15.7.3 Congenital Neonatal Infections Flashcards

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1
Q

Definition:
Neonate
Bacterial sepsis in a neonate
Prenatal or congenital infection
Perinatal infection
Postnatal infection
Bacteraemia

A

Neonate: A baby in the first 28 days of life
Bacterial sepsis in a neonate: Clinical syndrome of systemic signs of infection accompanied by bacteremia in a neonate
Prenatal or congenital infection: Infection acquired before birth of the baby/during pregnancy
Perinatal infection: Infection acquired during pregnancy or delivery
Postnatal infection: Infection acquired after birth
Bacteremia: fever, lethargic, vomiting, diarhoea

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2
Q

Congenital infections big picture

A

Maternal infection in the first half of the pregnancy, particularly the first trimester, poses the greatest risk to the fetus

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3
Q

When should you think of congenital infections?

A
  • IUGR infants
  • Hepatosplenomegaly
  • Thrombocytopenia
  • Unusual rash
  • Concerning maternal history
  • “Classic” findings of any specific infection
  • Hydrops fetalis
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4
Q

SCORTCH (acronym used for congenital infections)

A

T : Toxoplasmosis
O : (Others) Hepatitis B, TB, Varicella, Parvo, SARS-CoV-2, Zika
R : Rubella
C : Cytomegalovirus
H : Herpes, HIV
E : Enterovirus
S : Syphilis

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5
Q

Diagnosis of congenital infection

A
  • Good maternal/prenatal history
    ➡️Remember most infections of concern are mild illnesses often unrecognized
  • Thorough exam of infant
  • Directed labs/studies based on most likely diagnosis…
    ➡️TORCH TITERS is not examination of choice
    ➡️IgG –maternal IgM –fetal
    ➡️Specific tests for specific infections e.g. PCR
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6
Q

Toxoplasmosis:
Transmission and pathogenesis
Clinical manifestations
Prevention

A
  • Toxoplasma gondii, a parasite found worldwide, causes congenital infection in about 1/10,000 to 80/10,000 births
  • Cats definitive host, humans intermediate host
  • Humans become infected after ingestion of raw meat, unpasteurized milk, ingestion of water or soil contaminated with oocytes from cat faeces
  • Highest risk of transmission in 3rd trimester

Transplacental transmission from mother to foetus:
1. Acute primary infection 3 months prior to pregnancy or during pregnancy
2. Pregnant mother immune to 1 strain who becomes infected with a new strain
3. Reactivation of toxoplasmosis during pregnancy in a severely immunocompromised mother

Clinical manifestations
- Most (70-90%) are asymptomatic at birth
- Classic triad of symptoms:
➡️Chorioretinitis
➡️Hydrocephalus
➡️Intracranial calcifications

Prevention
- Use precautions when handling cat litter box
- Do not eat inadequately cooked meat

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7
Q

Hepatitis B virus
Epidemiology
Transmission
Complications

A
  • Global prevalence of hepatitis B infections ranges between 4.2% and 6%

Transmission
- Mothers can transmit HBV to their fetusesin uteroin 3–9%
- Exact mechanism for prenatal transmission of HBV not clearly known
- >90% of neonatal HBV infections occur during peripartum period
- Infants born to HBeAg positive mothers may remain at the risk of infection
- Increased risk of acquiring the infection if the mother is HBeAg positive and/or has high levels of HBV DNA.
- Evidence for transmission with preterm rupture of membranes is uncertain
- Evidence for elective caesarean section to prevent the transmission is limited
- Postnatal transmission during care or through breast milk (postpartum transmission) not important mode of transmission

Clinical presentation
- Majority asymptomatic
- Mild ↑ liver enzymes by 2-6 months (chronic antigenemia in immune tolerant phase)
- Some present with acute hepatitis by 2 months (even acute fulminant hepatitis)
- Few develop chronic liver disease (risk of cirrhosis and hepatocellular carcinoma)

Complications (are immunisations available)
- Hepatic: chronic active hepatitis and cirrhosis liver failure and hepatocellular Ca
- Risk chronic infection: 90% of newborns
30% 1-5 years and 5-10% older children
- Nephrosis
- HBV immunisations available

