43 research outputs found
Tailored Pre-Operative Antibiotic Prophylaxis to Prevent Post-Operative Surgical Site Infections in General Surgery
No full textThe average American today undergoes three inpatient and two outpatient surgical procedures during one’s life, each of which carries with it a risk of post-operative infection. It has long been known that post-operative infections cause significant morbidity in the immediate peri-operative period, but recent evidence suggests that they can have long-term consequences as well, increasing a patient’s risk of infectious complications in unrelated surgeries performed months or even years later. While there are several theories on the origin of this association, including bacterial colonization of a post-operative infectious wound site, antimicrobial resistance from curative courses of antibiotics, subclinical immunosuppression, or the creation of an inflammatory “pathobiome” following an infectious insult, it is ultimately still unclear why patients who experience a single post-operative infection seem to be at a significantly higher risk of experiencing subsequent ones. Regardless, this association has significant implications for the routine use of pre-operative antibiotic prophylaxis. Indeed, while the prescription of antibiotics pre-operatively has dramatically reduced the rate of post-operative infections, the chosen prophylaxis regimens are typically standardized according to national guidelines, are facing increasing antimicrobial resistance patterns, and have been unable to reduce the risk of post-operative infection to acceptably low levels for certain surgeries. As a result, some clinicians have speculated that tailoring pre-operative antibiotic prophylaxis according to a patient’s prior infectious and operative history could improve efficacy and further reduce the rate of post-operative infections. The purpose of this review is to describe the evidence for the link between multiple post-operative infections and explore the efficacy of individualized pre-operative prophylaxis
Intestinal anastomotic injury alters spatially defined microbiome composition and function
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Anastomotic leak in rats exposed to pre-operative radiation and intestinal <i>P. aeruginosa</i>.
No full text<p>(A) Sketch of anastomosis model and treatment groups. Treatment groups: I, anastomosis only; II, anastomosis + cecal injection of <i>P. aeruginosa</i> MPAO1, 10<sup>7</sup> CFU; III, radiation + anastomosis; IV, radiation +anastomosis + cecal injection of <i>P. aeruginosa</i> MPAO1 (10<sup>7</sup> CFU). Black arrows indicate the anastomotic site. (B) Excised and exposed suture lines of anastomotic sites. All suture lines are grossly intact except for group IV where ulceration/dehiscence is noted by the black arrow. (C) H&E staining of anastomotic tissues. Arrows and brackets indicate width of tissue apposition at suture line. (D, D’, E) Methylene blue assessment of anastomotic integrity demonstrating rare to no leaks in groups I–III (D) and gross extravasation in group IV (D’). Arrows indicate the site of anastomosis. (E) Incidence of anastomotic leak between groups. n = 12 (group I), n = 16 (group II), n = 9 (group III), n = 18 (group IV), *p<0.01.</p
Intestinal anastomotic injury alters spatially defined microbiome composition and function
No full textBackgroundWhen diseased intestine (i.e., from colon cancer, diverticulitis) requires resection, its reconnection (termed anastomosis) can be complicated by non-healing of the newly joined intestine resulting in spillage of intestinal contents into the abdominal cavity (termed anastomotic leakage). While it is suspected that the intestinal microbiota have the capacity to both accelerate and complicate anastomotic healing, the associated genotypes and functions have not been characterized.ResultsUsing 16S rRNA amplicon sequencing of samples collected on the day of surgery (postoperative day 0 (POD0)) and the 6th day following surgery (postoperative day 0 (POD6)), we analyzed the changes in luminal versus tissue-associated microbiota at anastomotic sites created in the colon of rats. Results indicated that anastomotic injury induced significant changes in the anastomotic tissue-associated microbiota with minimal differences in the luminal microbiota. The most striking difference was a 500-fold and 200-fold increase in the relative abundance of Enterococcus and Escherichia/Shigella, respectively. Functional profiling predicted the predominance of bacterial virulence-associated pathways in post-anastomotic tissues, including production of hemolysin, cytolethal toxins, fimbriae, invasins, cytotoxic necrotizing factors, and coccolysin.ConclusionTaken together, our results suggest that compositional and functional changes accompany anastomotic tissues and may potentially accelerate or complicate anastomotic healing
SNP mutation in <i>MexT</i> is responsible for P2 phenotype.
No full text<p>(A) Genome DNA sequence comparative map of <i>P. aeruginosa</i> MPAO1-P1 and MPAO1-P2 at the DSM-1707 backbone annotated with the MexT locus. Grey and teal bands: annotated coding regions; red tick: location of MexT locus; green ticks: tRNAs; black ticks: rRNAs; inner circle GC content. (B–D) swarming motility in (B) MPAO1-P1 (P1), (C) MPAO1-P2 (P2), and (D) MPAO1-P2 in which <i>mexT</i> was replaced by <i>mexT</i> gene amplified from MPAO1-P1 (P2/<i>mexT</i><sub>P1</sub>). (E) Growth curves at 100 µg/ml chloramphenicol demonstrating acquisition of chloramphenicol resistance in P2/<i>mexT</i><sub>P1.</sub> (F) Collagenase activity measured by fluorescence of fluorescent labeled gelatin as a substrate. n = 6, *p<0.01. Results are representative of 3 independent experiments.</p
