Effective Disinfection of Orthodontic Pliers

Objective:: Pathogenic microbes may be transmitted directly from the orthodontist to the patient or from the patient to the doctor, and indirectly from patient to patient. The latter may occur via contaminated instruments or surfaces, and is referred to as cross-contamination. The objective of this study was to evaluate the extent of bacterial contamination of orthodontic pliers and the efficacy of the disinfection techniques applied after clinical use. We also sought to examine under standardized conditions the virucidal, bactericidal and fungicidal effects of disinfection techniques used in practice. Materials and Methods:: The efficacy of various disinfection methods was determined after clinical use in-vivo on 10 test subjects and in-vitro with deliberate contamination. The following disinfection methods were tested: 1. Iso-Septol spray 2. Incidur® spray 3. Trough disinfection in combination with 5% Sekusept® Plus solution 4. Ultrasound bath in combination with 5% Sekusept® Plus solution 5. Thermal disinfection For in-vitro contamination we used the test organisms Staphylococcus aureus, Escherichia coli, Candida albicans, Coxsackie virus B4, HSV 1, and Adenovirus type 5. The tests were carried out six to eight times for each organism. The Weingart pliers and distalend cutters were tested. The criteria for effective disinfection were a reduction in infectiosity of five log steps (for bacteria and fungi) or four log steps (viruses). Statistical analysis was carried out using the Wilcoxon and Whitney U-test. Results:: The presence of contamination following clinical use was not adequately eliminated with all disinfection methods. The spray methods exhibited shortcomings in disinfection. For the type of contamination defined, trough disinfection with 5% Sekusept® Plus and the Incidur® and Iso-Septol spray disinfection methods provided insufficient disinfection. Conversely, the ultrasound bath with 5% Sekusept® Plus solution and steam disinfection met the criteria for effective disinfection for all microbes. No statistically significant difference was found between the oiled and unoiled states. In some cases, there were slightly higher rates of contamination with the Weingart pliers as with the distalend cutters. However, these were not statistically significant. Conclusions:: It should be possible to disinfect lipophilic viruses and the usual bacterial infections adequately with all methods, provided that the use of sprays and trough disinfection is preceded by cleaning with brush and water, followed by drying. With hydrophilic viruses, however, the spray and trough disinfection methods are limited in their efficacy and cannot be considered adequate. Exclusively chemical methods are therefore less effective than thermal or physical-chemical methods. Thermal disinfection and the ultrasound bath in combination with 5% Sekusept® Plus are clearly superior to spray disinfection and trough disinfection alone. The ultrasound bath and thermal disinfection can therefore be recommended for the disinfection of orthodontic pliers. We recommend that the pliers be cleaned beforehand due to their uneven surface

SIL1 mutations and clinical spectrum in patients with Marinesco-Sjögren syndrome

Marinesco-Sjögren syndrome is a rare autosomal recessive multisystem disorder featuring cerebellar ataxia, early-onset cataracts, chronic myopathy, variable intellectual disability and delayed motor development. More recently, mutations in the SIL1 gene, which encodes an endoplasmic reticulum resident co-chaperone, were identified as the main cause of Marinesco-Sjögren syndrome. Here we describe the results of SIL1 mutation analysis in 62 patients presenting with early-onset ataxia, cataracts and myopathy or combinations of at least two of these. We obtained a mutation detection rate of 60% (15/25) among patients with the characteristic Marinesco-Sjögren syndrome triad (ataxia, cataracts, myopathy) whereas the detection rate in the group of patients with more variable phenotypic presentation was below 3% (1/37). We report 16 unrelated families with a total of 19 different SIL1 mutations. Among these mutations are 15 previously unreported changes, including single- and multi-exon deletions. Based on data from our screening cohort and data compiled from the literature we found that SIL1 mutations are invariably associated with the combination of a cerebellar syndrome and chronic myopathy. Cataracts were observed in all patients beyond the age of 7 years, but might be missing in infants. Six patients with SIL1 mutations had no intellectual disability, extending the known wide range of cognitive capabilities in Marinesco-Sjögren syndrome to include normal intelligence. Modestly constant features were somatic growth retardation, skeletal abnormalities and pyramidal tract signs. Examination of mutant SIL1 expression in cultured patient lymphoblasts suggested that SIL1 mutations result in severely reduced SIL1 protein levels irrespective of the type and position of mutations. Our data broaden the SIL1 mutation spectrum and confirm that SIL1 is the major Marinesco-Sjögren syndrome gene. SIL1 patients usually present with the characteristic triad but cataracts might be missing in young children. As cognitive impairment is not obligatory, patients without intellectual disability but a Marinesco-Sjögren syndrome-compatible phenotype should receive SIL1 mutation analysis. Despite allelic heterogeneity and many families with private mutations, the phenotype related to SIL1 mutations is relatively homogenous. Based on SIL1 expression studies we speculate that this may arise from a uniform effect of different mutations on protein expressio