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8
Q

Hepatitis C

A
  • 5% of infected woman transmit HCV.
  • Transmission only if mother HSV RNA positive
  • Can breastfeed
  • 25% have jaundice and LFT abnormalities
  • 85% persistent infection 70% chronic hepatitis 20% cirrhosis ,Ca
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9
Q

Hepatitis A

A

Unlikely to contact virus, but can lead to hepatitis in newborn

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10
Q

Congenital Varicella Zoster
Epidemiology
Syndrome

A

Epidemiology
- Most women immune by childbearing age (+/- 90%)
- Intrauterine infection: occurs in 25% women (T1+T2)
- Can lead to intrauterine demise
- 2-12% incidence of CVS if fetus infected

Syndrome
- Skin lesions in dermatomal distribution
- Limb hypoplasia
- Neurological: cortical or spinal cord atrophy, limb paresis, seizures, microcephaly, encephalitis
- Eye: micropthalmia, chorioretinitis, cataracts, nystagmus, optic atrophy
- IUGR
- GI and GU abnormalities

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11
Q

Perinatal VZN

A
  • Risk period = 5 days pre to 2 days post partum
  • Diagnosis:
    Maternal history
    Infant’s rash
    Virus isolation (vesicular fluid)
  • Neonatal wards exposure if a mother is ill
  • Dx- skin scraping, viral culture, serology

Clinical presentation
Slide 26

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12
Q

Congenital Rubella
Clinical presentation
Epidemiology

A

Clinical presentation (depends on when mom got inffected)
- microcephaly
- PDA
- cataracts
Slide 30

Epidemiology
- Rare in South Africa as most women of child-bearing are immune (98% >25 years)
- > 80% risk if mother infected during 1st month, drops to 5% in 4th month of gestation.
- Teratogenic
- Fetal age determines extent of damage
- Infection:
< 8 weeks severe effects in 10-60% → most likely eye and heart
> 13-16 weeks: fewer than 30% affected → hearing loss

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13
Q

Herpes Simplex Virus
Epidemiology
Neonatal

A
  • HSV1 or HSV2
  • Primarily transmitted through infected maternal genital tract
    ➡️Rationale for C-section delivery prior to membrane rupture
  • Primary infection with greater transmission risk than reactivation

Neonatal
- Type 1 & 2 (Genital herpes)
- Neonatal herpes:
Direct contact at delivery
Ascending infection-PROM
- Risks for postnatal infection:
Caregivers with orolabial herpes, herpetic whitlow

Clinical presentation
- Most are asymptomatic at birth
- 3 patterns of ~ equal frequency with symptoms between birth and 4wks:
➡️Skin, eyes, mouth (SEM) -> best outcome
➡️CNS disease
➡️Disseminated disease (present earliest) -> highest mortality
- Initial manifestations very nonspecific with skin lesions NOT necessarily present
- Disseminated disease: With treatment-mortality ~ 50 %
- CNS disease:
Long-term sequelae:
Microcephaly, mental retardation,
blindness, etc.
- Localized skin, mucosa: best outcome

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14
Q

Congenital CMV
Transmission and Pathogenesis
Clinical presentation

A

Transmission and pathogenesis
- Double stranded DNA virus (herpesvirus family)
- Primary infection (highest risk)→latency (can reactivate)
- Incidence 0.2-2% of all live births
- 5-10% symptomatic at birth
- Transmitted via direct contact with infected body fluids
- Intrauterine transmission: CMV crosses the placenta in a primary {highest risk of transmission and systemic disease} or latent (reactivation) infection
- Primary infection increased transmission and risk of symptomatic disease
- Peripartum exposure common (premature), pneumonitis, hepatitis, enteritis
- Term babies postpartum acquired- less severe illness
- High risk-women working in daycare

Clinical presentation
- Slide 41

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15
Q

Congenital syphilis
Transmission & Pathogenesis
Features
Late congenital syphilis
Prevention

A

Transmission & pathogenesis
- Spirochete Treponema pallidum transmitted transplacentally from mother to foetus by contact with active lesion during labour
- Transmission risk: 70-100% if untreated primary syphilis vs 40% if latent
- Risk factors: co-infection HIV, promiscuity, failure to implement safer sexual practices drug use –particular among adolescents and young adults, insufficient public health resources
- 66% asymptomatic at birth

