The microbial cell has the means to sense stresses such as those leading to ribosomal disruption (e.g., heat stress) or modification in cell membrane fluidity (e.g., cold shock). Response to these stresses is presumed beneficial to the cell, but it occasionally has detrimental consequences. Protective responses require physiological adaptations to compensate for stress damage and permit the cell to continue its growth and ensure its survival. Similarly, the bacterial cell responds to stress induced by inherent physiological change. Entry of a cell population into the stationary phase, for example, triggers a general stress response, which results in microbial resistance to multiple stresses. Adaptive stress response involves the induction of a number of genetic and physiological mechanisms, as well as morphological events, which include: (1) synthesis of protective proteins that participate in damage repair, cell maintenance, or suppression of stress agents, (2) temporary increase in resistance to lethal factors, (3) transformation of cells to a latent state, e.g., spore formation or induction of viable-but-not-culturable state, (4) evasion of the host's defense mechanisms, and (5) adaptive mutations [1,2,4-7].
Environmental or physiological conditions may hinder a cell's ability to respond to stress. Chilled or metabolically exhausted cells, for example, may not respond to radiation stress. Similarly, when dormant bacterial spores are exposed to an injurious stress they are incapable of responding until conditions are favorable for germination and outgrowth. Lack of response to a stress may sensitize a microbial cell to subsequent stresses that are otherwise innocuous. Response to a stress also may exhaust a cell's ability to cope with subsequent stresses, causing a stress-sensitizing effect.
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