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Background Clostridium difficile infection (CDI) is a major infectious concern, accounting for substantial morbidity and resource utilization. Advances in microbiological and molecular techniques have resulted in an increasing number of testing options for CDI. A glutamate dehydrogenase (GDH) enzyme immunoassay (EIA) and a DNA amplification (DNA-A) test for the diagnosis of CDI have recently become commercially available. Aims The aim of this prospective study was to compare the test performance characteristics of the traditional diagnostic modality for CDI diagnosis, the toxin A/B (TOX) EIA, with those of the GDH EIA and DNA-A test, utilizing enriched toxigenic culture (TGC) as the gold standard. Clinical variables predictive of CDI were also studied. Methods Participants fulfilled one or more criteria placing them at increased risk for CDI. Each stool sample was tested by each of the methods mentioned above. Clinical data parameters were collected via a 12-month review of the electronic medical record prior to the index date of the first stool test. Results A total of 272 stool samples from 144 admissions of 139 patients were evaluated for CDI. The sensitivity and positive predictive value (PPV) of the TOX EIA were 86.1 and 58.4 %, respectively, whereas the sensitivity and PPV of the GDH EIA and DNA-A test were 100 %. 1.8 % of the GDH tests yielded inconclusive results. Using TGC as the gold standard, nosocomial exposure with emphasis on nursing home residence, history of previous CDI, and female gender were predictive of CDI. Conclusions Test performance characteristics of the DNA-A test and GDH EIA were superior to those of the traditional TOX EIA. The GDH test is limited by inconclusive test results and requires a multi-step diagnostic algorithm. Therefore, the DNA-A test should be implemented as the diagnostic method of choice for CDI. CDI clinical predictors are important for diagnostic decision-making.

Epstein-Barr virus (EBV) is a human herpesvirus which causes infectious mononucleosis and is associated with two cancers, Burkitt's lymphoma and nasopharyngeal carcinoma. To understand the biologic activity of EBV, it is crucial to understand how EBV infects cells, and what viral components are important to this process. Epstein-Barr virus infects two cell types, B lymphocytes and epithelial cells. To examine the early events in virus infection, binding and fusion, we have adapted an assay that measures membrane fusion. Virus membranes were labeled with concentrations of octadecylrhodamine (R$\\sb{18}$) or 5-(N-octadecanoyl)aminofluorescein (AF) at which fluorescence is self-quenched. The fluorescence of AF is also sensitive to changes in pH. Fusion and mixing of virus and cell membranes was measured in terms of relief of self-quenching and was monitored kinetically. The assay was used to compare virus fusion with lymphoblastoid cell lines, lymphocytes recently transformed with EBV, normal B lymphocytes and epithelial cells. Entry of EBV into all cell types occurred independent of exposure to low pH. However, virus fusion with normal and recently transformed lymphocytes occurred from within endocytic vesicles, whereas fusion with lymphoblastoid and epithelial cells occurred at the plasma membrane. The contribution to fusion made by virus envelope proteins to fusion was studied with monoclonal antibodies that neutralized virus infectivity. Antibody to glycoprotein gp85 inhibited fusion with all cells except epithelial cells. Antibody to glycoprotein gp350, responsible for virus attachment to CR2 on lymphocytes, only partially inhibited virus binding to epithelial cells and the remaining bound virus did not fuse. Soluble CR2 inhibited virus binding to lymphocytes but only partially inhibited binding to epithelial cells. These studies document clear differences between virus entry into lymphocytes and epithelial cells and suggest that the virus proteins involved in fusion with the two cell types may be distinct.