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
