LaPlante K.L.,University of Rhode Island |
LaPlante K.L.,Brown University |
Woodmansee S.,Infectious Diseases Research Laboratory |
Mermel L.A.,Brown University
American Journal of Health-System Pharmacy | Year: 2012
Purpose. The compatibility and stability of telavancin and vancomycin in heparin or sodium citrate lock solutions were evaluated. Methods. Telavancin and vancomycin hydrochloride injection powder lyophilized for solution were reconstituted with 0.9% sodium chloride injection at room temperature according to the manufacturer's instructions and then further diluted with (1) commercially available heparin sodium to reach a final heparin concentration of 2500 units/mL or (2) sodium citrate solution 2.2% or 4% to achieve final telavancin and vancomycin concentrations of 2 and 5 mg/mL. Physical stability, chemical compatibility, and biological anticoagulant stability were analyzed for each antibiotic-anticoagulant combination immediately after preparation and at 24, 48, and 72 hours. Changes in coagulation were measured at each time point and compared using two-way analysis of variance. Results. Both telavancin and vancomycin retained at least 90% of the initial concentration after incubation at 37°C over 72 hours. The biological stability of vancomycin 2 mg/mL and telavancin 2 mg/mL did not significantly alter prothrombin time when compared with that of 0.9% sodium chloride injection. However, telavancin 5 mg/mL and vancomycin 5 mg/mL significantly increased the activated partial thromboplastin time at 72 hours compared with the control solution. Visual precipitation only occurred with vancomycin-containing solutions; however, this dissipated after 10 minutes. Conclusion. Telavancin 2 and 5 mg/mL was physically compatible in combination with heparin 2500 units/mL and with sodium citrate 2.2% and 4% over 72 hours. Vancomycin 2 and 5 mg/mL initially precipitated in the sodium citrate 2.2% formulation, but no precipitation was noted after 10 minutes of incubation at 37°C. Telavancin and vancomycin 2 and 5 mg/mL retained over 90% of the initial concentration after incubation at 37°C over 72 hours.
Masia M.,University Miguel Hernandez |
Padilla S.,University Miguel Hernandez |
Fernandez M.,Infectious Diseases Research Laboratory |
Rodriguez C.,Centro Sanitario Sandoval |
And 6 more authors.
PLoS ONE | Year: 2016
Objective We aimed to assess whether oxidative stress is a predictor of mortality in HIV-infected patients. Methods We conducted a nested case-control study in CoRIS, a contemporary, multicentre cohort of HIV-infected patients, antiretroviral-naïve at entry, launched in 2004. Cases were patients who died with available stored plasma samples collected. Two age and sex-matched controls for each case were selected. We measured F2-isoprostanes F2-IsoPs and malondialdehyde MDA plasma levels in the first blood sample obtained after cohort engagement. Results 54 cases and 93 controls were included. Median F2-IsoPs and MDA levels were significantly higher in cases than in controls. When adjustment was performed for age, HIV- Transmission category, CD4 cell count and HIV viral load at cohort entry, and subclinical inflammation measured with highly-sensitive C-reactive protein hsCRP, the association of F2-IsoPs with mortality remained significant adjusted OR per 1 log10 increase, 2.34 [1.23- 4.47], P = 0.009. The association of MDA with mortality was attenuated after adjustment: Adjusted OR 95% CI per 1 log10increase, 2.05 [0.91-4.59], P = 0.080. Median hsCRP was also higher in cases, and it also proved to be an independent predictor of mortality in the adjusted analysis: OR 95% CI per 1 log10 increase, 1.39 1.01-1.91, P = 0.043; and OR 95% CI per 1 log10 increase, 1.46 1.07-1.99, P = 0.014, respectively, when adjustment included F2-IsoPs and MDA. Oxidative stress is a predictor of all-cause mortality in HIV-infected patients. For plasma F2- IsoPs, this association is independent of HIV-related factors and subclinical inflammation. © 2016 Masiá et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Elhadad D.,Infectious Diseases Research Laboratory |
Elhadad D.,Tel Aviv University |
McClelland M.,University of California at Irvine |
Rahav G.,Infectious Diseases Research Laboratory |
And 3 more authors.
