Building Implementation Science Capacity in Academic Pharmacy: Report of the 2020-2021 AACP Research and Graduate Affairs Committee.

The 2020-2021 AACP Research and Graduate Affairs Committee (RGAC) continued the work begun by the 2019-2020 RGAC to increase awareness of and capacity for implementation research to advance practice transformation in academic pharmacy. AACP President Anne Lin charged the RGAC with developing resources and programs for training faculty and graduate students in implementation science. The committee was further charged with developing a mechanism to pair pharmacy faculty and implementation experts on practice advancement projects.

The opportunistic pathogen Enterococcus faecalis resists phagosome acidification and autophagy to promote intracellular survival in macrophages.

While many strains of Enterococcus faecalis have been reported to be capable of surviving within macrophages for extended periods, the exact mechanisms involved are largely unknown. In this study, we found that after phagocytosis by macrophages, enterococci-containing vacuoles resist acidification, and E. faecalis is resistant to low pH.

Surface protein Esp enhances pro-inflammatory cytokine expression through NF-κB activation during enterococcal infection.

Enterococcal surface protein (Esp) is encoded on a pathogenicity island in Enterococcus faecalis and E. faecium and is involved in biofilm formation and binding to epithelial cells. In this study, using Esp-expressing E.

Roles of TLR/MyD88/MAPK/NF-κB Signaling Pathways in the Regulation of Phagocytosis and Proinflammatory Cytokine Expression in Response to E. faecalis Infection.

Enterococcus faecalis is a commensal bacterium residing in the gastrointestinal tract of mammals, but in certain situations it is also an opportunistic pathogen which can cause serious disease. Macrophages have been shown to play a critical role in controlling infections by commensal enterococci and also have an important role in mediating chromosomal instability and promoting colon cancer during high-level enterococcal colonization in genetically susceptible mice. However, the molecular mechanisms involved in the interaction of macrophages with enterococci during infection are not fully understood.

A TIR domain protein from E. faecalis attenuates MyD88-mediated signaling and NF-κB activation.

Toll-like receptor signaling, mediated by functional Toll/interleukin-1 receptor (TIR) domains, plays a critical role in activating the innate immune response responsible for controlling and clearing infection. Bacterial protein mimics of components of this signaling pathway have been identified and function through inhibition of interactions between Toll-like receptors (TLRs) and their adaptor proteins, mediated by TIR domains. A previously uncharacterized gene, which we have named tcpF (for TIR domain-containing protein in E.

Enterococcus faecalis infection activates phosphatidylinositol 3-kinase signaling to block apoptotic cell death in macrophages.

Apoptosis is an intrinsic immune defense mechanism in the host response to microbial infection. Not surprisingly, many pathogens have evolved various strategies to manipulate this important pathway to benefit their own survival and dissemination in the host during infection. To our knowledge, no attempts have been made to explore the host cell survival signals modulated by the bacterium Enterococcus faecalis.

Transcriptional regulator PerA influences biofilm-associated, platelet binding, and metabolic gene expression in Enterococcus faecalis.

Enterococcus faecalis is an opportunistic pathogen and a leading cause of nosocomial infections, traits facilitated by the ability to quickly acquire and transfer virulence determinants. A 150 kb pathogenicity island (PAI) comprised of genes contributing to virulence is found in many enterococcal isolates and is known to undergo horizontal transfer. We have shown that the PAI-encoded transcriptional regulator PerA contributes to pathogenicity in the mouse peritonitis infection model.

Biofilm and planktonic Enterococcus faecalis elicit different responses from host phagocytes in vitro.

Enterococcus faecalis is a commensal organism of the gastrointestinal tract but can also cause serious opportunistic infections. In addition to high levels of antibiotic resistance, the ability to form biofilms on abiotic surfaces and on in-dwelling devices within the host complicates treatment strategies and successful outcomes of antibiotic therapy. Despite rapid advances made in recent years in understanding the genomics and virulence of this organism, much remains to be learned regarding the host response to enterococcal infections.

In vivo trafficking and immunostimulatory potential of an intranasally-administered primary dendritic cell-based vaccine.

Background: Coccidioidomycosis or Valley fever is caused by a highly virulent fungal pathogen: Coccidioides posadasii or immitis. Vaccine development against Coccidioides is of contemporary interest because a large number of relapses and clinical failures are reported with antifungal agents. An efficient Th1 response engenders protection.

A novel conjugative plasmid from Enterococcus faecalis E99 enhances resistance to ultraviolet radiation.

Enterococcus faecalis has emerged as a prominent healthcare-associated pathogen frequently encountered in bacteremia, endocarditis, urinary tract infection, and as a leading cause of antibiotic-resistant infections. We recently demonstrated a capacity for high-level biofilm formation by a clinical E. faecalis isolate, E99.

Genetic variation and evolution of the pathogenicity island of Enterococcus faecalis.

Enterococcus faecalis is a leading cause of nosocomial infections and is known for its ability to acquire and transfer virulence and antibiotic resistance determinants from other organisms. A 150-kb pathogenicity island (PAI) encoding several genes that contribute to pathogenesis was identified among antibiotic-resistant clinical isolates. In the current study, we examined the structure of the PAI in a collection of isolates from diverse sources in order to gain insight into its genesis and dynamics.

An AraC-type transcriptional regulator encoded on the Enterococcus faecalis pathogenicity island contributes to pathogenesis and intracellular macrophage survival.

