How Silver Kills Bacteria
The germ killing ability of silver at low concentrations is a documented fact.
Study Title:A review of the use of silver in wound care: facts and fallacies.
This review traces the use of silver in wound care, discussing its merits as an antibacterial agent and constituent of many new dressings, which are increasingly tailored to the treatment of wounds ranging from acute surgical lesions to chronic and diabetic leg ulcers. Misconceptions regarding the biological properties of silver, its possible physiological value in the human body and wound bed, absorption through the skin, and safety factors are addressed. The article aims to present silver and the new range of sustained silver-release dressings as important features in the management of skin wounds, providing effective control of wound infections while ensuring patient comfort and quality of life.
Selected quotes from study:
Discussion on the presumed mechanism(s) of silver and related compounds should acknowledge that:
From the earliest reliable studies, the microbicidal action of silver products has been directly related to the amount and rate of silver released and its ability to inactivate target bacterial and fungal cells.39 The oligodynamic microbicidal action of silver compounds at low concentrations probably does not reflect any remarkable effect of a comparatively small number of ions on the cell, but rather the ability of bacteria, trypanosomes and yeasts to take up and concentrate silver from very dilute solutions.4,5,40
Therefore, bacteria killed by silver may contain 105–107 Ag+ per cell, the same order of magnitude as the estimated number of enzyme-protein molecules per cell.41 In culture media, uptake and toxicity of silver ions in Pseudomonas stutzeri is influenced by sodium chloride, which results in precipitation of relatively insoluble silver chloride.42 Kuschner found variations in the sensitivity of mutant strains of Salmonella typhimurium to the biocidal action of metals such as copper, cobalt, nickel and chromium, whereas both parent and mutant strains of the bacterium remained equally sensitive to silver (and mercury).43
Chemically, metallic silver is relatively inert but its interaction with moisture on the skin surface and with wound fluids leads to the release of silver ion and its biocidal properties. Silver ion is a highly reactive moiety and avidly binds to tissue proteins, causing structural changes in bacterial cell walls and intracellular and nuclear membranes.44 These lead to cellular distortion and loss of viability.45,46
Silver binds to and denatures bacterial DNA and RNA, thereby inhibiting replication.47,48 A recent study demonstrated the inhibitory action of silver on two strains of Gram-negative Escherichia coli and Gram-positive Staphylococcus aureus. It found that silver-nitrate exposure lead to the formation of electron-light regions in their cytoplasm and condensation of DNA molecules.49
Granules of silver were observed in the cytoplasm, but RNA and DNA damage and protein inactivation seemed to be the principal mechanisms for bacteriostasis. Intracellular protective mechanisms against silver differed in the Gram-positive and Gram-negative bacteria. The action of silver on bacterial infections in water supplies has also increased our understanding of its microbicidal action. Cell penetration of silver is considered the principal objective in the development of copper/silver ionisation techniques.50
Positively charged copper ions form electrostatic bonds at negatively charged sites on bacterial cell walls, and the resulting damage permits the uptake and release of silver ions. Silver-related degenerative changes in bacterial RNA and DNA, mitochondrial respiration and cytosolic protein lead to cell death. Silver filters and metal used in the control of Legionella suggest that silver and copper ion concentrations are 40:400g/l respectively.51
The action of silver ion on cell walls is illustrated by reference to the yeast Candida albicans. Silver has been shown to inhibit the enzyme phosphomannose isomerase (PIM) by binding cysteine residues.52 This enzyme plays an essential role in the synthesis of the yeast cell wall, and defects lead to the release of phosphate, glutamine and other vital nutrients.53 Silver ion did not inhibit PIM in Escherichia coli cultures.53
Recent literature suggests that the microbicidal action of silver products is partly related to the inhibitory action of silver ion on cellular respiration and cellular function, although the contribution made by ‘other’ silver radicals generated is also acknowledged.54 The exact nature of these silver radicals is not clear but Ovington44 noted that nanocrystalline silver products (Acticoat, Smith and Nephew) can release a cluster of highly reactive silver cations and radicals, which provide a high antibacterial potency on account of unpaired electrons in outer orbitals. Silver and silver radicals released from Acticoat also cause impaired electron transport, bacterial DNA inactivation, cell membrane damage, and binding and precipitation of insoluble complexes with cytosolic anions, proteins and sulphydryl moieties.5,50,55
Lansdown AB. A review of the use of silver in wound care: facts and fallacies. Br J Nurs. 2004 March 13(6 Suppl):S6-19.
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