434 Modern Food Microbiology
content and more lipid saturation. According to this investigator, cells cannot grow at temperatures
below the solidification point of their lipids. Marr and Ingraham
33 showed a progressive increase
in saturated fatty acids and a corresponding decrease in unsaturated fatty acids in E. coli as the
temperature of growth increased. The general decrease in the proportion of unsaturated fatty acids
as growth temperatures increase has been found to occur in a large variety of animals and plants.
Saturated fatty acids form stronger hydrophobic bonds than do unsaturated. Among the saturated fatty
acids are branched-chain acids. The preferential synthesis of branched heptadecanoic acid and the total
elimination of unsaturated fatty acids by two thermophilic Bacillus spp. have been demonstrated.
60
Mesophilic bacteria display changes in their membrane lipids when grown significantly above or
below their normal growth range. When D 57 ◦ C values of four heat-adapted strains of E. coli (including
E. coli 0157:H7 and a rpoS mutant) were determined, the values were up to 3.9 minutes longer
than controls for all strains.
64 Palmitic acid (16:0) and cis-vaccenic acid (18:1 7c) increased in
the membrane of two strains. Total intracellular verotoxin decreased in the heat-adapted strain but
extracellular toxin increased in the heat-adapted cells, apparently the result of increased membrane
fluidity.
64
Cellular Membranes
The nature of cellular membranes affects thermophilic growth. Brock
11 reported that the molecular
mechanism of thermophilism is more likely to be related to the function and stability of cellular
membranes than to the properties of specific macromolecules. This investigator pointed out that there
is no evidence that organisms are killed by heat because of the inactivation of proteins or other
macromolecules, a view that is widely held. According to Brock, an analysis of thermal death curves
of various microorganisms shows them to be a first-order processes compatible with an effect of heat
on some large structure such as the cell membrane, as a single hole in the membrane could result in
leakage of cell constituents and subsequent death. Brock has also pointed out that thermal killing due to
the inactivation of heat-sensitive enzymes, or heat-sensitive ribosomes, of which there are many copies
in the cell, should not result in simple first-order kinetics. The leakage of ultraviolet light-absorbing
and other material from cells undergoing “cold shock” would tend to implicate the membrane in hightemperature death. Because most animals die when body temperatures reach between 40
◦ C and 45
◦ C
and most psychrophilic bacteria are killed at about this temperature range, the suggestion that lethal
injury is due to the melting of lipid constituents of the cell or cell membrane is not only plausible, it
has been supported by the findings of various investigators. The unit cell membrane consists of layers
of lipid surrounded by layers of protein and depends on the lipid layers for its biological functions.
The disruption of this structure would be expected to cause cell damage and perhaps death. In view of
the changes in cellular lipid saturation noted above, cellular membrane integrity appears to be critical
to growth and survival at thermophilic temperatures.
Effect of Temperature
Brock
11 called attention to the fact that thermophiles apparently do not grow as fast at their optimum
temperatures as one would predict or is commonly believed. Arrhenius plots of thermophile growth
compared to E. coli over a range of temperatures indicated that, overall, the mesophilic types were
more efficient. Brock noted that thermophile enzymes are inherently less efficient than mesophiles
because of thermal stability; that is, the thermophiles have had to discard growth efficiency in order
to survive at all.
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