Sepsis occurs in infants < 28days old, () and is still a major cause of mortality and morbidity in new-bornstoday, with an incidence ranging from 1-10/1000 live-births being affected, ().The systemic infection can be categorised as early-onset or late-onset, (),with microorganisms such as E.coli and Coagulase-negative staphylococci beingassociated with the infection.
Early-onset sepsis (EOS) is defined as theinfection occurring within the first 72 hours of life, () with the mortalityrate for EOS currently reaching ~3% among term new-borns and ~16% invery-low-birth-weight (VLBW) infants, (). Late-onset sepsis (LOS) tends tooccur during the first 7 days of life, (), and is generally acquired from theenvironment (). With LOS, mortality rates have been observed to increase withpostnatal age, reaching 36% in new-borns aged 8-14 days and 52% in those aged15-28 days, (). Several recent studies – including one carried out in Egypt whichobserved the incidence of sepsis in neonates over a 12-month period – havehighlighted the occurrence of multidrug resistant organisms being leadingcauses of early and late onset sepsis (). Both gram-negative bacilli andgram-positive cocci are noted to be highly resistant to various microbials,including ampicillin, (). This was not only noted in LOS cases, but resistancewas also observed in infants diagnosed with early onset sepsis, (). Thus, the increasingresistance to certain antibiotics for treatment of neonatal sepsis has beenbought to global attention with demands for antibiotic regulations beingcalled.
Septicaemia is one of the mostprominent infections responsible for the 1.6 million deaths that are caused byneonatal infections in developing countries annually, (). The bacterial blood stream infection (BSI)can be classified according to the time of onset of the disease – early onset(EOS) which occurs within the first 3 days of life, and late onset (LOS) whereinfection tends to appear anytime between first week and first month of life,depending on whether the infant was term or born prematurely, (). With EOS, theacquisition of the microorganisms occurs as a result of transplacentalinfection, or colonisation of the mother’s genitourinary (GU) tract, (), thusresulting in the bacterial pathogens being transmitted vertically from motherto infant before or during delivery ().
Microorganisms most commonly associatedwith EOS are Group B Streptococcus (GBS), Escherichia coli (E. coli) – which is the second leadingcause of EOS, accounting for 24% of all cases, with 81% occurring in preterminfants, () – as well as Coagulase-negative Staphylococcus (CoNS) andHaemophilus influenzae (). Theseorganisms typically colonise the maternal GU tract leading to contamination ofthe amniotic fluid, placenta, cervix or vaginal canal, (). Contaminationof the amniotic fluid can occur prior or during labour, meaning the infant mayacquire the pathogen in utero orintrapartum, (). In late-onset sepsis, the pathogens are acquired after birth,normally from nosocomial or community sources, (). There is some contemplationas to when the period for late-onset sepsis begins, however generally infectionis deemed late-onset when it occurs after 6 days of life, ().
With LOS, 70% ofinfections were associated with Gram-positive organisms; Coagulase-negativeStaphylococci contributed 48% of cases and Gram-negative (such as E. coli) bacteria 18%, (). Invasivemicroorganisms from the environment may colonise the infant’s skin, respiratorytract, conjunctivae, GI tract and umbilicus, and can acquired vertically orhorizontally, (). Both the E. coliand Staph pathogens are importantbacterial agents of sepsis; however, E. coliis a more prominent cause in EOS, whilst CoNS is a major cause for LOS, ().
Escherichia coli (E.coli), is responsible for asubstantial proportion of mortality in infants and is part of one of the mostdiverse bacterial species (). The complex antigenic structure as well as certainvirulence factors have been important in neonatal sepsis – the best describedvirulence factor is the K1 capsular antigen which is present in certain strainsand is closely linked to neonatal meningitis, (). This polysialic acid impairsopsonophagocytic killing meaning those infected with the K1 antigenic strainshave an increased morbidity and mortality in comparison to those with otherstrains, ().
The severity of the disease is associated to the amount andpersistence of the K1 antigen in the cerebrospinal fluid, ().