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Page 2 of 16 Tejiram et al. Plast Aesthet Res. 2025;12:9 https://dx.doi.org/10.20517/2347-9264.2024.109

to determine bacterial taxonomy characteristics. Graft loss was determined at clinic follow-up.

Results: In ABX patients, there were 29 enriched bacterial taxa within wound beds at dressing takedown [log(LDA)
≥ 2, P ≤ 0.05] and greater than 10 bacterial taxa in buccal swabs at follow-up [log(LDA) ≥ 2, P ≤ 0.05]. There was
increasing alpha diversity in ABX patients intraoperatively and at dressing takedown. There were no significant
differences in graft loss between groups. Extremophile infiltration was noted in oral and wound microbiomes in
ABX patients.

Conclusion: Though not affected clinically, these data suggest that a single preoperative antibiotic dose
significantly impacts the wound and oral microbiome. Innovative approaches to examining the antibiotic impact on
the host microbiome of burn patients may help better tailor antibiotic stewardship.

Keywords: Antibiotics, antibiotic resistance, burn injury, infection, microbial diversity, microbiome, preoperative,
wound

INTRODUCTION
Advances in burn care and wound management in recent decades, including the use of topical
antimicrobials, improved resuscitation strategies, judicious systemic antibiotics, and early excision and
grafting, have resulted in improved wound healing and mortality. However, burn wound sepsis remains a
[1]
significant cause of morbidity and mortality, accounting for approximately 50% of all burn-related deaths .
Disruption of the skin barrier due to burn injury attenuates homeostasis mechanisms and represents an
entry point for bacteria, fungi, and viruses. Increased burn injury size is correlated with increased risk for
local and systemic infection . Dermal ischemia and avascular necrotic tissue provide a protein-rich
[2-4]
environment that is advantageous for the colonization of microbes . Rapid onset of burn wound edema
[5]
promotes an infectious environment by deoxygenating surrounding tissues. This environment, along with
an early systemic hyperinflammatory response, increases vasodilation and vascular permeability, leading to
microvascular leakage . A dysregulation of homeostatic mechanisms follows, resulting in both local and
[3-6]
[7]
systemic responses to injury .
Burn-injured patients present in a more immunocompromised state due to the significant inflammatory
response that follows their injury and the loss of their skin integrity, which functions as a natural barrier
against infection. Initial burn wound colonization is gram-positive in nature as commensal colonizers of the
skin easily infect the wound and include species such as Staphylococcus, Enterococcus, Streptococcus,
Corynebacterium, and Micrococcus species (spp.) [2,8-11] . Due to the induction of gut permeability in more
severe burn injuries, the microbial community eventually shifts to a predominantly gram-negative
environment with Pseudomonas aeruginosa, Acinetobacter baumannii, Escherichia coli, Enterobacter cloacae,
Klebsiella spp., and Enterococcus spp. representing common pathogens of infection. Multi-drug resistant
organisms (MDRO) such as methicillin-resistant Staphylococcus aureus (MRSA), resistant Acinetobacter,
and Pseudomonas spp. may develop during prolonged hospital stays and pose a significant risk to morbidity
and mortality in patients with severe burn injury [2,8-12] . Extended hospitalization facilitates transmission of
MDRO, leading to hospital-acquired infections (HAI). Therapy for these microbes is confounded by their
drug resistance, requiring increasing demand for the development of novel antibiotics and meticulous
[2]
isolation protocols . Early tangential burn wound excision reduces the interval between injury and removal
of the damaged, inflammatory necrotic tissue, and subsequent closure through skin grafting helps attenuate
this risk . However, wound infections, particularly from common MDROs like MRSA or other microbes,
[10]
contribute to significant graft loss and wound healing morbidity. Studies on the microbiome in patients
with burn injury are limited, and even fewer have examined the effect of antibiotics on the microbiome in