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Tejiram et al. Plast Aesthet Res. 2025;12:9 https://dx.doi.org/10.20517/2347-9264.2024.109 Page 13 of 16

wound bed is exposure from the environment. The hospital exposome could serve as the partial source of
invasion through contact with water during debridement or other sources [1,42] . There is a paucity of literature
examining antibiotic resistant patterns in extremophiles in general, including the use of cefazolin; however,
some mechanisms have been suggested. Similar to other resistant bacterial species, extremophiles may
accumulate genes or plasmids for multiple drug resistance. This may lead to the development of enzymes
[49]
like penicillinase that enable propagation in spite of antimicrobial use . Another enriched organism of the
wound bacteriome at this time point was Acinetobacter. Acinetobacter is prevalent in burn wound infections
and multi-drug resistant Acinetobacter has notably been associated with delayed healing sepsis, shock, and
death . The only member enriched in the no-ABX wound bed at takedown was of the phylum
[4]
Verrucomicrobia, which is commonly found in the environment and is relatively inactive.

Despite the enrichment of extremophiles and pathogenic species as well as enrichment of the whole domain
of Bacteria at follow-up in the wound bed, alpha diversity of the wound bed was not significantly different at
any time point. Instead, wound bed diversity was slightly elevated in ABX patients. This is contrary to
several studies that point to a resulting dysbiosis and lower community richness due to burn injury
dynamics alone and after antibiotic treatment [1,5,42,50] . By decreasing the number of commensal microbes,
antibiotics may allow for the invasion of species that are more niche-specific, which may not otherwise have
an opportunity. The increasing enrichment of non-commensal microbes throughout the time course (from
dressing removal through clinical follow-up) leads to the question of when the microbial transition from
burn wound dysbiosis to normal healed wound homeostasis occurs and what role clinical therapeutic agents
play in that transition.

Preoperative antibiotics and the oral microbiome
The oral microbiome at follow-up in ABX patients displayed enrichment of endogenous flora such as
Corynebacterium, Lactobacillus, Rothia, and Granulicatella. Corynebacterium has been associated with a
decrease in sepsis in burn patients and a decrease in S. aureus virulence [1,51] . Delanghe et al. found that
Lactobacilli play a profound role in inhibiting skin pathogens by modulating the inflammatory response,
producing antimicrobial metabolites, and enhancing skin barrier function . Rothia is a known commensal
[52]
of the oral microbiome. Though it can be pathogenic, its virulence as an opportunistic pathogen is mainly a
concern for immunocompromised individuals.

In the no-ABX oral microbiome at follow-up, Defluviitaleaceae of the phylum Firmicutes were enriched.
This finding is similar to Tsuzukibashi et al.’s rat study of non-antibiotic cutaneous post-burn bacteriome,
[53]
in which Firmicutes accounted for 63.8% of the enriched microbial members . The abundance of
commensal flora in the oral microbiome at follow-up, in contrast to the entirety of the domain of Bacteria
in the wound bed, suggests the integrity and continuity of the oral microbiome despite ABX treatment. The
compositional differences in the post-burn microbiome in the oral cavity and wound bed are striking
because commensals are not present where they would be most effective in supporting host immune
deficiencies (i.e., the wound bed). Further research could characterize and contrast microbiome differences
in sites localized to the burn injury, uninjured distant skin, the oral microbiome, and the gut microbiome to
bolster our understanding of the global response to post-burn perioperative antibiotic treatment.

Study limitations
This work represents a preliminary investigation into the effect of a short course of antibiotics on the burn
patient microbiome. This study has several limitations. While the total sample size of the study is large, the
number of patients included is small. Given the translational nature of the study, the need for microbiome
analysis, and sample collection techniques, the number of participants we could enroll was limited. Having
an adequately powered study is critical to draw more robust and definitive conclusions about the full