Copper Killing Mechanism
Before discussing mechanisms of copper killing, the following finding is of great practical significance to those interested in integrating antimicrobial copper surfaces into their built environment.
Unlike antibiotic resistance, bacteria resistant to dry copper surfaces have NOT been isolated. After exposure of over 10 billion bacteria* to a dry copper surface, all but 1 or 2 individual bacteria occasionally survive. When these survivors retested, they also die at the same rapid rate as the initial 10 billion bacteria. Thus these survivors have NOT developed resistance to dry copper surface killing.
Together these results - Rapid Killing AND NO Copper Surface Resistance - clearly indicate that copper surfaces in your environment will be a consistent, long lived, easily maintained, and powerful weapons in the fight against the spread of bacteria* that cause infections.
Different mechanisms of copper surface killing have been discussed in the literature. The Membrane Attack hypothesis discussed below is the most straightforward, requires the fewest assumptions, and best explains the absence of copper alloy surface exposure resistance. Copper alloy surface killing is quite distinct from killing due to exposure of bacteria to liquids with high concentrations of dissolved copper, such as water in copper mines. Studies have shown that so-called copper resistant bacteria strains isolated from copper mines are not resistance to copper alloy surfaces. Thus, the mechanisms are distinct.
Membrane Attack Theory of Bacterial Killing on Dry Copper Surfaces
The copper killing mechanism is not fully understood but certain aspects are known. Copper has the ability to transition between two oxidation states, cuprous (Cu+) and cupric (Cu++), and the transition catalyzes the formation of reactive oxygen species (ROS). The most common ROS formed is a highly reactive hydroxyl radical (OH*) that causes oxidative damage to various cellular targets. The primary target of copper surface bacterial killing is the cell’s membrane. In summary, the sequence of events are shown below. NOTE: All occur within a matter of a few minutes and under typical indoor ambient room conditions.
Copper ions form at the interface between the copper surface and the bacterial cell.
Hydroxyl ROS radicals form as a product of the cuprous to cupric ion transition.
Hydroxyl radicals oxidize essential components of the bacterial membrane, specifically the long-chain unsaturated fatty acids of the lipid bilayer.
Oxidative damage causes breaks the long-chain fatty acids leading to serious distortions of the lipid bilayer, irreversible structural alterations, and loss of membrane integrity.
The bacterial membrane is compromised resulting in its rupture, the release and degradation of cellular components, and rapid death.
"Copper - The New 'Old' Weapon in the Fight Against Infectious Disease"