Escherichia coli (E. coli) is a bacterium commonly found in the lower intestine of warm-blooded animals. It is a versatile microorganism, capable of thriving in diverse environments outside of a host, such as soil and water. Temperature is a primary environmental factor that governs the proliferation and survival of this bacterium. The ability of E. coli to sense and rapidly adjust its cellular machinery to shifts in temperature is fundamental to its success as a widespread organism. Understanding these thermal responses offers insights into bacterial physiology and has practical implications for public health and food safety.
Optimal Growth Conditions and Growth Rate
E. coli is classified as a mesophile, adapted to flourish in moderate temperatures. The optimal growth temperature for most strains is approximately 37°C, which mirrors the internal body temperature of its primary mammalian hosts. At this ideal temperature, under nutrient-rich conditions, the bacterium achieves its fastest rate of reproduction, allowing the population to increase exponentially.
Reproduction rate is quantified by the generation time, the interval required for the population to double. Under favorable laboratory conditions, E. coli can exhibit a doubling time as short as 20 minutes. As the temperature deviates from the 37°C optimum, the growth rate declines predictably, reflecting decreased metabolic efficiency. For instance, some strains show a generation time of over 80 minutes at 30°C compared to their optimal rate.
Bacterial growth follows a typical curve, starting with a lag phase followed by an exponential phase of rapid division. Temperature strongly influences the duration and speed of these phases. Because 37°C is the host temperature, the bacterium is well-equipped to immediately enter the exponential growth phase upon intestinal colonization.
Molecular Mechanisms of Thermal Adaptation
The bacterial cell uses molecular systems to cope with sudden temperature changes that destabilize cellular components. These responses are categorized into two primary mechanisms: the heat shock response (for increases) and the cold shock response (for decreases). Both involve the rapid, transient production of specific proteins that stabilize the cell’s internal environment.
Upon a sudden upshift in temperature, the cell activates the heat shock response to prevent protein denaturation. A sensor mechanism detects the accumulation of misfolded or aggregated proteins, which triggers the stabilization and accumulation of the \(\sigma^{32}\) transcription factor. This factor initiates the transcription of genes encoding Heat Shock Proteins (HSPs), which function as molecular chaperones. Major HSPs, such as the DnaK and GroEL/GroES systems, bind to damaged proteins, assisting in their proper refolding and preventing toxic aggregation.
The cold shock response is triggered when the temperature drops, causing two main issues: decreased cell membrane fluidity and hindered transcription/translation machinery. To combat membrane rigidification, E. coli alters its fatty acid composition in a process called homeoviscous adaptation. This involves increasing the proportion of unsaturated fatty acids, such as cis-vaccenic acid, which helps maintain the necessary permeability and flexibility of the membrane at lower temperatures.
Concurrently, the cell induces the production of Cold Shock Proteins (CSPs), with CspA being a well-studied example. These proteins help destabilize the secondary structures that form in messenger RNA (mRNA) and DNA at low temperatures, which would otherwise impede transcription and translation. By functioning as RNA chaperones, CSPs facilitate the movement of ribosomes and allow the synthesis of necessary proteins to continue, enabling the cell to acclimate and resume a slower growth rate. The cold shock also causes changes in DNA supercoiling, which can repress the transcription of certain genes, further contributing to the complexity of the adaptation process.
Survival Limits: Cold Inhibition and Thermal Death
Temperatures outside the growth range lead to either inhibition or cell death, with significant implications for food preservation and sterilization. Refrigeration temperatures, typically 4°C, represent a point of cold inhibition for E. coli. At this temperature, the bacterium’s metabolism slows drastically, and cell division effectively halts.
Cold temperature does not kill the bacteria but instead induces a state of stasis or dormancy, allowing the organism to survive for extended periods. While growth is inhibited, the cell remains viable and can resume proliferation quickly once returned to a warmer environment. This is why refrigeration slows food spoilage but does not eliminate the risk of bacterial contamination.
Conversely, exposure to high temperatures results in thermal death due to the irreversible damage of cellular components. Temperatures at or above 60°C cause denaturation, where the three-dimensional structure of proteins and enzymes is permanently disrupted, leading to the loss of biological function. This is the principle behind thermal processing methods like pasteurization, designed to inactivate harmful bacteria.
For instance, the High-Temperature Short-Time (HTST) pasteurization standard involves heating to 72°C for 15 seconds, a regimen proven to kill pathogenic E. coli. Some strains previously subjected to sublethal heat stress can acquire a transient increase in heat tolerance. However, temperatures above 65°C rapidly reduce the bacterial population to safe levels.