Kristina L. Guyton

Bacterial colonization and succession in a newly opened hospital

Patients share their microbiota with their rooms and with nursing staff, and this shapes the microbial ecology of the hospital environment. A new hospital teems with life Lax et al. conducted a yearlong survey of the bacterial diversity associated with the patients, staff, and built surfaces in a newly opened hospital. They found that the bacterial communities on patient skin strongly resembled those found in their rooms. The authors demonstrated that the patient skin microbial communities were shaped by a diversity of clinical and environmental factors during hospitalization. They found little effect of intravenous or oral antibiotic treatment on the skin microbiota of patients. The microorganisms that inhabit hospitals may influence patient recovery and outcome, although the complexity and diversity of these bacterial communities can confound our ability to focus on potential pathogens in isolation. To develop a community-level understanding of how microorganisms colonize and move through the hospital environment, we characterized the bacterial dynamics among hospital surfaces, patients, and staff over the course of 1 year as a new hospital became operational. The bacteria in patient rooms, particularly on bedrails, consistently resembled the skin microbiota of the patient occupying the room. Bacterial communities on patients and room surfaces became increasingly similar over the course of a patient’s stay. Temporal correlations in community structure demonstrated that patients initially acquired room-associated taxa that predated their stay but that their own microbial signatures began to influence the room community structure over time. The α- and β-diversity of patient skin samples were only weakly or nonsignificantly associated with clinical factors such as chemotherapy, antibiotic usage, and surgical recovery, and no factor except for ambulatory status affected microbial similarity between the microbiotas of a patient and their room. Metagenomic analyses revealed that genes conferring antimicrobial resistance were consistently more abundant on room surfaces than on the skin of the patients inhabiting those rooms. In addition, persistent unique genotypes of Staphylococcus and Propionibacterium were identified. Dynamic Bayesian network analysis suggested that hospital staff were more likely to be a source of bacteria on the skin of patients than the reverse but that there were no universal patterns of transmission across patient rooms.

The gut microbiota and gastrointestinal surgery

Surgery involving the gastrointestinal tract continues to prove challenging because of the persistence of unpredictable complications such as anastomotic leakage and life-threatening infections. Removal of diseased intestinal segments results in substantial catabolic stress and might require complex reconstructive surgery to maintain the functional continuity of the intestinal tract. As gastrointestinal surgery necessarily involves a breach of an epithelial barrier colonized by microorganisms, preoperative intestinal antisepsis is used to reduce infection-related complications. The current approach to intestinal antisepsis varies widely across institutions and countries with little understanding of its mechanism of action, effect on the gut microbiota and overall efficacy. Many of the current approaches to intestinal antisepsis before gastrointestinal surgery run counter to emerging concepts of intestinal microbiota contributing to immune function and recovery from injury. Here, we review evidence outlining the role of gut microbiota in recovery from gastrointestinal surgery, particularly in the development of infections and anastomotic leak. To make surgery safer and further reduce complications, a molecular, genetic and functional understanding of the response of the gastrointestinal tract to alterations in its microbiota is needed. Methods can then be developed to preserve the health-promoting functions of the microbiota while at the same time suppressing their harmful effects.

Morphine Promotes Colonization of Anastomotic Tissues with Collagenase - Producing Enterococcus faecalis and Causes Leak

BackgroundDespite ever more powerful antibiotics, newer surgical techniques, and enhanced recovery programs, anastomotic leaks remain a clear and present danger to patients. Previous work from our laboratory suggests that anastomotic leakage may be caused by Enterococcus faecalis strains that express a high collagenase phenotype (i.e., collagenolytic). Yet the mechanisms by which the practice of surgery shifts or selects for collagenolytic phenotypes to colonize anastomotic tissues remain unknown.MethodsHere, we hypothesized that morphine, an analgesic agent universally used in gastrointestinal surgery, promotes tissue colonization with collagenolytic E. faecalis and causes anastomotic leak. To test this, rats were administered morphine in a chronic release form as would occur during routine surgery or vehicle. Rats were observed for 6 days and then underwent exploratory laparotomy for anastomotic inspection and tissue harvest for microbial analysis. These results provide further rationale to enhanced recovery after surgery (i.e., ERAS) programs that suggest limiting or avoiding the use of opioids in gastrointestinal surgery.ResultsResults demonstrated that compared to placebo-treated rats, morphine-treated rats demonstrated markedly impaired anastomotic healing and gross leaks that correlated with the presence of high collagenase-producing E. faecalis adherent to anastomotic tissues. To determine the direct role of morphine on this response, various isolates of E. faecalis from the rats were exposed to morphine and their collagenase activity and adherence capacity determined in vitro. Morphine increased both the adhesiveness and collagenase production of four strains of E. faecalis harvested from anastomotic tissues, two that were low collagenase producers at baseline, and two that were high collagenase producers at baseline.ConclusionThese results provide further rationale to enhanced recovery after surgery (i.e., ERAS) programs that suggest limiting or avoiding the use of opioids in gastrointestinal surgery.

