scholarly journals Modeling Surface Disinfection Needs To Meet Microbial Risk Reduction Targets

2018 ◽  
Vol 84 (18) ◽  
Author(s):  
Amanda M. Wilson ◽  
Kelly A. Reynolds ◽  
Jonathan D. Sexton ◽  
Robert A. Canales

ABSTRACTNosocomial viral infections are an important cause of health care-acquired infections where fomites have a role in transmission. Using stochastic modeling to quantify the effects of surface disinfection practices on nosocomial pathogen exposures and infection risk can inform cleaning practices. The purpose of this study was to predict the effect of surface disinfection on viral infection risks and to determine needed viral reductions to achieve risk targets. Rotavirus, rhinovirus, and influenza A virus infection risks for two cases were modeled. Case 1 utilized a single fomite contact approach, while case 2 assumed 6 h of contact activities. A 94.1% viral reduction on surfaces and hands was measured following a single cleaning round using an Environmental Protection Agency (EPA)-registered disinfectant in an urgent care facility. This value was used to model the effect of a surface disinfection intervention on infection risk. Risk reductions for other surface-cleaning efficacies were also simulated. Surface reductions required to achieve risk probability targets were estimated. Under case 1 conditions, a 94.1% reduction in virus surface concentration reduced infection risks by 94.1%. Under case 2 conditions, a 94.1% reduction on surfaces resulted in median viral infection risks being reduced by 92.96 to 94.1% and an influenza A virus infection risk below one in a million. Surface concentration in the equations was highly correlated with dose and infection risk outputs. For rotavirus and rhinovirus, a >99.99% viral surface reduction would be needed to achieve a one-in-a-million risk target. This study quantifies reductions of infection risk relative to surface disinfectant use and demonstrates that risk targets for low-infectious-dose organisms may be more challenging to achieve.IMPORTANCEIt is known that the use of EPA-registered surface disinfectant sprays can reduce infection risk if used according to the manufacturer's instructions. However, there are currently no standards for health care environments related to contamination levels on surfaces. The significance of this research is in quantifying needed reductions to meet various risk targets using realistic viral concentrations on surfaces for health care environments. This research informs the design of cleaning protocols by demonstrating that multiple applications may be needed to reduce risk and by highlighting a need for more models exploring the relationship among microbial contamination of surfaces, patient and health care worker behaviors, and infection risks.

2001 ◽  
Vol 75 (1) ◽  
pp. 499-505 ◽  
Author(s):  
Naomi Yamamoto ◽  
Shunsuke Suzuki ◽  
Yuzo Suzuki ◽  
Akira Shirai ◽  
Masatoshi Nakazawa ◽  
...  

ABSTRACT To study which phase of viral infection promotes antigen sensitization via the airway and which type of antigen-presenting cells contributes to antigen sensitization, BALB/c mice were sensitized by inhalation of ovalbumin (OA) during the acute phase or the recovery phase of influenza A virus infection, and then 3 weeks later animals were challenged with OA. The numbers of eosinophils and lymphocytes, the amounts of interleukin-4 (IL-4) and IL-5 in the bronchoalveolar lavage fluid, and the serum levels of OA-specific immunoglobulin G1 (IgG1) and IgE increased in mice sensitized during the acute phase (acute phase group), while a high level of gamma interferon production was detected in those sensitized during the recovery phase (recovery phase group). In the acute phase group, both major histocompatibility complex class II molecules and CD11c were strongly stained on the bronchial epithelium; in the recovery phase group, however, neither molecule was detected. OA-capturing dendritic cells (DCs) migrated to the regional lymph nodes, and a small number of OA-capturing macrophages were also observed in the lymph nodes of the acute phase group. In the recovery group, however, no OA-capturing DCs were detected in either the lungs or the lymph nodes, while OA-capturing macrophages were observed in the lymph nodes. These results indicate that the timing of antigen sensitization after viral infection determines the type of immune response.


mBio ◽  
2016 ◽  
Vol 7 (4) ◽  
Author(s):  
Ryan M. Reddinger ◽  
Nicole R. Luke-Marshall ◽  
Anders P. Hakansson ◽  
Anthony A. Campagnari

ABSTRACTStaphylococcus aureusis a ubiquitous opportunistic human pathogen and a major health concern worldwide, causing a wide variety of diseases from mild skin infections to systemic disease.S. aureusis a major source of severe secondary bacterial pneumonia after influenza A virus infection, which causes widespread morbidity and mortality. While the phenomenon of secondary bacterial pneumonia is well established, the mechanisms behind the transition from asymptomatic colonization to invasive staphylococcal disease following viral infection remains unknown. In this report, we have shown thatS. aureusbiofilms, grown on an upper respiratory epithelial substratum, disperse in response to host physiologic changes related to viral infection, such as febrile range temperatures, exogenous ATP, norepinephrine, and increased glucose. Mice that were colonized withS. aureusand subsequently exposed to these physiologic stimuli or influenza A virus coinfection developed pronounced pneumonia. This study provides novel insight into the transition from colonization to invasive disease, providing a better understanding of the events involved in the pathogenesis of secondary staphylococcal pneumonia.IMPORTANCEIn this study, we have determined that host physiologic changes related to influenza A virus infection causesS. aureusto disperse from a biofilm state. Additionally, we report that these same host physiologic changes promoteS. aureusdissemination from the nasal tissue to the lungs in an animal model. Furthermore, this study identifies important aspects involved in the transition ofS. aureusfrom asymptomatic colonization to pneumonia.


Cell Reports ◽  
2021 ◽  
Vol 35 (7) ◽  
pp. 109159
Author(s):  
Xiaoyuan Bai ◽  
Wenxian Yang ◽  
Xiaohan Luan ◽  
Huizi Li ◽  
Heqiao Li ◽  
...  

2007 ◽  
Vol 88 (10) ◽  
pp. 2627-2635 ◽  
Author(s):  
Alexey A. Matskevich ◽  
Karin Moelling

In mammals the interferon (IFN) system is a central innate antiviral defence mechanism, while the involvement of RNA interference (RNAi) in antiviral response against RNA viruses is uncertain. Here, we tested whether RNAi is involved in the antiviral response in mammalian cells. To investigate the role of RNAi in influenza A virus-infected cells in the absence of IFN, we used Vero cells that lack IFN-α and IFN-β genes. Our results demonstrate that knockdown of a key RNAi component, Dicer, led to a modest increase of virus production and accelerated apoptosis of influenza A virus-infected cells. These effects were much weaker in the presence of IFN. The results also show that in both Vero cells and the IFN-producing alveolar epithelial A549 cell line influenza A virus targets Dicer at mRNA and protein levels. Thus, RNAi is involved in antiviral response, and Dicer is important for protection against influenza A virus infection.


2012 ◽  
Vol 206 (4) ◽  
pp. 495-503 ◽  
Author(s):  
Jie Zhou ◽  
Kelvin Kai-Wang To ◽  
Hui Dong ◽  
Zhong-Shan Cheng ◽  
Candy Choi-Yi Lau ◽  
...  

Virulence ◽  
2012 ◽  
Vol 3 (7) ◽  
pp. 603-608 ◽  
Author(s):  
Jason Waithman ◽  
Justine D. Mintern

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