Abstract
Since bacterial destruction is a cavitation-dependent effect of ultrasound, it is possible to draw conclusions regarding the factors affecting cavitation by studying bacterial destruction. To destroy bacteria, cavities must form and collapse within several [mu] of the bacterial cells so that the resulting collapse shock wave will have a high enough energy to rupture the cell wall. Cavitation near the cell occurs most readily when the interfacial linkages between the cell and the surrounding liquid are weakest. When surface-active agents, which strengthen the interfacial linkages, are added to the bacterial suspension, cavitation is inhibited and the ultrasonic death rate decreases markedly. If the bacterial suspension is heated, increasing the energy of the intramolecular bonds, the threshold sound pressure just necessary to kill bacteria is reduced, or, if the sound pressure is constant, the bacteria are destroyed at an increasing rate as the temp. increases. Likewise, if alternate cavitation nuclei which form weaker linkages with the surrounding liquid than with the initial bacteria are added to the bacterial suspension, the killing rate of the original bacteria is decreased.

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