Fundamental Food Microbiology, Third Edition - Fuad Fathir

FOOD BIOPRESERVATIVES OF MICROBIAL ORIGIN 237
D. Mode of Action 9–14
Bacteriocins of lactic acid bacteria kill sensitive bacterial cells very rapidly and the
highly potent one at a very low concentration [minimum inhibitory concentration
(MIC) ~ 0.01mg/ml for pediocin AcH to Listeria monocytogenes]. Their antibacterial
actions can be summarized as follows:
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1. They differ greatly in the spectra of antibacterial activity against sensitive Grampositive
bacteria (e.g., nisin and pediocin have wider spectra than leucocin or
sakacin).
2. Their relative potency (MIC) against a sensitive strain differs greatly (e.g., pediocin
is more potent than leucocin against Lis. monocytogenes).
3. Bactericidal efficiency of a bacteriocin increases at acidic pH, higher temperature,
in the presence of a detergent, and against exponentially growing cells.
4. Even in the population of a most sensitive strain, there are variant cells that are
resistant to a bacteriocin, but this property is not stable, because in the absence
of the bacteriocin they become sensitive again.
5. A sensitive strain resistant to one bacteriocin can be sensitive to a second bacteriocin.
6. Gram-negative and resistant Gram-positive bacteria injured by a physical or chemical
stress become sensitive to a bacteriocin.
7. Bacterial spores of a sensitive bacterium are resistant to a bacteriocin, but become
sensitive following germination and outgrowth.
The bactericidal effect of a bacteriocin toward a sensitive bacterial cell is produced
primarily by destabilization of the function of the cytoplasmic membrane. It is
now accepted that, in general, the bacteriocin molecules are initially adsorbed on
the membrane surface and form transient pores, leading to loss of protein motive
force as well as the pH gradient across the membrane. This alters the permeability
of the membrane, causing leakage of small nutrient molecules, as well as affecting
the transport of nutrients and synthesis of ATP. These changes finally cause the
cell to lose viability. In addition, some bacteriocins can cause lysis of sensitive
cells. The exact mechanisms by which these changes are brought about differ with
bacteriocins and are explained here by using nisin A and pediocin AcH or PA-1
as two examples. In the case of nisin, several molecules initially bind (dock) to
the lipid II of the cell wall. This subsequently helps the molecules to come in
contact with the membrane, leading to pore formation. Pore formation by nisin
requires a voltage difference between the inside and outside of the membrane.
Nisin is thus more potent against growing cells as opposed to resting cells of a
target population. In contrast, the action of pediocin is not dependent on voltage
difference of the membrane and is thus effective against both growing and resting
cells. Pediocin also forms pores on the cytoplasmic membrane of target cells. As
the molecules come in contact with the membrane, their random conformation
changes to a defined structure. Several molecules then assemble in a cluster,
leading to formation of a pore in the membrane.