBC
- **Hb (normal **14.5-24.5)
- **↑/↓ WBC (normal **5-30)
- Ratio of immature to total neutrophil (Band form: left shift of neutrophil lineage)
- **Thrombocytopenia (normal **>150)
2. CRP (2x negative rule out infection), ESR, IL6
3. Culture
- Blood
- Urine
- CSF
—> CSF / Blood glucose ratio (normal **>0.6)
—> Protein (normal **
<0.5)
—> RBC (a few can be present due to traumatic tap)
- Gastric aspirate, Ear, Eyes etc.
4. X-ray

Treatment:
1. **Penicillin (or Ampicillin) for Gram +ve
2. **
Aminoglycoside (or Cephalosporin) for Gram -ve
3. Combination for Empirical treatment

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11
Q

Group B Streptococcus (GBS)

A

Streptococcus agalactiae:
- Colonised in maternal genital tract 15-20%
- **Asymptomatic in mother
—> May cause **
in-utero infection —> **Abortion / **IUD
—> **Premature labour
—> **
Perinatal infection
- Colonisation difficult to eradicate
- Sensitive to ***Penicillin

Perinatal GBS infection:
- 1% of colonised pregnancy
- Vertical transmission 50-70%
- Neonatal colonisation rate 8-25%
- Early onset (usually **<=3 days) —> **Pneumonia, **Septicaemia
- Late onset (up to **
90 days) —> ***Meningitis

Prevention of Perinatal GBS infection:
- Intrapartum maternal **Penicillin / **Ampicillin prophylaxis (to known carrier mothers) at onset of labour reduce maternal and neonatal GBS infection (50% ***early onset infection)
- Risk factor approach: treat whenever risk factors are present (no carrier detection)

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12
Q

Neonatal O2 saturation

A
  • Normal: SpO2 >95% breathing in room air

Cyanosis:
- DeoxyHb >5g/dL
- Central cyanosis vs Peripheral cyanosis

Causes of Cyanosis:
1. Pulmonary
2. Cardiac
3. Persistent pulmonary hypertension
4. Others (e.g. Methaemoglobinaemia)

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13
Q

Lumbar puncture in neonates (Phoebe Lam)

A

Indication:
- When clinical suspicion is high (e.g. bulging fontanelle, seizure, s/s of meningitis)

Insert LP needle between vertebral bodies:
- L4-5 / L3-4 (not lower otherwise no fluid will come out)
- Spinal cord ends at L1

Possible complications:
1. Local trauma to spinal cord
2. Bleeding / Haematoma
- correct coagulopathy
- if DIC in sepsis, then do LP with FFP and platelet transfusion?
3. Introduce infection
4. Cardiopulmonary decompensation during positioning
- ∵ need to flex baby’s head and buttock to straighten spinal cord —> monitor for bradycardia / desaturation —> release / defer LP till baby more stable
5. Coning
- when there is ↑ ICP (unlikely in neonates because pressure can be released through open fontanelles (but may happen in obstructed hydrocephalus e.g. spinal cord pathologies like myelomeningocele, known brain malformation)

CSF interpretation:
1. CSF / Blood glucose ratio (normal **>0.6)
2. Protein (normal **
<0.5)
3. RBC (a few can be present due to traumatic tap)

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14
Q

Normal CSF value (from HNNS09)

A

Protein: 0.15-0.45 g/L
Glucose: 2.8-3.9 mmol/L
Cell counts: 0-3 / mm^3
Organism: None
Appearance: Clear

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