A gene encoding a putative AraC-type transcriptional regulator was identified on the 153-kb pathogenicity island (PAI) found among virulent Enterococcus faecalis strains. In an effort to understand the function of this regulator, designated PerA (for pathogenicity island-encoded regulator), we first examined the expression of the perA gene in the original PAI strain MMH594 and in an unrelated clinical isolate E99 by reverse transcription-PCR. Interestingly, expression analysis revealed no detectable perA transcript in MMH594, whereas a transcript was observed in strain E99.

Academic pharmacy administrators' perceptions of core requirements for entry into professional pharmacy programs.

Objectives: To determine which basic and social science courses academic pharmacy administrators believe should be required for entry into the professional pharmacy program and what they believe should be the required length of preprofessional study.

Methods: An online survey was sent to deans of all colleges and schools of pharmacy in the United States. Survey respondents were asked to indicate their level of agreement as to whether the basic and social science courses listed in the survey instrument should be required for admission to the professional program.

Systems biology approach for mapping the response of human urothelial cells to infection by Enterococcus faecalis.

Background: To better understand the response of urinary epithelial (urothelial) cells to Enterococcus faecalis, a uropathogen that exhibits resistance to multiple antibiotics, a genome-wide scan of gene expression was obtained as a time series from urothelial cells growing as a layered 3-dimensional culture similar to normal urothelium. We herein describe a novel means of analysis that is based on deconvolution of gene variability into technical and biological components.

Results: Analysis of the expression of 21,521 genes from 30 minutes to 10 hours post infection, showed 9553 genes were expressed 3 standard deviations (SD) above the system zero-point noise in at least 1 time point.

Horizontal transfer of virulence genes encoded on the Enterococcus faecalis pathogenicity island.

Enterococcus faecalis, a leading cause of nosocomial antibiotic resistant infections, frequently possesses a 150 kb pathogenicity island (PAI) that carries virulence determinants. The presence of excisionase and integrase genes, conjugative functions and multiple insertion sequence elements suggests that the PAI, or segments thereof, might be capable of horizontal transfer. In this report, the transfer of the E.

Presence of pathogenicity island genes in Enterococcus faecalis isolates from pigs in Denmark.

Enterococcus faecalis isolates of porcine origin were screened for the presence of a previously identified pathogenicity island (PAI). By using the esp gene as a genetic marker for the presence of this PAI, 9 esp-positive and 10 esp-negative isolates of porcine origin were investigated by use of a designed oligonucleotide array. The results indicated the clustering of esp-positive strains by multilocus sequence typing (MLST), but surprisingly, all strains investigated contained parts of the PAI.

Putative surface proteins encoded within a novel transferable locus confer a high-biofilm phenotype to Enterococcus faecalis.

Enterococci are opportunistic pathogens and among the leading causes of nosocomial infections. Enterococcus faecalis, the dominant species among infection-derived isolates, has recently been recognized as capable of forming biofilms on abiotic surfaces in vitro as well as on indwelling medical devices. A few bacterial factors known to contribute to biofilm formation in E.

The N-terminal domain of enterococcal surface protein, Esp, is sufficient for Esp-mediated biofilm enhancement in Enterococcus faecalis.

Enterococci have emerged as one of the leading causes of nosocomial bloodstream, surgical site, and urinary tract infections. More recently, enterococci have been associated with biofilms, which are bacterial communities attached to a surface and encased in an extracellular polymeric matrix. The enterococcal cell surface-associated protein, Esp, enhances biofilm formation by Enterococcus faecalis in a glucose-dependent manner.

Enterococcal surface protein Esp does not facilitate intestinal colonization or translocation of Enterococcus faecalis in clindamycin-treated mice.

Enterococcal surface protein (Esp) is a cell wall-associated protein of Enterococcus faecalis that has been identified as a potential virulence factor. We used a mouse model to examine whether Esp facilitates intestinal colonization or translocation of E. faecalis to mesenteric lymph nodes.

Enterococcal surface protein, Esp, enhances biofilm formation by Enterococcus faecalis.

Enterococci play a dual role in human ecology. They serve as commensal organisms of the gastrointestinal tract and are also leading causes of multiple antibiotic-resistant hospital-acquired infection. Many nosocomial infections result from the ability of microorganisms to form biofilms.

Enterococcal cytolysin: activities and association with other virulence traits in a pathogenicity island.

Enterococcal cytolysin is a structurally novel bacterial toxin expressed by some strains of E. faecalis and is distantly related to the class of bacteriocins known as lantibiotics. The cytolysin can be encoded by large pheromone-responsive plasmids, or on the chromosome within pathogenicity island.

A novel putative enterococcal pathogenicity island linked to the esp virulence gene of Enterococcus faecium and associated with epidemicity.

Enterococcus faecalis harbors a virulence-associated surface protein encoded by the esp gene. This gene has been shown to be part of a 150-kb putative pathogenicity island. A gene similar to esp has recently been found in Enterococcus faecium isolates recovered from hospitalized patients.

Association between the presence of enterococcal virulence factors gelatinase, hemolysin, and enterococcal surface protein and mortality among patients with bacteremia due to Enterococcus faecalis.

The potential virulence factors of enterococci include production of enterococcal surface protein (Esp), gelatinase, and hemolysin. Gelatinase- and hemolysin-producing strains of Enterococcus faecalis have been shown to be virulent in animal models of enterococcal infections. Esp production has been shown to enhance the persistence of E.