Microbial Stress Response in the Food Environment ◾ 101
The cells of the pathogens were initially acid adapted by exposing them to pH 5.0. They were then
suspended in orange, apple, or grape juice (pH 3.5–3.9) and heated to 56°C. In all instances, the
D values of acid-adapted cells as compared with those of control cells increased significantly. For
Lis. monocytogenes, D values for control and acid-adapted cells were 2.1 and 3.8 minutes in orange
juice, 1.6 and 5.0 minutes in apple juice, and 2.3 and 4.6 minutes in grape juice, respectively.
These results suggest that stress adaptation of microorganisms can occur both in culture broth
and in food systems. In food processing and preservation methods, results of studies developed
with normal cells (not stress adapted) may not be effective to control or kill stress-adapted foodborne pathogens and spoilage bacteria. To overcome this problem, it is necessary to understand
the underlying mechanisms that confer resistance to stress-adapted cells and develop methods to
control them.
Mechanisms of Stress Adaptation 8–10
An earlier theory was that bacterial cells cope with stress (such as temperature stress) by changing
the lipid composition of the cytoplasmic or inner membrane so that the fluid state is maintained.
Thus, at lower or higher ranges of growth temperature, the membrane lipid accumulates more lowmolecular weight and unsaturated fatty acids, but at optimum growth temperature, it accumulates
more high-molecular-weight saturated fatty acids. In recent years, stress adaptation by bacterial
cells (and other microorganisms) is viewed to be mediated through the synthesis of many types of
shock proteins or stress proteins, some of which are specific for specific stress, whereas others are
nonspecific and expressed against more than one stress. Stress proteins provide protection to structures that could be otherwise adversely affected by the stress, such as DNA and many enzymes.
Synthesis of stress proteins in large quantities is mediated through the expression of stress-related
gene systems, some of which are inducible, whereas others are constitutive but expressed at a low
level when cells are not under stress. As some of the gene systems are global, gene expression by
one stress can also help cells to adapt to other related stresses.
Expression of stress-related genes is initiated by specific polypeptides or sigma factor (σ) synthesized by specific genes. Some of these, such as σ B or σ 37 (encoded by gene sig B), help cope
with general stress in Gram-positive bacteria; σ 32 (encoded by the rpoH gene) and σ 24 (encoded
by the rpoE gene) help cope with heat response; and σ 38 or σ s (encoded by the rpoS gene) helps
cope with general stress and starvation in Gram-negative bacteria. Under a specific stress (such
as under heat-shock condition), rpoH is turned on to affect the synthesis of rpoH or σ 32 protein
in high amounts (Figure 10.2). This sigma factor (also called a regulon) then combines with the
core RNA polymerase (consisting of four subunits, ααββ) to form the complete RNA polymerase
enzyme or holoenzyme. This holoenzyme then binds to the promoter of a heat-shock gene family,
leading to synthesis of heat-shock proteins (e.g., in Esc. coli), which then protects the structural
and functional units of stressed cells susceptible to heat damage (e.g., DNA and proteins). They
can also protect against other stresses. Involvement of different sigma factors in protecting against
stresses (such as cold, heat, low pH, UV) has been studied with several species of foodborne
bacteria.
Importance of Stress-Adapted Microorganisms in Food 11–13
As indicated previously, during the handling of food and food ingredients from the farm to the
table, foodborne bacteria are exposed to different suboptimal physical and chemical environments.
This can enable foodborne pathogens and spoilage bacteria as well as beneficial bacteria to develop
The cells of the pathogens were initially acid adapted by exposing them to pH 5.0. They were then
suspended in orange, apple, or grape juice (pH 3.5–3.9) and heated to 56°C. In all instances, the
D values of acid-adapted cells as compared with those of control cells increased significantly. For
Lis. monocytogenes, D values for control and acid-adapted cells were 2.1 and 3.8 minutes in orange
juice, 1.6 and 5.0 minutes in apple juice, and 2.3 and 4.6 minutes in grape juice, respectively.
These results suggest that stress adaptation of microorganisms can occur both in culture broth
and in food systems. In food processing and preservation methods, results of studies developed
with normal cells (not stress adapted) may not be effective to control or kill stress-adapted foodborne pathogens and spoilage bacteria. To overcome this problem, it is necessary to understand
the underlying mechanisms that confer resistance to stress-adapted cells and develop methods to
control them.
Mechanisms of Stress Adaptation 8–10
An earlier theory was that bacterial cells cope with stress (such as temperature stress) by changing
the lipid composition of the cytoplasmic or inner membrane so that the fluid state is maintained.
Thus, at lower or higher ranges of growth temperature, the membrane lipid accumulates more lowmolecular weight and unsaturated fatty acids, but at optimum growth temperature, it accumulates
more high-molecular-weight saturated fatty acids. In recent years, stress adaptation by bacterial
cells (and other microorganisms) is viewed to be mediated through the synthesis of many types of
shock proteins or stress proteins, some of which are specific for specific stress, whereas others are
nonspecific and expressed against more than one stress. Stress proteins provide protection to structures that could be otherwise adversely affected by the stress, such as DNA and many enzymes.
Synthesis of stress proteins in large quantities is mediated through the expression of stress-related
gene systems, some of which are inducible, whereas others are constitutive but expressed at a low
level when cells are not under stress. As some of the gene systems are global, gene expression by
one stress can also help cells to adapt to other related stresses.
Expression of stress-related genes is initiated by specific polypeptides or sigma factor (σ) synthesized by specific genes. Some of these, such as σ B or σ 37 (encoded by gene sig B), help cope
with general stress in Gram-positive bacteria; σ 32 (encoded by the rpoH gene) and σ 24 (encoded
by the rpoE gene) help cope with heat response; and σ 38 or σ s (encoded by the rpoS gene) helps
cope with general stress and starvation in Gram-negative bacteria. Under a specific stress (such
as under heat-shock condition), rpoH is turned on to affect the synthesis of rpoH or σ 32 protein
in high amounts (Figure 10.2). This sigma factor (also called a regulon) then combines with the
core RNA polymerase (consisting of four subunits, ααββ) to form the complete RNA polymerase
enzyme or holoenzyme. This holoenzyme then binds to the promoter of a heat-shock gene family,
leading to synthesis of heat-shock proteins (e.g., in Esc. coli), which then protects the structural
and functional units of stressed cells susceptible to heat damage (e.g., DNA and proteins). They
can also protect against other stresses. Involvement of different sigma factors in protecting against
stresses (such as cold, heat, low pH, UV) has been studied with several species of foodborne
bacteria.
Importance of Stress-Adapted Microorganisms in Food 11–13
As indicated previously, during the handling of food and food ingredients from the farm to the
table, foodborne bacteria are exposed to different suboptimal physical and chemical environments.
This can enable foodborne pathogens and spoilage bacteria as well as beneficial bacteria to develop