DISCUSSION
VGS-BSI can cause life-threatening complications in children with cancer
and early initiation of appropriate antibiotic therapy is essential.
With increasing penicillin-resistance amongst VGS
isolates,12 febrile neutropaenia monotherapy with an
extended spectrum B-lactam agent may be suboptimal in patients at high
risk of VGS-BSI.13 However, the universal addition of
vancomycin to empiric febrile neutropaenia therapy has not shown
benefit, increases nephrotoxicity,18 and the emergence
of resistance,19 and is not routinely
recommended.15,20 A risk-stratified approach limits
the addition of empiric vancomycin to febrile neutropaenia therapy for
high-risk and clinically unstable patients, maximising utility and
minimising the potential for harm. This report demonstrates that this
approach is safe and effective, guiding appropriate therapy and
supporting good clinical outcomes in VGS-BSI.
The proportion of non-penicillin susceptible VGS isolates (57.9%) was
comparable to previous paediatric studies (29.6% to
67.5%).6,9,21 Reassuringly, there were no VGS-BSI
related deaths and all VGS isolates in high-risk patients were
susceptible to the recommended empiric antibiotics. Whilst four
non-high-risk patients had a non-penicillin susceptible VGS-BSI,
vancomycin was added within 24 hours and all recovered without incident.
The clinical stability observed in these patients, despite the slight
delay in vancomycin therapy, may attest to the lower pathogenicity of
VGS in lower risk populations.
Modern laboratory methods allow continuous assessment of blood culture
samples, allowing early notification and time-to-positivity assessment.
In this study, all blood cultures were detected as positive for VGS-BSI
within 17 hours, indicating that empiric vancomycin targeting VGS can be
safely discontinued in stable patients at 24 hours if cultures remain
negative.
This study is limited by the single-centre design and small sample size
but given the limited data assessing such a risk-stratified approach,
the findings remain important. Secondly, we employed a pragmatic
definition of BSI including all single VGS isolates, which may have led
to an overestimation of VGS-BSI episodes. The definition of VGS-BSI is
not standardised and whilst some previous surveillance studies required
isolation of VGS from two samples,7,9 several other
studies have defined VGS-BSI as any single isolation of
VGS6,8,22 as this would result in treatment initiation
from a clinical perspective. Notably, all VGS-BSI episodes in this study
were associated with fever and were treated as true episodes of
bacteremia.22
In conclusion, this data demonstrates the safety of a risk-stratified
approach targeting the addition of empiric vancomycin to febrile
neutropaenia therapy in children with cancer at high-risk of VGS-BSI.
The majority of patients received appropriate antibiotic cover for
VGS-BSI and no episodes progressed to VGS-BSI related shock requiring
ICU admission; there were no VGS-BSI associated deaths. All VGS isolates
flagged positive within 24 hours indicating empiric vancomycin can be
discontinued after 24 hours in clinically stable patients. Broader
assessment of this risk-stratified approach is warranted.