Design and preliminary validation of a mobile application-based expert system to facilitate repair of medical equipment in resource-limited health settings.

BACKGROUND: One of the greatest barriers to safe surgery is the availability of functional biomedical equipment. Biomedical technicians play a major role in ensuring that equipment is functional. Following in-field observations and an online survey, a mobile application was developed to aid technicians in troubleshooting biomedical equipment. It was hypothesized that this application could be used to aid technicians in equipment repair, as modeled by repair of a pulse oximeter. METHODS: To identify specific barriers to equipment repair and maintenance for biomedical technicians, an online survey was conducted to determine current practices and challenges. These findings were used to guide the development of a mobile application system that guides technicians through maintenance and repair tasks. A convenience sample of technicians in Ethiopia tested the application using a broken pulse oximeter task and following this completed usability and content validity surveys. RESULTS: Fifty-three technicians from 13 countries responded to the initial survey. The results of the survey showed that technicians find equipment manuals most useful, but these are not easily accessible. Many do not know how to or are uncomfortable reaching out to human resources. Thirty-three technicians completed the broken pulse oximeter task using the application. All were able to appropriately identify and repair the equipment, and post-task surveys of usability and content validity demonstrated highly positive scores (Agree to Strongly Agree) on both scales. DISCUSSION: This research demonstrates the need for improved access to resources for technicians and shows that a mobile application can be used to address a gap in the access to knowledge and resources in low- and middle-income countries. Further research will include prospective studies to determine the impact of an application on the availability of functional equipment in a hospital and the effect on the provision and safety of surgical care.

The binary toxin CDT enhances Clostridium difficile virulence by suppressing protective colonic eosinophilia.

Clostridium difficile is the most common hospital acquired pathogen in the USA, and infection is, in many cases, fatal. Toxins A and B are its major virulence factors, but expression of a third toxin, known as C. difficile transferase (CDT), is increasingly common. An adenosine diphosphate (ADP)-ribosyltransferase that causes actin cytoskeletal disruption, CDT is typically produced by the major, hypervirulent strains and has been associated with more severe disease. Here, we show that CDT enhances the virulence of two PCR-ribotype 027 strains in mice. The toxin induces pathogenic host inflammation via a Toll-like receptor 2 (TLR2)-dependent pathway, resulting in the suppression of a protective host eosinophilic response. Finally, we show that restoration of TLR2-deficient eosinophils is sufficient for protection from a strain producing CDT. These findings offer an explanation for the enhanced virulence of CDT-expressing C. difficile and demonstrate a mechanism by which this binary toxin subverts the host immune response.

Microbiota-Regulated IL-25 Increases Eosinophil Number to Provide Protection during Clostridium difficile Infection.

Clostridium difficile infection (CDI) is the most common cause of hospital-acquired infection in the United States. Host susceptibility and the severity of infection are influenced by disruption of the microbiota and the immune response. However, how the microbiota regulate immune responses to mediate CDI outcome remains unclear. Here, we have investigated the role of the microbiota-linked cytokine IL-25 during infection. Intestinal IL-25 was suppressed during CDI in humans and mice. Restoration of IL-25 reduced CDI-associated mortality and tissue pathology even though equivalent levels of C. difficile bacteria and toxin remained in the gut. IL-25 protection was mediated by gut eosinophils, as demonstrated by an increase in intestinal eosinophils and a loss of IL-25 protection upon eosinophil depletion. These findings support a mechanism whereby the induction of IL-25-mediated eosinophilia can reduce host mortality during active CDI. This work may provide targets for future development of microbial or immune-based therapies.