Neonatal Sepsis Microbiology
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Direct answer
Neonatal sepsis is systemic infection in the first 28 days of life, and its microbiology divides by the time of onset. Early-onset disease, within 72 hours of birth, is led by Group B streptococcus and Escherichia coli acquired from the maternal genital tract. Late-onset disease, from 72 hours to 28 days, is led by coagulase-negative staphylococci, Staphylococcus aureus and Klebsiella acquired from the hospital or community.
What you must remember
- Early onset: Within 72 hours of birth, usually from the maternal genital tract, with Group B streptococcus leading in Western series, followed by E. coli and Listeria monocytogenes; Indian NICUs report mostly gram-negative bacilli.
- Late onset: From 72 hours to 28 days, usually from hospital or community contact, with coagulase-negative staphylococci, S. aureus, Klebsiella and Candida as common causes.
- Group B streptococcus screening: A rectovaginal swab culture at about 35 to 37 weeks of gestation guides intrapartum antibiotic prophylaxis for colonised women.
- Listeria: A gram-positive bacillus that causes early-onset sepsis and meningitis after maternal infection that may be mild or unrecognised, and ampicillin is the drug of choice.
- E. coli K1: Its capsular K1 antigen is linked to neonatal meningitis and helps the organism resist complement.
- Candida: Causes late-onset invasive disease in preterm infants on broad-spectrum antibiotics, central lines or parenteral nutrition.
- Gram-negative resistance: Klebsiella and other nosocomial gram-negative bacilli cause NICU outbreaks, so local antibiogram data shape empirical therapy.
- Sepsis screen: Blood culture before antibiotics, CSF examination when meningitis is suspected, and serial CRP help confirm and monitor disease.
Early versus late onset at a glance
Neonatal sepsis is a clinical syndrome with nonspecific signs, so the microbiology sets the empirical treatment. Timing of onset is the first clue to the likely organism and its source.
| Feature | Early onset (under 72 hours) | Late onset (72 hours to 28 days) |
|---|---|---|
| Source | Maternal genital tract | Hospital environment or community |
| Leading organisms | Group B streptococcus, E. coli, Listeria | Coagulase-negative staphylococci, S. aureus, Klebsiella, Candida |
| Typical picture | Respiratory distress and rapid deterioration | Meningitis, focal infection or central line sepsis |
| Key tests | Blood culture and maternal history | Blood and CSF cultures, line swabs |
| Empirical focus | Ampicillin with an aminoglycoside pending culture | Choice guided by local antibiogram and MRSA risk |
The timing points to the likely source, whereas culture confirms the species and its susceptibility. Early-onset organisms are largely maternal, which is why antenatal screening for Group B streptococcus matters. A baby who looks well at birth but deteriorates within hours still needs a full sepsis screen, because early Group B streptococcal disease can progress quickly.
Where the exam tries to catch you
Neonatal sepsis questions usually test whether the candidate uses the time of onset to choose the organism.
- Trap: Treating all neonatal sepsis as early-onset Group B streptococcus. Correct: Late-onset disease in NICU infants is commonly due to coagulase-negative staphylococci or Klebsiella, so the organism changes after 72 hours.
- Trap: Discarding a negative blood culture as proof of no sepsis. Correct: Small neonatal volumes and prior antibiotics reduce the yield, so clinical signs and repeat sampling still matter.
- Trap: Ignoring Listeria because the mother had no fever. Correct: Maternal infection can be mild or silent, so Listeria stays on the differential, and ampicillin with gentamicin covers it empirically.
- Trap: Assuming every gram-negative bacillus in a neonate is E. coli. Correct: Klebsiella, Pseudomonas and Enterobacter also cause late-onset disease, so culture identification is needed.
Frequently asked questions
Which organism causes most early-onset neonatal sepsis?
Group B streptococcus is the leading cause of early-onset neonatal sepsis, acquired from the maternal genital tract during labour. Escherichia coli, especially K1 strains, is the second major cause, and Listeria monocytogenes is also important.
Why does Listeria matter in neonatal sepsis?
Listeria monocytogenes causes early and late neonatal sepsis and meningitis, often after maternal infection that is mild or unrecognised. It is a gram-positive bacillus, and ampicillin is the drug of choice, usually combined with gentamicin in neonates.
How is Group B streptococcus carriage detected in pregnancy?
A rectovaginal swab culture taken at about 35 to 37 weeks of gestation identifies women colonised with Group B streptococcus. Positive women receive intrapartum antibiotic prophylaxis, usually penicillin, to prevent early-onset disease in the newborn.
What is the onset window for late-onset neonatal sepsis?
Late-onset neonatal sepsis begins after 72 hours of life and up to 28 days, usually from hospital or community contact. Coagulase-negative staphylococci, Staphylococcus aureus and Klebsiella are common causes, and central lines are a key risk factor.
Which fungus causes late-onset neonatal infection in preterm infants?
Candida species, including C. albicans and C. parapsilosis, cause late-onset invasive infection in preterm infants receiving broad-spectrum antibiotics, central lines or parenteral nutrition. Diagnosis is by blood culture, and antifungal treatment is started promptly when invasive candidiasis is suspected.