Assessment and risk reduction of infectious pathogens on chiropractic treatment tables

<p>Abstract</p> <p>Background</p> <p>To investigate the presence of pathogenic microbes on chiropractic treatment tables in one outpatient teaching clinic. Additional aims were to test inexpensive disinfectants on tables that may kill microbes and suggest infection control measures for chiropractic offices, clinics and classrooms. The aim of the study was to assess the presence of pathogenic microbes on treatment tables in one outpatient teaching clinic and determine a simple behavioral model for infection control including table disinfection and accepted hand washing and sanitizing protocols.</p> <p>Methods</p> <p>10 treatment tables were selected and sampled for possible microbial flora on face and hand pieces. Samples were cultured on MacConky's agar and mannitol salt agar, labeled and incubated for up to 48 hours. Confirmatory testing of microbes to determine if drug resistant flora were present was performed. Among tables tested, 5 were selected to test disinfectants. One-half of the face piece and 1 hand piece were treated with two different wipes and then post-tested for microbes.</p> <p>Results</p> <p>Pathogenic microbes were present on chiropractic treatment tables including methicillin-resistant <it>Staph aureus</it>. Simple disinfectants neutralized the pathogens. A rudimentary disinfection procedure and infection control measures are suggested based on the findings.</p> <p>Conclusion</p> <p>Pathogenic microbes may be present on chiropractic treatment tables and can be effectively killed with proper disinfecting. Hand washing/sanitizing is an important measure in infection control as is table disinfecting. Rudimentary behavioral changes to improve chiropractic clinic infection control are needed. More comprehensive behavioral models are needed. All teaching clinics and private chiropractic offices should adopt infection control practices including routine table disinfecting and hand sanitizing. Effective measures can be put in place at minimal costs. Accrediting bodies of chiropractic institutions should mandate an infection control plan for member institutions immediately.</p

A Novel Tool for the Assessment of Pain: Validation in Low Back Pain

Joachim Scholz and colleagues develop and validate an assessment tool that distinguishes between radicular and axial low back pain

The Golgin GMAP210/TRIP11 Anchors IFT20 to the Golgi Complex

Eukaryotic cells often use proteins localized to the ciliary membrane to monitor the extracellular environment. The mechanism by which proteins are sorted, specifically to this subdomain of the plasma membrane, is almost completely unknown. Previously, we showed that the IFT20 subunit of the intraflagellar transport particle is localized to the Golgi complex, in addition to the cilium and centrosome, and hypothesized that the Golgi pool of IFT20 plays a role in sorting proteins to the ciliary membrane. Here, we show that IFT20 is anchored to the Golgi complex by the golgin protein GMAP210/Trip11. Mice lacking GMAP210 die at birth with a pleiotropic phenotype that includes growth restriction, ventricular septal defects of the heart, omphalocele, and lung hypoplasia. Cells lacking GMAP210 have normal Golgi structure, but IFT20 is no longer localized to this organelle. GMAP210 is not absolutely required for ciliary assembly, but cilia on GMAP210 mutant cells are shorter than normal and have reduced amounts of the membrane protein polycystin-2 localized to them. This work suggests that GMAP210 and IFT20 function together at the Golgi in the sorting or transport of proteins destined for the ciliary membrane

AAV Exploits Subcellular Stress Associated with Inflammation, Endoplasmic Reticulum Expansion, and Misfolded Proteins in Models of Cystic Fibrosis

Barriers to infection act at multiple levels to prevent viruses, bacteria, and parasites from commandeering host cells for their own purposes. An intriguing hypothesis is that if a cell experiences stress, such as that elicited by inflammation, endoplasmic reticulum (ER) expansion, or misfolded proteins, then subcellular barriers will be less effective at preventing viral infection. Here we have used models of cystic fibrosis (CF) to test whether subcellular stress increases susceptibility to adeno-associated virus (AAV) infection. In human airway epithelium cultured at an air/liquid interface, physiological conditions of subcellular stress and ER expansion were mimicked using supernatant from mucopurulent material derived from CF lungs. Using this inflammatory stimulus to recapitulate stress found in diseased airways, we demonstrated that AAV infection was significantly enhanced. Since over 90% of CF cases are associated with a misfolded variant of Cystic Fibrosis Transmembrane Conductance Regulator (ΔF508-CFTR), we then explored whether the presence of misfolded proteins could independently increase susceptibility to AAV infection. In these models, AAV was an order of magnitude more efficient at transducing cells expressing ΔF508-CFTR than in cells expressing wild-type CFTR. Rescue of misfolded ΔF508-CFTR under low temperature conditions restored viral transduction efficiency to that demonstrated in controls, suggesting effects related to protein misfolding were responsible for increasing susceptibility to infection. By testing other CFTR mutants, G551D, D572N, and 1410X, we have shown this phenomenon is common to other misfolded proteins and not related to loss of CFTR activity. The presence of misfolded proteins did not affect cell surface attachment of virus or influence expression levels from promoter transgene cassettes in plasmid transfection studies, indicating exploitation occurs at the level of virion trafficking or processing. Thus, we surmised that factors enlisted to process misfolded proteins such as ΔF508-CFTR in the secretory pathway also act to restrict viral infection. In line with this hypothesis, we found that AAV trafficked to the microtubule organizing center and localized near Golgi/ER transport proteins. Moreover, AAV infection efficiency could be modulated with siRNA-mediated knockdown of proteins involved in processing ΔF508-CFTR or sorting retrograde cargo from the Golgi and ER (calnexin, KDEL-R, β-COP, and PSMB3). In summary, our data support a model where AAV exploits a compromised secretory system and, importantly, underscore the gravity with which a stressed subcellular environment, under internal or external insults, can impact infection efficiency