Shifting the Discourse on Disability: Moving to an Inclusive, Intersectional Focus

Individuals with disabilities comprise one of the largest marginalized groups in the United States and experience systemic barriers in healthcare. In Westernized communities, disability has historically been conceptualized via the medical model, which considers disability an individual-level deficit in need of correction. Although other models of disability (e.g., social model) have been developed to address the medical model’s ableist shortcomings, these fail to consistently acknowledge intersectionality. Specifically, these models fail to consider that (a) a disabled individual may hold other marginalized or oppressed identities and (b) these intersecting oppressions may exacerbate health inequities. Intersectionality, which originates from Black feminist literature, describes the ways that systems of power and oppression (e.g., racism, sexism) interact to form an individual’s unique experience. To date, the intersection of disability and other marginalized identities has been neglected in psychology and related fields, leaving little guidance for how scholars, clinicians, and other stakeholders can address disability via an intersectional lens. The current paper discusses how a disability-affirmative, intersectional approach can serve as a strategy for challenging and reforming oppressive systems across the field of psychology. We assert that, ultimately, this approach has the potential to optimize and expand access to equitable, inclusive mental health care, and we propose actionable steps psychologists can take in research, practice, and training in pursuit of this aim

Exposure of Bacterial Biofilms to Electrical Current Leads to Cell Death Mediated in Part by Reactive Oxygen Species.

Bacterial biofilms may form on indwelling medical devices such as prosthetic joints, heart valves and catheters, causing challenging-to-treat infections. We have previously described the 'electricidal effect', in which bacterial biofilms are decreased following exposure to direct electrical current. Herein, we sought to determine if the decreased bacterial quantities are due to detachment of biofilms or cell death and to investigate the role that reactive oxygen species (ROS) play in the observed effect. Using confocal and electron microscopy and flow cytometry, we found that direct current (DC) leads to cell death and changes in the architecture of biofilms formed by Gram-positive and Gram-negative bacteria. Reactive oxygen species (ROS) appear to play a role in DC-associated cell death, as there was an increase in ROS-production by Staphylococcus aureus and Staphylococcus epidermidis biofilms following exposure to DC. An increase in the production of ROS response enzymes catalase and superoxide dismutase (SOD) was observed for S. aureus, S. epidermidis and Pseudomonas aeruginosa biofilms following exposure to DC. Additionally, biofilms were protected from cell death when supplemented with antioxidants and oxidant scavengers, including catalase, mannitol and Tempol. Knocking out SOD (sodAB) in P. aeruginosa led to an enhanced DC effect. Microarray analysis of P. aeruginosa PAO1 showed transcriptional changes in genes related to the stress response and cell death. In conclusion, the electricidal effect results in death of bacteria in biofilms, mediated, at least in part, by production of ROS

Evaluation of the Enterococcus faecalis Biofilm-Associated Virulence Factors AhrC and Eep in Rat Foreign Body Osteomyelitis and In Vitro Biofilm-Associated Antimicrobial Resistance.

Enterococcus faecalis can cause healthcare-associated biofilm infections, including those of orthopedic devices. Treatment of enterococcal prosthetic joint infection is difficult, in part, due to biofilm-associated antimicrobial resistance. We previously showed that the E. faecalis OG1RF genes ahrC and eep are in vitro biofilm determinants and virulence factors in animal models of endocarditis and catheter-associated urinary tract infection. In this study, we evaluated the role of these genes in a rat acute foreign body osteomyelitis model and in in vitro biofilm-associated antimicrobial resistance. Osteomyelitis was established for one week following the implantation of stainless steel orthopedic wires inoculated with E. faecalis strains OG1RF, ΩahrC, and ∆eep into the proximal tibiae of rats. The median bacterial loads recovered from bones and wires did not differ significantly between the strains at multiple inoculum concentrations. We hypothesize that factors present at the infection site that affect biofilm formation, such as the presence or absence of shear force, may account for the differences in attenuation in the various animal models we have used to study the ΩahrC and ∆eep strains. No differences among the three strains were observed in the planktonic and biofilm antimicrobial susceptibilities to ampicillin, vancomycin, daptomycin, linezolid, and tetracycline. These findings suggest that neither ahrC nor eep directly contribute to E. faecalis biofilm-associated antimicrobial resistance. Notably, the experimental evidence that the biofilm attachment mutant ΩahrC displays biofilm-associated antimicrobial resistance suggests that surface colonization alone is sufficient for E. faecalis cells to acquire the biofilm antimicrobial resistance phenotype

Flow cytometric analysis of biofilms exposed to 200 μA direct current (DC) for 24 hours, and controls.

<p><i>S</i>. <i>aureus</i> control (<b>A</b>) and DC exposure (<b>B</b>); <i>S</i>. <i>epidermidis</i> control (<b>C</b>) and DC exposure (<b>D</b>); and <i>P</i>. <i>aeruginosa</i> control (<b>E</b>) and DC exposure (<b>F</b>). Experiments were performed in triplicate for each organism; a representative graph is shown for each bacterium.</p

The electricidal effect is enhanced in PAO1Δ<i>sodAB</i>.

<p><i>P</i>. <i>aeruginosa</i> PAO1Δ<i>sodAB</i> compared with parental control following exposure to 200 μA direct current (DC) for 24 hours, *p = 0.0495, n = 3 for all samples. Samples not exposed to DC are shown as 0 μA.</p

Scanning electron micrographs of biofilm-laden discs exposed to 200 μA direct current (DC) or no exposure for 24 hours.

<p><i>S</i>. <i>aureus</i> control (<b>A</b>) or 200 μA DC (<b>B</b>); <i>S</i>. <i>epidermidis</i> control (<b>C</b>) or 200 μA DC <b>D</b>); <i>P</i>. <i>aeruginosa</i> control (<b>E</b>) or 200 μA DC (<b>F</b>). All images were taken at 10K magnification and a minimum of three fields were observed. A representative field for each bacterial biofilm sample is shown.</p

Lipid peroxidation in response to DC.

<p>Lipid peroxidation measured by MDA production in <i>S</i>. <i>aureus</i> (<b>A</b>), <i>S</i>. <i>epidermidis</i> (<b>B</b>) and <i>P</i>. <i>aeruginosa</i> (<b>C</b>) following no exposure (shown as 0 μA) or exposure to 200 μA direct current for 5 or 10 minutes. Samples were read in triplicate and normalized to the log₁₀ cfu/cm².</p