The intestinal microbiome and surgical disease

As we have seen throughout this monograph, microbes play a key role in both human health, disease, response to surgery and pharmacologic intervention. Advancing the understanding of these complex relationships is in its infancy. Technological advances in analysis, large data management and interpretation of data are rapidly evolving to address disease states which have eluded investigator and clinicians. What has been learned so far, however is both exciting and humbling.

Surgeon-patient communication during awake procedures.

BACKGROUND Surgeons are increasingly performing procedures on awake patients. Communication during such procedures is complex and underexplored in the literature. METHODS Surgeons were recruited from the faculty of 2 hospitals to participate in an interview regarding their approaches to communication during awake procedures. Three researchers used the constant comparative method to transcribe, code, and review interviews until saturation was reached. RESULTS Twenty-three surgeons described the advantages and disadvantages of awake procedures, their communication with the awake patient, their interactions with staff and with trainees, the environment of awake procedures, and how communication in this context is taught and learned. CONCLUSIONS Surgeons recognized communication during awake procedures as important and reported varied strategies for ensuring patient comfort in this context. However, they also acknowledged challenges with multiparty communication during awake procedures, especially in balancing commitments to teaching with their duty to comfort the patient.

Prevention of Perioperative Anastomotic Healing Complications: Anastomotic Stricture and Anastomotic Leak

The anastomotic healing complications of postoperative leak and stricture continue to plague surgeons despite many broadly targeted interventions. Evaluation of preventive measure efficacy is difficult due to inconsistent definitions and reporting of these complications. Few interventions have been shown to impact rates of leakage or stricture. However, new evidence is emerging that the intestinal microbiota can play an important role in the development of anastomotic complications. A more holistic approach to understanding the mechanisms of anastomotic complications is needed in order to develop tailored interventions to reduce their frequency. Such an approach may require a more complete definition of the role of the microbiota in anastomotic healing.

Media from macrophages co-incubated with Enterococcus faecalis induces epithelial cell monolayer reassembly and altered cell morphology

Signal exchange between intestinal epithelial cells, microbes and local immune cells is an important mechanism of intestinal homeostasis. Given that intestinal macrophages are in close proximity to both the intestinal epithelium and the microbiota, their pathologic interactions may result in epithelial damage. The present study demonstrates that co-incubation of murine macrophages with E. faecalis strains producing gelatinase (GelE) and serine protease (SprE) leads to resultant condition media (CM) capable of inducing reassembly of primary colonic epithelial cell monolayers. Following the conditioned media (CM) exposure, some epithelial cells are shed whereas adherent cells are observed to undergo dissolution of cell-cell junctions and morphologic transformation with actin cytoskeleton reorganization resulting in flattened and elongated shapes. These cells exhibit marked filamentous filopodia and lamellipodia formation. Cellular reorganization is not observed when epithelial monolayers are exposed to: CM from macrophages co-incubated with E. faecalis GelE/SprE-deficient mutants, CM from macrophages alone, or E. faecalis (GelE/SprE) alone. Flow cytometry analysis reveals increased expression of CD24 and CD44 in cells treated with macrophage/E. faecalis CM. This finding in combination with the appearance colony formation in matrigel demonstrate that the cells treated with macrophage/E. faecalis CM contain a higher proportion progenitor cells compared to untreated control. Taken together, these findings provide evidence for a triangulated molecular dialogue between E. faecalis, macrophages and colonic epithelial cells, which may have important implications for conditions in the gut that involve inflammation, injury or tumorigenesis.

Parastomal Hernia: An Ounce of Prevention

Parastomal hernia is a common consequence of creating an intestinal stoma. Though many patients with parastomal hernias are asymptomatic, complications from a parastomal hernia (PSH) can be life threatening. Parastomal hernia negatively impacts patient psychological well-being and quality of life and increases healthcare utilization. Numerous methods of PSH repair have been proposed and practiced, but recurrence after surgery remains common; therefore attention to PSH prevention has been a topic of interest in recent years. While many technical aspects of stoma creation are taught as surgical dogma, the two preventative techniques with the best evidence are the creation of an extraperitoneal stoma and the reinforcement of the fascial opening using prophylactic mesh. Despite increasing evidence supporting the efficacy of prophylactic mesh in the prevention of parastomal herniation, this technique has been slow to be adopted into current practice.