Bacterial Colonization in Computer Keyboards Posses Health Hazard

Computer keyboards of a teaching laboratory were examined and bacteria were isolated from computer keyboards. The subsequent tests were done for the bacterial isolates: methyl red, vogus proskaur, citrate utilization, urease and TSI. This study paves the way to look at an inanimate object like computer keyboard as potential reservoir of bacteria.

Can Humidifier Reservoir Bacteria Colonize the Circuit During Mechanical Ventilation?

Background:Although the circuit condensate, an ideal bacterial reservoir, may flow into the humidifier reservoir (HR), no study has investigated if HR-colonized bacteria colonize other circuit locations with airflow. Therefore, the objective of this study was to explore if bacterial growth in the HR leads to bacterial colonization in the ventilator circuit. Methods: A randomized controlled experiment was performed in a public tertiary hospital in Guangdong Province, China. In vitro mechanical ventilation models (n = 60), divided into sterile water samples (n = 30) and broth samples (n = 30), were established. Sterile water was used for humidification in the ventilation models. The sterile water group contained either Acinetobacter baumannii (n = 15) or Pseudomonas aeruginosa (n = 15) in humidifier water. The broth group was similar to the sterile water group, but brain heart infusion broth was added to the HR. After 24, 72, and 168 h of continuous ventilation, bacteria in the humidifier water and at different circuit locations were sampled and cultured, and the results were analyzed by the Chi-square test. The difference in bacterial concentration at the HR outlet was analyzed by the F test, and P < 0.05 was considered statistically significant.Results:Bacterial culture results of the sterile water samples were negative. Bacteria in the humidifier water continued to proliferate in the broth group, and the bacterial concentration at different times was not significantly different (P > 0.05). With prolonged ventilation, the bacterial concentration at the HR outlet increased (P < 0.05). During continuous ventilation, no bacterial growth occurred at 10 cm from the HR outlet and the Y-piece of the ventilator circuit. The bacterial concentration at the HR outlet was higher in the P. aeruginosa group than in the A. baumannii group (P < 0.05).Conclusions:Sterile water in the HR was not conducive to bacterial growth. Although bacteria grew in the HR and could reach the HR outlet, colonization of other circuit locations was unlikely.

A Niclosamide-releasing hot-melt extruded catheter prevents Staphylococcus aureus experimental biomaterial-associated infection

Biomaterial-associated infections are a major healthcare challenge as they are responsible for high disease burden in critically ill patients. In this study, we have developed drug-eluting antibacterial catheters to prevent catheter-related infections. Niclosamide (NIC), originally a well-studied antiparasitic drug, was incorporated into the polymeric matrix of thermoplastic polyurethane (TPU) via solvent casting, and catheters were fabricated using hot-melt extrusion technology. The mechanical and physicochemical properties of TPU polymers loaded with NIC were studied. NIC was released in a sustained manner from the catheters and exhibited antibacterial activity against Staphylococcus aureus and Staphylococcus epidermidis in different in vitro models. Moreover, the antibacterial efficacy of NIC-loaded catheters was validated in an in vivo biomaterial-associated infection mouse model using a methicillin-susceptible and methicillin-resistant strain of S. aureus. The released NIC from the produced catheters reduced bacterial colonization of the catheter as well as of the surrounding tissue. A sustained in vivo release of NIC from the catheters for at least 14 days was observed. In summary, the NIC-releasing hot-melt extruded catheters prevented implant colonization and reduced the bacterial colonization of peri-catheter tissue by methicillin sensitive as well as resistant S. aureus in a biomaterial-associated infection mouse model and has good prospects for preclinical development.

Xanthomonas campestris pv. musacearum bacterial infection induces organ-specific callose and hydrogen peroxide production in banana

Xanthomonas campestris pv. musacearum (Xcm) bacteria cause banana Xanthomonas wilt (BXW), the most destructive disease of bananas in East and Central Africa. During early stages of infection in susceptible banana cultivars, incomplete systemic movement of Xcm limits bacterial colonization in the upper organs. Mechanistic basis of this delayed movement is unknown. We hypothesized that Xcm infection triggers basal pattern triggered immune (PTI) responses whose spatial and temporal variability along banana’s anatomical structure accounts for initially limiting Xcm in upper organs. Hence, we examined PTI responses such as callose deposition and hydrogen peroxide (H2O2) production in different organs in response to Xcm infection in BXW susceptible Kayinja and Mbwazirume banana cultivars and wild resistant progenitor Musa balbisiana. Xcm-induced callose increased and peaked at 14 days post inoculation (dpi) and 28dpi as assessed by fluorescence microscopy and enzyme-linked immunosorbent assays, respectively. The levels of Xcm-induced H2O2 and callose were highest in the pseudostems and corms, respectively, and were independent of host susceptibility or resistance to BXW. H2O2 production showed a biphasic transient pattern with an initial increase at 1-hour post Xcm-inoculation (hpi), followed by a decline 3-6hpi and then a second increase by 12hpi. Our findings point to organ-specific responses to Xcm infection in bananas. The corm which doubles as a subterranean parenating organ and interface between mother plants and lateral shoots, was the most responsive organ in callose production while the pseudostem was the most responsive organ in H2O2 production, suggesting the significance of these organs in banana response to BXW.