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UuStB Koeln(38)-8406254 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekSIGLEDEGerman

Sil1 Mutations and Clinical Spectrum in Patients with Marinesco-Sjogren Syndrome

Marinesco-Sjogren syndrome is a rare autosomal recessive multisystem disorder featuring cerebellar ataxia, early-onset cataracts, chronic myopathy, variable intellectual disability and delayed motor development. More recently, mutations in the SIL1 gene, which encodes an endoplasmic reticulum resident co-chaperone, were identified as the main cause of Marinesco-Sjogren syndrome. Here we describe the results of SIL1 mutation analysis in 62 patients presenting with early-onset ataxia, cataracts and myopathy or combinations of at least two of these. We obtained a mutation detection rate of 60% (15/25) among patients with the characteristic Marinesco-Sjogren syndrome triad (ataxia, cataracts, myopathy) whereas the detection rate in the group of patients with more variable phenotypic presentation was below 3% (1/37). We report 16 unrelated families with a total of 19 different SIL1 mutations. Among these mutations are 15 previously unreported changes, including single- and multi-exon deletions. Based on data from our screening cohort and data compiled from the literature we found that SIL1 mutations are invariably associated with the combination of a cerebellar syndrome and chronic myopathy. Cataracts were observed in all patients beyond the age of 7 years, but might be missing in infants. Six patients with SIL1 mutations had no intellectual disability, extending the known wide range of cognitive capabilities in Marinesco-Sjogren syndrome to include normal intelligence. Modestly constant features were somatic growth retardation, skeletal abnormalities and pyramidal tract signs. Examination of mutant SIL1 expression in cultured patient lymphoblasts suggested that SIL1 mutations result in severely reduced SIL1 protein levels irrespective of the type and position of mutations. Our data broaden the SIL1 mutation spectrum and confirm that SIL1 is the major Marinesco-Sjogren syndrome gene. SIL1 patients usually present with the characteristic triad but cataracts might be missing in young children. As cognitive impairment is not obligatory, patients without intellectual disability but a Marinesco-Sjogren syndrome-compatible phenotype should receive SIL1 mutation analysis. Despite allelic heterogeneity and many families with private mutations, the phenotype related to SIL1 mutations is relatively homogenous. Based on SIL1 expression studies we speculate that this may arise from a uniform effect of different mutations on protein expression.Wo

Adaptation of hepatitis C virus to mouse CD81 permits infection of mouse cells in the absence of human entry factors.

Hepatitis C virus (HCV) naturally infects only humans and chimpanzees. The determinants responsible for this narrow species tropism are not well defined. Virus cell entry involves human scavenger receptor class B type I (SR-BI), CD81, claudin-1 and occludin. Among these, at least CD81 and occludin are utilized in a highly species-specific fashion, thus contributing to the narrow host range of HCV. We adapted HCV to mouse CD81 and identified three envelope glycoprotein mutations which together enhance infection of cells with mouse or other rodent receptors approximately 100-fold. These mutations enhanced interaction with human CD81 and increased exposure of the binding site for CD81 on the surface of virus particles. These changes were accompanied by augmented susceptibility of adapted HCV to neutralization by E2-specific antibodies indicative of major conformational changes of virus-resident E1/E2-complexes. Neutralization with CD81, SR-BI- and claudin-1-specific antibodies and knock down of occludin expression by siRNAs indicate that the adapted virus remains dependent on these host factors but apparently utilizes CD81, SR-BI and occludin with increased efficiency. Importantly, adapted E1/E2 complexes mediate HCV cell entry into mouse cells in the absence of human entry factors. These results further our knowledge of HCV receptor interactions and indicate that three glycoprotein mutations are sufficient to overcome the species-specific restriction of HCV cell entry into mouse cells. Moreover, these findings should contribute to the development of an immunocompetent small animal model fully permissive to HCV