Quantification of the influence of trimethylamine-N-oxide (TMAO) on the heat resistance of Escherichia coli K12 at lethal temperatures.

AIM: To quantify the influence of trimethylamine-N-oxide (TMAO) on the heat resistance of Escherichia coli K12 MG1655 cells at static temperatures. METHODS AND RESULTS: Stationary-phase E. coli cells were inactivated at 52, 54 and 58°C. The heat resistance is described as reduction in the inactivation rate, k(max) , and/or an increase in the time for one decimal reduction, D, and/or an increase in the time for the fourth decimal reduction, t(4D) . CONCLUSIONS: Resistance of E. coli changed - increased - at all temperatures under study. Generally, the addition of TMAO to the growth medium protected E. coli cells, leading to an increase in their heat resistance, i.e. reduced k(max) and increased D and t(4D) values are obtained. SIGNIFICANCE AND IMPACT OF THE STUDY: Additional knowledge on the reaction of E. coli to heat in the presence of the organic osmolyte TMAO at lethal temperatures is provided. This work contributes to an improved understanding of the level of the resistance of bacteria to heat in the presence of osmolytes.

Towards the quantification of the effect of acid treatment on the heat tolerance of Escherichia coli K12 at lethal temperatures.

The aim of this work is to investigate the effect of acid treatment -before and during heat inactivation- on the heat resistance of Escherichia coli K12 MG1655 cells at lethal temperatures. E. coli cells were grown in Brain Heart Infusion broth until they reached the stationary phase (≈10(9) cfu/mL). Approximately 30 min before thermal inactivation the early stationary phase cells were added in Brain Heart Infusion broth with a specific pH value, achieved with addition of either acetic (50% (v/v)), lactic (50% (v/v)) or hydrochloric acid (30% (v/v)), and inactivation experiments took place at 54 °C and 58 °C. The inactivation dynamics are analysed using the inactivation model of Geeraerd et al. (2000). This enables to define the induced thermotolerance of E. coli as a prolongation of the shoulder and/or a reduction of the inactivation rate. Generally, addition of acids increased the heat resistance of E. coli. The induced resistance depends on the type of acid and on the quantity added, i.e. different levels of acidification lead to a different level of heat resistance. This work provides additional knowledge on the reaction of bacterial cultures to heat after acid treatment -before and during heat treatment- and, therefore, it contributes to an improved understanding of the effect of acid exposure on the bacterial heat resistance.