Development of Antibacterial and Antifouling Innovative and Eco-Sustainable Sol–Gel Based Materials: From Marine Areas Protection to Healthcare Applications

Bacterial colonization of surfaces is the leading cause of deterioration and contaminations. Fouling and bacterial settlement led to damaged coatings, allowing microorganisms to fracture and reach the inner section. Therefore, effective treatment of surface damaged material is helpful to detach bio-settlement from the surface and prevent deterioration. Moreover, surface coatings can withdraw biofouling and bacterial colonization due to inherent biomaterial characteristics, such as superhydrophobicity, avoiding bacterial resistance. Fouling was a past problem, yet its untargeted toxicity led to critical environmental concerns, and its use became forbidden. As a response, research shifted focus approaching a biocompatible alternative such as exciting developments in antifouling and antibacterial solutions and assessing their antifouling and antibacterial performance and practical feasibility. This review introduces state-of-the-art antifouling and antibacterial materials and solutions for several applications. In particular, this paper focuses on antibacterial and antifouling agents for concrete and cultural heritage conservation, antifouling sol–gel-based coatings for filtration membrane technology, and marine protection and textile materials for biomedicine. In addition, this review discusses the innovative synthesis technologies of antibacterial and antifouling solutions and the consequent socio-economic implications. The synthesis and the related physico-chemical characteristics of each solution are discussed. In addition, several characterization techniques and different parameters that influence the surface finishing coatings deposition were also described.

Osteochondral necrosis of the femoral condyles in Thoroughbred foals: eight cases (2008–2018)

OBJECTIVE To describe clinical, imaging, gross, and histopathological abnormalities associated with osteochondral necrosis of the femoral condyles in foals and identify features suggestive of a common pathogenesis. ANIMALS 8 Thoroughbred foals euthanized with a presumptive diagnosis of necrosis of the femoral condyles. PROCEDURES Postmortem CT was performed on all distal femoral epiphyseal samples. The articular epiphyseal cartilage complex (AECC) of affected distal femurs was examined grossly and histologically, focusing on lesions of interest identified on CT images. RESULTS 7 foals were between 9 and 23 days old at the time of euthanasia; 1 foal was 85 days old. Concurrent illness (neonatal maladjustment syndrome, neonatal isoerythrolysis, or infection such as enteritis and omphalitis) was diagnosed in 7 foals. The characteristic antemortem radiographic and postmortem CT finding was a crescent-shaped osteochondral flap displaced from the affected medial femoral condyle. Synovial fluid cytology from affected joints was either within normal limits or consistent with mild inflammation. Histologically, all lesions were characterized by osteochondral necrosis and detachment of the AECC. In 6 foals, polymorphonuclear cells were found within growth cartilage canals, representing septic cartilage canals. CLINICAL RELEVANCE Osteochondral necrosis was interpreted to be secondary to bacterial colonization of the distal femoral AECC, evidenced by septic cartilage canals identified in 6 of 8 foals. This uncommon condition was previously thought to arise from an ischemic event, but the disease process was not well understood. An improved understanding of the pathogenesis of osteochondral necrosis is the first step in formulating more successful preventative and treatment strategies.

