Decontamination of Hospital Surfaces With Multijet Cold Plasma: A Method to Enhance Infection Prevention and Control?

OBJECTIVE To evaluate the efficacy of a multijet cold-plasma system and its efficacy in decontaminating 2 surfaces commonly found in hospitals DESIGN An in vitro study of common causes of healthcare-acquired infection METHODS Log10 9 cultures of methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci, extended spectrum ß-lactamase-producing Escherichia coli, and Acinetobacter baumannii were applied to 5-cm2 sections of stainless steel and mattress. Human serum albumin (HSA) was used as a proxy marker for organic material, and atomic force microscopy (AFM) was used to study the impact on bacterial cell structure. The inoculated surfaces were exposed to a cold-air-plasma-generating multijet prototype for 15, 20, 30, and 45 seconds. RESULTS After 45 seconds, at least 3 to 4 log reductions were achieved for all bacteria on the mattress, while 3 to 6 log reductions were observed on stainless steel. The presence of HSA had no appreciable effect on bacterial eradication. The surfaces with bacteria exposed to AFM showed significant morphological changes indicative of "etching" due to the action of highly charged ions produced by the plasma. CONCLUSION This multijet cold-plasma prototype has the potential to augment current environmental decontamination approaches but needs further evaluation in a clinical setting to confirm its effectiveness. Infect Control Hosp Epidemiol 2017;38:1182-1187.

Surface microbial contamination in hospitals: A pilot study on methods of sampling and the use of proposed microbiologic standards.

Contamination of hospital surfaces by bacteria is increasingly recognized. We assessed commonly touched surfaces using contact plates and Petrifilms (3M, St. Paul, MN) and compared the results against proposed microbiology standards. Toilet door handles were the most heavily contaminated (7.97 ± 0.68 colony forming units [CFU]/cm(2)) and exceeded proposed standards on 74% of occasions. Petrifilms detected statistically higher CFU from bedside lockers. Further research is required on the use of standards and methods of sampling.

Cold-air atmospheric pressure plasma against Clostridium difficile spores: a potential alternative for the decontamination of hospital inanimate surfaces.

Clostridium difficile spores survive for months on environmental surfaces and are highly resistant to decontamination. We evaluated the effect of cold-air plasma against C. difficile spores. The single-jet had no effect while the multi-jet achieved 2-3 log10 reductions in spore counts and may augment traditional decontamination.

Detecting Clostridium difficile spores from inanimate surfaces of the hospital environment: which method is best?

The recovery of Clostridium difficile spores from hospital surfaces was assessed using rayon swabs, flocked swabs, and contact plates. The contact plate method was less laborious, achieved higher recovery percentages, and detected spores at lower inocula than swabs. Rayon swabs were the least efficient method. However, further studies are required in health care settings.

What is the best method? Recovery of methicillin-resistant Staphylococcus aureus and extended-spectrum ß-lactamase-producing Escherichia coli from inanimate hospital surfaces.

Environmental sampling in hospitals, when required, needs to be reliable. We evaluated different methods of sampling methicillin-resistant Staphylococcus aureus and extended-spectrum ß-lactamase-producing Escherichia coli on 5 materials of the hospital setting. Petrifilms and contact plates were superior to swabs for all of the surfaces studied.

Cold air plasma to decontaminate inanimate surfaces of the hospital environment.

The hospital environment harbors bacteria that may cause health care-associated infections. Microorganisms, such as multiresistant bacteria, can spread around the patient's inanimate environment. Some recently introduced biodecontamination approaches in hospitals have significant limitations due to the toxic nature of the gases and the length of time required for aeration. This study evaluated the in vitro use of cold air plasma as an efficient alternative to traditional methods of biodecontamination of hospital surfaces. Cultures of methicillin-resistant Staphylococcus aureus (MRSA), vancomycin-resistant enterococci (VRE), extended-spectrum-ß-lactamase (ESBL)-producing Escherichia coli, and Acinetobacter baumannii were applied to different materials similar to those found in the hospital environment. Artificially contaminated sections of marmoleum, mattress, polypropylene, powder-coated mild steel, and stainless steel were then exposed to a cold air pressure plasma single jet for 30 s, 60 s, and 90 s, operating at approximately 25 W and 12 liters/min flow rate. Direct plasma exposure successfully reduced the bacterial load by log 3 for MRSA, log 2.7 for VRE, log 2 for ESBL-producing E. coli, and log 1.7 for A. baumannii. The present report confirms the efficient antibacterial activity of a cold air plasma single-jet plume on nosocomial bacterially contaminated surfaces over a short period of time and highlights its potential for routine biodecontamination in the clinical environment.

