Biocidal Mechanisms of Metallic Copper Surfaces
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Abstract
Hospital acquired infections (HAI), also known as nosocomial infections, have a vast impact on patient and staff health and affect survival chances of patients with compromised immune system, elderly, and young children. Moreover, hospital environments are favoring the development of drug-resistant strains of bacteria, making treatment of such HAI more challenging. The Center of Disease Control estimates that one of the deadliest types of antibiotic-resistant bacteria, MRSA (methicillin-resistant Staphylococcus aureus), causes 19,000 death cases per year, whereas another superbug, Clostridium difficile, causes 500,000 incidents per year.
The natural medicinal and sanitizing properties of copper and its minerals were used throughout the ages by many civilizations. However, only recently have we started understanding the mechanisms of such bactericidal effects of copper. One of the latest research developments in this area is concerned with showing that metallic copper surfaces strongly reduce microbial surface-burden, both in laboratory settings and healthcare environments. Microbiologists and hygiene specialists are increasingly recognizing this unique antimicrobial property of metallic copper as a very promising novel tool for reducing HAI, which are known to spread through touching contaminated surfaces. Copper surfaces have universal microbe-inactivating properties against a wide variety of Gram-positive and Gram-negative microbes under moist (droplets of cell suspensions, mimicking splash-contamination) or dry (direct contact between cells and surfaces, mimicking touch surfaces) conditions.
This chapter reviews the molecular mechanisms underlying bactericidal properties of solid copper surfaces and factors that influence such processes: copper surface oxidation and corrosion, copper cell accumulation, copper alloy content and roughness, temperature, moisture, presence of chelators, osmotic stress, reactive oxygen species, cellular characteristics, cell wall structure, spores, genetic traits for copper resistance systems, anaerobiosis, viable but not culturable state (VBNC). Additionally, primary targets for metallic copper toxicity, DNA and lipids, are also included in discussion in this chapter.
Our understanding of the antimicrobial properties of metallic copper surfaces have made great strides in the last 5 years both under laboratories and healthcare conditions, highlighting safe, economical and sustainable application of metallic copper surfaces in hospital or any public settings for prevention of HAI.
Keywords
Metallic copper surface Antimicrobial Biocidal Toxicity Killing mechanism Membrane damage GenotoxicityList of Abbreviations
- BCS
Bathocuproine disulfonate
- BTA
Benzotriazole
- C=C–C•
Allylic radicals
- CFU
Colony forming units
- ComC
Copper-induced outer membrane component
- ComR
Copper-induced repressor
- CopA
Copper exporter P-type ATPase
- CopB
Cytoplasmic copper and delivers it to the P1B-type ATPase
- CopY
Copper-responsive repressor
- CopZ
Cytoplasmic copper binding chaperone
- CueP
Periplasmic copper binding protein
- CueR
Copper response cytoplasmic MerR-family activator/repressor
- CusCFBA
Copper/Silver transporting efflux system
- CusRS
Periplasmic copper two-component system sensor
- CycA
d-cycloserine uptake permease
- DNA
Deoxyribonucleic acid
- EDTA
Ethylenediaminetetraacetic acid
- FabR
Repressor for unsaturated fatty acids biosynthesis
- FAME
Fatty acid methyl esters
- GSH
Glutathione
- GSSG
Glutathione disulfide
- HAI
Healthcare-acquired infections
- ICP-MS
Inductively coupled plasma mass spectrometry
- L
Lipid
- L•
Lipid radical
- LO•
Lipid alkoyl radicals
- LOO•
Peroxyl radical
- MDA
Malondialdehyde
- MerR
Mercury resistance repressor
- Pco
Plasmid-borne copper resistance
- PMF
Proton motive force
- ROS
Reactive oxygen species
- TBARS
Thiobarbituric acid-reactive substances
- TetR
Tetracycline repressor protein
- Tris
Tris(hydroxymethyl)aminomethane
- VBNC
Viable-But-Not-Culturable
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