Neonatology - infections Flashcards
Risk factors for neonatal invasive Group B streptococcus (GBS) infection
Women who have faecal or vaginal carriage of Group B strep
In colonized mothers: Preterm Prolonged rupture of membranes Maternal fever during labour (>38°C) Maternal chorioamnionitis Previously infected infant
What disease does neonatal GBS cause
Early onset sepsis
Late onset sepsis up to 3 months with respiratory distress, apnoea and pneumonia
or
septicaemia and meningitis
mortality is up to 10%
Prophylaxis in mothers with GBS
Intrapartm iv antibiotics
2 approaches:
universal screenin at 35-38 weeks to identify carrier mothers
Risk-based approach - if risk factors, offered antbiotics
Investigations for a neonate with resp distress and temp instability
CXR Septic screen FBC for neutropenia Blood cultures CPR takes 12-24 hrs
management of suspected neonatal GBS
Antibiotics started immediately without waiting for cultures (usually broad-spectrum amoxicillin or benzylpenicillin)
If cultures negative and clinical signs return to normal, stop after 48 hours
If cultures are positive, then continue, check for neurological signs, examine and culture the CSF
Pathology of early onset sepsis
<48hrs after birth
Bacteria ascended from the birth canal and invaded the amniotic fluid
-this is connected to fetal lungs, thus usually presents with pneumonia and bacteraemia/septicaemia
In congenital viral infection and early-onset infection with Listeria monocytogenes, foetal infection is acquired via the placenta following maternal infection
Pathophyysiology of late-onset sepsis
> 48hrs after birth
Source is often infant’s environment
Usually non-specific presentation
In NICU, the main sources are:
indwelling central venous catheters for parenteral nutrition
Invasive procedures which break the skin
Tracheal tubes
Commonest pathogens in late onset sepsis
Staph epidermis is most common
Gram +ve (staph aureus, enterococcus faecalis)
Gram -ve (E.coli, Pseudomonas, Klebsiella)
Use of prolonged antibiotics can also predispose to invasive fungal infections in premature babies eg. Candida albicans
What is the commonest congenital infection. Features?
CMV 3-4/1000
90% are normal at birth and develop naturally
5% have clinical features at birth: hepatosplenomegaly and petechiae
Neurodevelopmental disabilties
5% develop problems later in life - mainly sensorineural hearing loss
Risks of maternal rubella infection in pregnancy
Before 8 weeks: deafness, congenital heart disease, cataracts >80%
13-16 weeks -30% have impaired hearing
Risk after 18 weeks is minimal
Diagnosis and prevention of rubella virus
Maternal infection must be confirmed serologically (clinical picture unreliable)
Childhood immunisation programme with MMR has made it extremely rare
What may cause acute infection with the protozoan Toxoplasma gondii
Consumption of raw or undercooked meat
Contact with faeces or recently infected cats
If during pregnancy, there is a 40% chance of transplacental infection
Congenital incidence is 1 in 10000
Clinical manifestations of congenital toxoplasmosis
Most are asymptomatic
Retinopathy
Cerebral calcification
Hydrocephalus
Usually there are long-term neurological disabilities
Clinical features of CMV, Rubella and Toxoplasmosis in the newborn
Growth restriction Eyye defects eg. cataracts Pneumonitis Hepatomegaly (jaundice and hepatitis) Bone abnormalities
Intracerebral calcification
Hydrocephalus
Microcephalus
Deafness
Heart defects: cardiomegaly
PDA
Rash: blueberry muffin or petechiak
Anaemia - Neutropenia, thrombocytopenia
Blood serology for Rubella, CMV and Tooplasmosis
Rubella-specific IgM, CMV-specific IgM, Toxoplasma-specific IgM
Persistently raised Toxoplasma IgG
Risks with HIV positive mothers
Likely to transmit if high viral load
Breastfeeding poses a 25-40% risk of perinatal transmission
Interventions in HIV positive mothers
Maternal antenatal, perinatal and postnatal antiretroviral drugs to achieve an undetectable maternal viral load at time of delivery
Avoidance of breastfeeding
Active management of labour and delivery to avoid prolonged rupture of the membranes or instrumental
Pre-labour C-section if the mother’s viral load is detectable close to time of delivery
What are the main risk factors for neonatal infection
Preterm (low IgG, and NO IgA and IgM at all)
Infection around cervix may cause preterm labour
Prolonged rupture of membranes (>18hrs)
Environmental: indwelling lines/catheters
Symptoms of neonatal syphilis
Very rare
FTT Fever Irritability No bridge to nose Early rash (small blisters) Large rash Rash to mouth, anus, genitalia Watery discharge from nose Splenomegaly/hepatomegaly Bone inflammation
Complications: blindness deafness deformities of face neurological problems
Treat with penicillin
Presentation of neonatal chlamydia
usually eyes - conjunctivitis
Swelling of eyelids at 1-2 weeks after birth or shortly after
Pneumonia at 4-6 weeks
Treat with oral erythromycin
Presentation of gonorrhoea
Associated with chorioamnionitis and increased risk of premature labour
40% of untreated maternal cases develop: ophthalmia neonatorum (purulent discharge, lid swelling and corneal haze within 4 days after birth) Needs urgent treatment to prevent blindness
Treat with penicillin or a third generation cephalosporin
Presentation of neonatal herpes
More common in preterm infants
Can present up to 4 weeks
Localised herpes lesions on skin/eye
Encephalitis
Disseminated disease
Local disease has low mortality, whereas in disseminated it is high
Common causes of bilious vomiting
Intussusception Obstruction Volvulus Malrotation Tumours Hirschprung's disease Constipation/meconium ileus
Basic treatment of early-onset sepsis
IV antibiotics
Penicillin + aminoglycosides (for Gram -ve)
-GBS
-Listeria monocytogenes
management of late onset sepsis
Cover staphylococci and gram -ve bacilli:
Flucloxacillin and gentamicin
If resistance, do specific antibiotics or broad-spectrum
eg. vancomycin for coagulase negative staphylococci or enterococci
management of suspected neonatal meningitis
Ampicillin or penicillin and a third-generation cephalosporin (eg. cefotaxime which penetrates CSF)
Clinical features of neonatal sepsis
Lethargy Fever or hypothermia Irritability Vomiting Poor feeding Apnoea Resp distress Abdominal distension Jaundice Neutropenia Hypo/hyperglycaemia Shock Seizures
Elements of the sepsis screen
FBC U and Es with glucose Blood culture Chest radiograph Lumbar puncture Urine culture and dip CRP CT or MRI for suspected meningitis
Risks to the newborn from maternal Hep B infection
Important cause of acute and chronic liver disease worldwide.
90% of infants who contract it are asymptomatic chronic carriers
There is no treatment for acute HBV infection
Diagnosis of perinatal Hep B
Detect HBV antigens and antibodies
IgM antibodies to the core antigen (anti-HBc) is positive in acute infections
positive hep B surface antigen (HBsAg) means ongoing infection
Risk of being a chronic HBV carrier
30-50% will develop chronic HBV liver disease - 10% of that progresses to cirrhosis
Long-term risk of hepatocellular carcinoma
Current treatment regimens have poor efficacy
Prevention of Hep B transmission perinatally
All pregnant women should have antenatal screening for HbsAg
If mother is HbsAg positive, give a coruse of Hep B vaccination with Hep B immunoglobulin.
Same with HbeAg positive
Check antibody response to the course - 5% of infants may require vaccination
