Evaluation of a Sporicidal Peracetic Acid/Hydrogen Peroxide–Based Daily Disinfectant Cleaner

2014 ◽  
Vol 35 (11) ◽  
pp. 1414-1416 ◽  
Author(s):  
Abhishek Deshpande ◽  
Thriveen S. C. Mana ◽  
Jennifer L. Cadnum ◽  
Annette C. Jencson ◽  
Brett Sitzlar ◽  
...  

OxyCide Daily Disinfectant Cleaner, a novel peracetic acid/hydrogen peroxide–based sporicidal disinfectant, was as effective as sodium hypochlorite for in vitro killing of Clostridium difficile spores, methicillin-resistant Staphylococcus aureus, and vancomcyin-resistant enterococci. OxyCide was minimally affected by organic load and was effective in reducing pathogen contamination in isolation roomsInfect Control Hosp Epidemiol 2014;35(11):1414–1416

2010 ◽  
Vol 76 (10) ◽  
pp. 3135-3142 ◽  
Author(s):  
K. Toté ◽  
T. Horemans ◽  
D. Vanden Berghe ◽  
L. Maes ◽  
P. Cos

ABSTRACT Bacteria and matrix are essential for the development of biofilms, and assays should therefore target both components. The current European guidelines for biocidal efficacy testing are not adequate for sessile microorganisms; hence, alternative discriminatory test protocols should be used. The activities of a broad range of biocides on Staphylococcus aureus and Pseudomonas aeruginosa biofilms were evaluated using such in vitro assays. Nearly all selected biocides showed a significant decrease in S. aureus biofilm viability, with sodium hypochlorite and peracetic acid as the most active biocides. Only hydrogen peroxide and sodium hypochlorite showed some inhibitory effect on the matrix. Treatment of P. aeruginosa biofilms was roughly comparable to that of S. aureus biofilms. Peracetic acid was the most active on viable mass within 1 min of contact. Isopropanol ensured a greater than 99.999% reduction of P. aeruginosa viability after at least 30 min of contact. Comparable to results with S. aureus, sodium hypochlorite and hydrogen peroxide markedly reduced the P. aeruginosa matrix. This study clearly demonstrated that despite their aspecific mechanisms of action, most biocides were active only against biofilm bacteria, leaving the matrix undisturbed. Only hydrogen peroxide and sodium hypochlorite were active on both the biofilm matrix and the viable mass, making them the better antibiofilm agents. In addition, this study emphasizes the need for updated and standardized guidelines for biofilm susceptibility testing of biocides.


2014 ◽  
Vol 35 (11) ◽  
pp. 1417-1420 ◽  
Author(s):  
Adrijana Gombosev ◽  
Salah E. Fouad ◽  
Eric Cui ◽  
Chenghua Cao ◽  
Leah Terpstra ◽  
...  

We surveyed infection prevention programs in 16 hospitals for hospital-associated methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci, extended-spectrum β-lactamase, and multidrug-resistant Acinetobacter acquisition, as well as hospital-associated MRSA bacteremia and Clostridium difficile infection based on defining events as occurring >2 days versus >3 days after admission. The former resulted in significantly higher median rates, ranging from 6.76% to 45.07% higherInfect Control Hosp Epidemiol 2014;35(11):1417–1420


1997 ◽  
Vol 41 (10) ◽  
pp. 2282-2285 ◽  
Author(s):  
Y Adachi ◽  
K Nakamura ◽  
Y Kato ◽  
N Hazumi ◽  
T Hashizume ◽  
...  

BO-3482, a dithiocarbamate carbapenem, inhibited clinical isolates of methicillin-resistant staphylococci (MRS) at 6.25 microg/ml (MIC at which 90% of isolates tested are inhibited [MIC90]), while the MIC90 of imipenem was > 100 microg/ml. BO-3482 was generally less active than imipenem against methicillin-susceptible Staphylococcus aureus, streptococci, enterococci, and gram-negative bacteria, although BO-3482 showed better activity (MIC90) than imipenem against Enterococcus faecium, Haemophilus influenzae, Proteus mirabilis, and Clostridium difficile. The affinities (50% inhibitory concentrations) of BO-3482 for penicillin-binding protein (PBP) PBP 2' of MRS and PBP 5 of E. faecium (both PBPs have low affinities for ordinary beta-lactam antibiotics) were 3.8 and 20 microg/ml, respectively, reflecting the greater activity of BO-3482 against MRS than against E. faecium.


2012 ◽  
Vol 33 (10) ◽  
pp. 1039-1042 ◽  
Author(s):  
Sirisha Kundrapu ◽  
Venkata Sunkesula ◽  
Lucy A. Jury ◽  
Brett M. Sitzlar ◽  
Curtis J. Donskey

In a randomized nonblinded trial, we demonstrated that daily disinfection of high-touch surfaces in rooms of patients with Clostridium difficile infection and methicillin-resistant Staphylococcus aureus colonization reduced acquisition of the pathogens on hands after contacting high-touch surfaces and reduced contamination of hands of healthcare workers caring for the patients.Infect Control Hosp Epidemiol 2012;33(10):1039-1042


Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1731
Author(s):  
Yu Maw Htwe ◽  
Huashan Wang ◽  
Patrick Belvitch ◽  
Lucille Meliton ◽  
Mounica Bandela ◽  
...  

Lung endothelial dysfunction is a key feature of acute lung injury (ALI) and clinical acute respiratory distress syndrome (ARDS). Previous studies have identified the lipid-generating enzyme, group V phospholipase A2 (gVPLA2), as a mediator of lung endothelial barrier disruption and inflammation. The current study aimed to determine the role of gVPLA2 in mediating lung endothelial responses to methicillin-resistant Staphylococcus aureus (MRSA, USA300 strain), a major cause of ALI/ARDS. In vitro studies assessed the effects of gVPLA2 inhibition on lung endothelial cell (EC) permeability after exposure to heat-killed (HK) MRSA. In vivo studies assessed the effects of intratracheal live or HK-MRSA on multiple indices of ALI in wild-type (WT) and gVPLA2-deficient (KO) mice. In vitro, HK-MRSA increased gVPLA2 expression and permeability in human lung EC. Inhibition of gVPLA2 with either the PLA2 inhibitor, LY311727, or with a specific monoclonal antibody, attenuated the barrier disruption caused by HK-MRSA. LY311727 also reduced HK-MRSA-induced permeability in mouse lung EC isolated from WT but not gVPLA2-KO mice. In vivo, live MRSA caused significantly less ALI in gVPLA2 KO mice compared to WT, findings confirmed by intravital microscopy assessment in HK-MRSA-treated mice. After targeted delivery of gVPLA2 plasmid to lung endothelium using ACE antibody-conjugated liposomes, MRSA-induced ALI was significantly increased in gVPLA2-KO mice, indicating that lung endothelial expression of gVPLA2 is critical in vivo. In summary, these results demonstrate an important role for gVPLA2 in mediating MRSA-induced lung EC permeability and ALI. Thus, gVPLA2 may represent a novel therapeutic target in ALI/ARDS caused by bacterial infection.


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