Introduction to Foodborne Pathogens
533
Listeria monocytogenes
Although Gram positive, this bacterium is significantly different from those noted above. The most
notable difference is that it is an intracellular pathogen. More specifically, it resides in the cytosol
where it replicates; and it apparently uses host-derived lipoic acid for its replication.
79 In order to
enter epithelial cells, the invasin internalin interacts with E-cadherin on human host cells (mouse
and rat E-cadherins are not receptors for internalin). The L. monocytogenes cells that lack internalin
are noninvasive
67 Although virulent strains produce the exocellular thiol-activated, pore-forming substance listeriolysin O (LLO), it does not per se cause the foodborne gastroenteritis syndrome. LLO
is a hemolysin involved in the invasion of the gut epithelium, and it contributes to the cell-to-cell
spread of the organism. Unlike the other syndromes above caused by Gram-positive bacteria (with the
exception of Clostridium perfringens), the ingestion of viable cells is necessary for listeric infection
to occur.
The PEST (P, pro.; E. glu.; S, ser.; T, thr.) sequence of LLO is essential for virulence and the
intracellular state of L. monocytogenes. This sequence induces host macrophages to degrade LLO
once it escapes from lysosomes. Mutants lacking the PEST sequence entered host cell cytosol and
killed the host cells.
33 LLO lacking PEST accumulated in the cytosol, suggesting that it targets LLO
for degradation.
33 In effect, PEST prevents LLO from prematurely destroying host cells.
Virulent strains of L. monocytogenes can breach the mucous barrier as noted above, and they then
enter epithelial cells, but just how is unclear. Also, gastrointestinal symptoms are seen in only around
one-third of human cases.
49 The body’s early defense against these organisms consists of resident
macrophages, especially the Kupffer cells of the liver.
91 They gain entry into these cells by being
internalized in M cells nondestructively.
58 This is followed by the induction of host T-cell-mediated
immunity, which is further described in Chapter 25. Polymorphonuclear neutrophils (PMNs) lyse
Listeria-infected parenchymal cells and thus expose the bacteria to professional phagocytes. The
PMNs contain superoxide anions, proteolytic enzymes, and other factors. When PMNs interact with
L. monocytogenes, they show increases in cytokines such as interleukin-Iβ, interleukin-6 (IL-6),
and tumor necrosis factor (TNF).
91 Once listeriae are phagocytized, the cells escape by lysing the
vacuolar membrane with the aid of LLO, move about the cytosol by actin filaments, and then spread
to neighboring cells where the process is repeated. Although virulent strains contain other substances
that may contribute to virulence, what sets this species apart from the nonpathogenic Listeria is the
capacity to adhere to and breach the mucosal/epithelial barrier, and to spread from cell to cell with the
aid of LLO. It may be postulated that these virulence factors in listeriae were acquired independently,
probably from other Gram-positive bacteria that produce thiol-activated toxins.
Gram-Negative Bacteria
The pathogenesis and virulence properties of this group are considerably different and far more
complex than for Gram-positive bacteria. Great effort was devoted to finding enterotoxins for most,
and while these pursuits were successful for some, the significance of the enterotoxins in foodborne
pathogenesis seems questionable. The findings on some of these organisms during the past two decades
or so are summarized below.
Salmonellae
It is estimated that Salmonella and Escherichia arose from a common ancestor about 120–160 million
years ago.
39 All S. enterica serovars carry pathogenicity islands 1 and 2 (SPI-1, SPI-2), which were
533
Listeria monocytogenes
Although Gram positive, this bacterium is significantly different from those noted above. The most
notable difference is that it is an intracellular pathogen. More specifically, it resides in the cytosol
where it replicates; and it apparently uses host-derived lipoic acid for its replication.
79 In order to
enter epithelial cells, the invasin internalin interacts with E-cadherin on human host cells (mouse
and rat E-cadherins are not receptors for internalin). The L. monocytogenes cells that lack internalin
are noninvasive
67 Although virulent strains produce the exocellular thiol-activated, pore-forming substance listeriolysin O (LLO), it does not per se cause the foodborne gastroenteritis syndrome. LLO
is a hemolysin involved in the invasion of the gut epithelium, and it contributes to the cell-to-cell
spread of the organism. Unlike the other syndromes above caused by Gram-positive bacteria (with the
exception of Clostridium perfringens), the ingestion of viable cells is necessary for listeric infection
to occur.
The PEST (P, pro.; E. glu.; S, ser.; T, thr.) sequence of LLO is essential for virulence and the
intracellular state of L. monocytogenes. This sequence induces host macrophages to degrade LLO
once it escapes from lysosomes. Mutants lacking the PEST sequence entered host cell cytosol and
killed the host cells.
33 LLO lacking PEST accumulated in the cytosol, suggesting that it targets LLO
for degradation.
33 In effect, PEST prevents LLO from prematurely destroying host cells.
Virulent strains of L. monocytogenes can breach the mucous barrier as noted above, and they then
enter epithelial cells, but just how is unclear. Also, gastrointestinal symptoms are seen in only around
one-third of human cases.
49 The body’s early defense against these organisms consists of resident
macrophages, especially the Kupffer cells of the liver.
91 They gain entry into these cells by being
internalized in M cells nondestructively.
58 This is followed by the induction of host T-cell-mediated
immunity, which is further described in Chapter 25. Polymorphonuclear neutrophils (PMNs) lyse
Listeria-infected parenchymal cells and thus expose the bacteria to professional phagocytes. The
PMNs contain superoxide anions, proteolytic enzymes, and other factors. When PMNs interact with
L. monocytogenes, they show increases in cytokines such as interleukin-Iβ, interleukin-6 (IL-6),
and tumor necrosis factor (TNF).
91 Once listeriae are phagocytized, the cells escape by lysing the
vacuolar membrane with the aid of LLO, move about the cytosol by actin filaments, and then spread
to neighboring cells where the process is repeated. Although virulent strains contain other substances
that may contribute to virulence, what sets this species apart from the nonpathogenic Listeria is the
capacity to adhere to and breach the mucosal/epithelial barrier, and to spread from cell to cell with the
aid of LLO. It may be postulated that these virulence factors in listeriae were acquired independently,
probably from other Gram-positive bacteria that produce thiol-activated toxins.
Gram-Negative Bacteria
The pathogenesis and virulence properties of this group are considerably different and far more
complex than for Gram-positive bacteria. Great effort was devoted to finding enterotoxins for most,
and while these pursuits were successful for some, the significance of the enterotoxins in foodborne
pathogenesis seems questionable. The findings on some of these organisms during the past two decades
or so are summarized below.
Salmonellae
It is estimated that Salmonella and Escherichia arose from a common ancestor about 120–160 million
years ago.
39 All S. enterica serovars carry pathogenicity islands 1 and 2 (SPI-1, SPI-2), which were