Staphylococcus aureus protein A binding to osteoblast tumour necrosis factor receptor 1 results in activation of nuclear factor kappa B and release of interleukin-6 in bone infection.

Staphylococcus aureus is the major pathogen among the staphylococci and the most common cause of bone infections. These infections are mainly characterized by bone destruction and inflammation, and are often debilitating and very difficult to treat. Previously we demonstrated that S. aureus protein A (SpA) can bind to osteoblasts, which results in inhibition of osteoblast proliferation and mineralization, apoptosis, and activation of osteoclasts. In this study we used small interfering RNA (siRNA) to demonstrate that osteoblast tumour necrosis factor receptor-1 (TNFR-1) is responsible for the recognition of and binding to SpA. TNFR-1 binding to SpA results in the activation of nuclear factor kappa B (NFκB). In turn, NFκB translocates to the nucleus of the osteoblast, which leads to release of interleukin 6 (IL-6). Silencing TNFR-1 in osteoblasts or disruption of the spa gene in S. aureus prevented both NFκB activation and IL-6 release. As well as playing a key role in proinflammatory reactions, IL-6 is also an important osteotropic factor. Release of IL-6 from osteoblasts results in the activation of the bone-resorbing cells, the osteoclasts. Consistent with our results described above, both silencing TNFR-1 in osteoblasts and disruption of spa in S. aureus prevented osteoclast activation. These studies are the first to demonstrate the importance of the TNFR-1-SpA interaction in bone infection, and may help explain the mechanism through which osteoclasts become overactivated, leading to bone destruction. Anti-inflammatory drug therapy could be used either alone or in conjunction with antibiotics to treat osteomyelitis or for prophylaxis in high-risk patients.

Staphylococcus aureus protein A plays a critical role in mediating bone destruction and bone loss in osteomyelitis.

Staphylococcus aureus is the most frequent causative organism of osteomyelitis. It is characterised by widespread bone loss and bone destruction. Previously we demonstrated that S. aureus protein A (SpA) is capable of binding to tumour necrosis factor receptor-1 expressed on pre-osteoblastic cells, which results in signal generation that leads to cell apoptosis resulting in bone loss. In the current report we demonstrate that upon S. aureus binding to osteoblasts it also inhibits de novo bone formation by preventing expression of key markers of osteoblast growth and division such as alkaline phosphatase, collagen type I, osteocalcin, osteopontin and osteocalcin. In addition, S. aureus induces secretion of soluble RANKL from osteoblasts which in turn recruits and activates the bone resorbing cells, osteoclasts. A strain of S. aureus defective in SpA failed to affect osteoblast growth or proliferation and most importantly failed to recruit or activate osteoclasts. These results suggest that S. aureus SpA binding to osteoblasts provides multiple coordinated signals that accounts for bone loss and bone destruction seen in osteomyelitis cases. A better understanding of the mechanisms through which S. aureus leads to bone infection may improve treatment or lead to the development of better therapeutic agents to treat this notoriously difficult disease.

Staphylococcus aureus protein A binds to osteoblasts and triggers signals that weaken bone in osteomyelitis.

Osteomyelitis is a debilitating infectious disease of the bone. It is predominantly caused by S. aureus and is associated with significant morbidity and mortality. It is characterised by weakened bones associated with progressive bone loss. Currently the mechanism through which either bone loss or bone destruction occurs in osteomyelitis patients is poorly understood. We describe here for the first time that the major virulence factor of S. aureus, protein A (SpA) binds directly to osteoblasts. This interaction prevents proliferation, induces apoptosis and inhibits mineralisation of cultured osteoblasts. Infected osteoblasts also increase the expression of RANKL, a key protein involved in initiating bone resorption. None of these effects was seen in a mutant of S. aureus lacking SpA. Complementing the SpA-defective mutant with a plasmid expressing spa or using purified protein A resulted in attachment to osteoblasts, inhibited proliferation and induced apoptosis to a similar extent as wildtype S. aureus. These events demonstrate mechanisms through which loss of bone formation and bone weakening may occur in osteomyelitis patients. This new information may pave the way for the development of new and improved therapeutic agents to treat this disease.