Features
Slide 47

Late congenital syphilis
- Hutchinson’s triad
➡️Dentition: Hutchinson’s teeth
➡️Eye: Interstitial keratitis
➡️ CN8 deafness
- Skin& face: Rhagades, saddle nose
- Bones and joints: pseudo paralysis of Parrot, short maxilla, high palatal arch, Higoumenakia sign, Saber shin, Scaphoid scapulae, Clutton joints [Slide 53}
- CNS: developmental delay, hydrocephalus
- Please consult ppt on Syphilis

Prevention
- Antenatal screening in early pregnancy and at delivery
- Treatment with 3 monthly RPR -titer follow-up for 1 year
- Vaccines in development; none in human clinical trials
- Neonates treated for congenital syphilis need to be notified

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16
Q

Parvovirus
Epidemiology
Pathophysiology

A

Epidemiology
- DNA virus, only a single serotype exists
- Humans are only known host
- Transmission is by respiratory droplets and by blood
- Incubation period is 4 to 20 day
- 50% of woman child bearing age immune
- If acquired in pregnancy –less than 10% transmission risk to fetus
- Can cause anemia and hydrops in fetus
- Intra-uterine transfusion

Pathophysiology
- Virus crosses the placenta and destroys red cell precursors
- Fetal anemia –> high output congestive heart failure –> hydrops fetalis
- Virus also directly injures myocardial cells

17
Q

Neonatal conjunctivitis

A
  • Prevention at birth forN Gonorrhea:
    Thick, copious, yellow
    Peri-orbital edema
  • Gram stain

Common causes
- slide 61

18
Q

Neonatal fungal infections

A
  • Most common: Candida albicans
  • Risk factors for systemic fungemia:
    Prematurity ,Cephalosporin and Carbapenum
    Host immunosuppression (steroids)
    Indwelling central venous lines
  • Skin: Thrush, perineal diaper rash (common in healthy babies ,in isolation not sign of immune depression)
19
Q

Oral thrush / candidiasis

A
  • Oral candidiasis the most common presentation
  • Causes feeding problems
  • White sticking to inside of cheeks
20
Q

Neonatal infections

A
  • Neonatal infections are primarily bacterial in origin, and include pneumonia, sepsis, and meningitis.
  • Incidence
    1-10/1000 live births –developed countries
    2-25/1000 live births –developing countries
  • Neonatal infections result in over 550 000 neonatal deaths every year
21
Q

Maternal risk factors that can predispose to neonatal infection

A
  • Chorioamnionitis
  • Intrapartum maternal temperature (  38 ℃)
  • Delivery at < 37 weeks gestational age (GA)
  • Prolonged rupture of membrane (> 18 hours)
  • Maternal GBS colonization
    ➡️Positive vaginal-rectal screen
    ➡️Previous infant with GBS disease
    ➡️GBS bacteriuria during current pregnancy
22
Q

Neonatal risk factors that can predispose to neonatal infection

A
  • Prematurity
  • Low birth weight
  • Male gender
  • Asphyxia
  • Congenital abnormalities
  • Barrier function (skin, invasive procedures and central lines, CPAP use etc)
23
Q

Immune system (cellular and humoral)

A

Neutrophils (PMNs) NB in killing of bacteria:
Neonatal PMNs are
- deficient in chemotaxis (decreased adherence to endothelial lining of blood vessels,
- reduced ability to migrate into the tissues) and
- reduced killing capacity (once in tissues may fail to degranulate)
Impaired macrophage chemotaxis and decreased cytokine production

= function impairedSome preformed immunoglobulin acquired via placenta from mother (most are transferred in last trimester..mainly IgG)
Decreased ability and response to generate immunoglobulin in response to antigenic stimulation (few IgM)
Breastfeeding transmits some IgA to newborn
Immature complement cascade – impaired killing of especially Gram negative organisms

24
Q

Timing of neonatal sepsis

A
  • Early-onset sepsisis defined as the onset of symptoms within the first 72 hours/1 week of life; infection from birth canal
  • Late-onset sepsisis defined as the onset of symptoms from an onset at ≥7 days of age; maternal or external source of infection
25
Q

Early onset sepsis

A

Slide 69

26
Q

Late onset sepsis

A
27
Q

Continue on slides

A