Germline Variants of CYBA and TRPM4 Predispose to Familial Colorectal Cancer

Familial colorectal cancer (CRC) is only partially explained by known germline predisposing genes. We performed whole genome sequencing in 15 Polish families of many affected individuals, without mutations in known CRC predisposing genes. We focused on loss-of-function variants and functionally characterized them. We identified a frameshift variant in the CYBA gene (c.246delC) in one family and a splice site variant in the TRPM4 gene (c.25-1 G&gt;T) in another family. While both variants were absent or extremely rare in gene variant databases, we identified four additional Polish familial CRC cases and two healthy elderly individuals with the CYBA variant (odds ratio 2.46, 95% confidence interval 0.48-12.69). Both variants led to a premature stop codon and to a truncated protein. Functional characterization of the variants showed that knockdown of CYBA or TRPM4 depressed generation of reactive oxygen species (ROS) in LS174T and HT-29 cell lines. Knockdown of TRPM4 resulted in decreased MUC2 protein production. CYBA encodes a component in the NADPH oxidase system which generates ROS and controls, e.g., bacterial colonization in the gut. Germline CYBA variants are associated with early onset inflammatory bowel disease, supported with experimental evidence on loss of intestinal mucus barrier function due to ROS deficiency. TRPM4 encodes a calcium-activated ion channel, which in a human colonic cancer cell line controls calcium-mediated secretion of MUC2, a major component of intestinal mucus barrier. We suggest that the gene defects in CYBA and TRPM4 mechanistically involve intestinal barrier integrity through ROS and mucus biology, which converges in chronic bowel inflammation.

What Flips the Switch? Signals and Stress Regulating Extraintestinal Pathogenic Escherichia coli Type 1 Fimbriae (Pili)

Pathogens are exposed to a multitude of harmful conditions imposed by the environment of the host. Bacterial responses against these stresses are pivotal for successful host colonization and pathogenesis. In the case of many E. coli strains, type 1 fimbriae (pili) are an important colonization factor that can contribute to diseases such as urinary tract infections and neonatal meningitis. Production of type 1 fimbriae in E. coli is dependent on an invertible promoter element, fimS, which serves as a phase variation switch determining whether or not a bacterial cell will produce type 1 fimbriae. In this review, we present aspects of signaling and stress involved in mediating regulation of type 1 fimbriae in extraintestinal E. coli; in particular, how certain regulatory mechanisms, some of which are linked to stress response, can influence production of fimbriae and influence bacterial colonization and infection. We suggest that regulation of type 1 fimbriae is potentially linked to environmental stress responses, providing a perspective for how environmental cues in the host and bacterial stress response during infection both play an important role in regulating extraintestinal pathogenic E. coli colonization and virulence.

Effect of Implantoplasty on Fatigue Performance and Surface Roughness of Narrow Diameter Dental Implants

Implantoplasty (IP) is used in dental implants with peri-implantitis and aims to remove threads and polish rough surfaces in order to prevent bacterial colonization. As a result of this procedure, implant strength might be compromised. We tested 20 tapered screw-shaped Ti6Al4V dental implants with a simulated bone loss of 50%. Ten implants underwent IP and 10 served as controls. Surface topography (Sa, Sz, Ssk and Sdr) was analyzed with a confocal optical microscope. Subsequently, cyclic loads were applied with a servo-hydraulic mechanical testing machine (5x106 cycles at 15 Hz, between the maximal compression force - 529N in the IP group and 735N in the control group - and 10% of that force). We recorded the number of cycles until failure and the type of failure. Implant failure was analyzed by visual inspection and scanning electron microscopy. Implantoplasty reduced the median Sa from 1.76 (IQR=0.11) to 0.49 (IQR=0.16). The fatigue limits of the control and implantoplasty groups were 551 N and 529 N, respectively. The scanning electron micrographs showed fatigue striations indicating fatigue failure. The infinite life range of the dental implants evaluated was largely above the threshold of usual chewing forces. Implantoplasty seems to render a fairly smooth surface and has a limited impact upon fatigue resistance.

Microbiota in Pancreatic Diseases: A Review of the Literature

The gut microbiota is a critical element in the balance between human health and disease. Its impairment, defined as dysbiosis, is associated with gastroenterological and systemic diseases. Pancreatic secretions are involved in the composition and changes of the gut microbiota, and the gut microbiota may colonize the pancreatic parenchyma and be associated with the occurrence of diseases. The gut microbiota and the pancreas influence each other, resulting in a “gut microbiota-pancreas axis”. Moreover, the gut microbiota may be involved in pancreatic diseases, both through direct bacterial colonization and an indirect effect of small molecules and toxins derived from dysbiosis. Pancreatic diseases such as acute pancreatitis, chronic pancreatitis, autoimmune pancreatitis, and pancreatic cancer are common gastroenterological diseases associated with high morbidity and mortality. The involvement of the microbiota in pancreatic diseases is increasingly recognized. Therefore, modifying the intestinal bacterial flora could have important therapeutic implications on these pathologies. The aim of this study is to review the literature to evaluate the alterations of the gut microbiota in pancreatic diseases, and the role of the microbiota in the treatment of these diseases.