Journal of Infectious Diseases | Year: 2015
Human infection with typhoidal Salmonella serovars causes a febrile systemic disease, termed enteric fever. Here we establish that in response to a temperature equivalent to fever (39°C-42°C) Salmonella enterica serovars Typhi, Paratyphi A, and Sendai significantly attenuate their motility, epithelial cell invasion, and uptake by macrophages. Under these feverlike conditions, the residual epithelial cell invasion of S. Paratyphi A occurs in a type III secretion system (T3SS) 1-independent manner and results in restrained disruption of epithelium integrity. The impaired motility and invasion are associated with down-regulation of T3SS-1 genes and class II and III (but not I) of the flagella-chemotaxis regulon. In contrast, we demonstrate up-regulation of particular Salmonella pathogenicity island 2 genes (especially spiC) and increased intraepithelial growth in a T3SS-2-dependent manner. These results indicate that elevated physiological temperature is a novel cue controlling virulence phenotypes in typhoidal serovars, which is likely to play a role in the distinct clinical manifestations elicited by typhoidal and nontyphoidal salmonellae. © 2014 The Author.
McConeghy K.W.,University of Rhode Island |
McConeghy K.W.,Infectious Diseases Research Laboratory |
LaPlante K.L.,University of Rhode Island |
LaPlante K.L.,Infectious Diseases Research Laboratory
Diagnostic Microbiology and Infectious Disease | Year: 2010
We investigated the activity of tigecycline in combination with gentamicin for the treatment of biofilm-forming methicillin-resistant and sensitive Staphylococcus aureus in an in vitro pharmacodynamic model. Tigecycline monotherapy demonstrated bacteriostatic activity throughout 48 h (-0.24 ± 0.17 log10 CFU/mL), whereas tigecycline in combination with gentamicin demonstrated significant (P < 0.002) kill (-3.66 ± 0.26 log10 CFU/mL) at 48 h. The addition of gentamicin to tigecycline significantly improved the killing activity of tigecycline in biofilm-forming S. aureus. © 2010 Elsevier Inc.
Neoh C.Y.,National Skin Center |
Tan A.W.H.,National Skin Center |
Mohamed K.,National Skin Center |
Sun Y.J.,Infectious Diseases Research Laboratory |
Tan S.H.,National Skin Center
Clinical and Experimental Dermatology | Year: 2010
Background. Pityriasis rosea (PR) is a common cutaneous papulosquamous disorder affecting young adults. Previous studies have suggested possibilities of a viral aetiology and the involvement of cell-mediated immunity, but these remain unproven to date. Aim. To elucidate the possible pathomechanisms in PR by characterizing the inflammatory cellular infiltrate in herald patches and fully developed PR eruptions. Methods. In total, 12 biopsy specimens from 6 patients diagnosed with PR were examined. For each patient, biopsies were taken from both a herald patch and a secondary patch. Specimens were processed for histopathological examination and immunohistochemical staining with a large panel of monoclonal antibodies. Results. Histopathologically, all specimens showed epidermal changes such as parakeratosis, orthokeratosis, epidermal hyperplasia and spongiosis. Less common results included epidermal exocytosis and focal parakeratosis. In all biopsies, the dermal infiltrate of lymphocytes stained positively for monoclonal antibodies specific for T cells. The ratio of the CD4+ (helper) vs. CD8+ (cytotoxic) T cells in the dermal infiltrate was increased in most specimens. Increased staining for Langerhans cells was seen within the dermis of lesional sk There were no marked differences found in histopathology and immunohistochemistry between the herald patch and secondary lesions. Overall, there was a lack of natural killer cell and B-cell activities in PR lesions. Conclusions. Our results support a predominantly T-cell mediated immunity in the development of PR. © 2009 British Association of Dermatologists.