534 Modern Food Microbiology
acquired via horizontal transfer either by plasmids or phages.
8 In S. Typhimurium, at least 60 genes
are required for virulence,
52 and the two SPIs are known to contain at least 42 of these genes. By
comparison of the 16S and 23S rRNA sequence data, the salmonellae have been shown to be closely
related to E. coli and shigellae, with the monophasic salmonellae serovars being adapted to mammals
and the diphasic to reptiles.
21 Regarding their evolution, up to 35 kilobases (kb) of the DNA that
encompasses the SPI region of Salmonella at centisome 63 may have been acquired as a block
from another microorganism as they evolved toward becoming pathogens.
48 This is supported by
the observation that S. enterica and E. coli contain a high incidence of mutator phenotypes that lead
to increased mutation rates and enhanced recombination among the diverse species.
70
A 29-kDa polypeptide enterotoxin has been demonstrated in S. Typhimurium that has the following
features: it cross-reacts with cholera toxin, it activates adenylate cyclase, its preferred host cell receptor
is ganglioside GM 1 , and it is positive in the ileal loop test.
75 This suggests that the toxins could play a
role in causing the diarrheal part of the salmonellae syndrome, but their role in intracellular invasion
and the subsequent pathogenesis is unclear. Production of other cytotoxic proteins has also been
reported in nontyphoid salmonellae.
28
Virulent strains of S. enterica initiate infection in nonphagocytic cells by attaching to the intestinal
mucosa with the aid of fimbrial adhesins encoded by a gene on SPI-1.
96 This is followed by the penetration of the intestinal mucosa, mainly at the lymphoid follicles of Peyer’s patches. Their initial site of
infection is the ileum of the small intestine. Once inside, they invade the M cells of Peyer’s patches
60
From the vesicles of these cells, they enter the lysosome. Virulent strains of S. enterica secrete into
the cytoplasm a protein (SpiC) that prevents the fusion of vesicles with lysosomes. S. Typhimurium
contains fimbriae that selectively adhere to M cells, and although they can enter any intestinal epithelial cell type, M cells are preferred. Their entry into nonphagocytic cells is aided by a type III
(also known as “contact”) secretion system. As Gal´ an
48 has noted, this entry mechanism involves
a rather intimate interaction between the bacterium and host cells that results in “cross-talk.” As a
consequence, cytoskeletal rearrangements, membrane ruffling, and bacterial uptake by macropinocytosis take place. The migration of neutrophils across the epithelial cells occurs and cytokines (e.g.,
interleukin-8) are produced. Once inside these cells, they remain inside membrane-bound vacuoles
during their entire intracellular stage.
84 Following multiplication, the cells ultimately burst and the
pathogen is spread. The entry of salmonellae into macrophages is accompanied also by membrane
ruffling and macropinocytosis.
84 Once inside, they are found inside the membrane-bound phagosomes,
which become enlarged. Salmonella Typhimurium induces apoptosis in macrophages. For a review of
Salmonellae Enteritis, see reference 99.
The nontyphoid salmonellae serovars differ in their degree of human pathogenicity with S. Pullorum
and S. Gallinarium being among the least pathogenic, and S. Choleraesuis, S. Dublin, and S. Enteritidis
being the most pathogenic. Salmonella serovar Choleraesuis is isolated from blood more often than
from stools of victims, and it, along with Salmonella serovar Dublin, is associated with higher mortality
than other serovars.
87 In the case of S. Choleraesuis, intestinal involvement and excretion are rare but
septicemia is common. In one study of 19 cases of salmonellosis caused by this serovar, all victims had
septicemia.
3 Just what sets these serovars apart from the more commonly occurring S. Typhimurium
relative to the locus of enterocyte effacement (LEE) and secretion system is unclear.
Escherichia coli
The disease-causing strains of this organism are placed in 5–6 virulence or pathogenicity groups and
they are discussed in Chapter 27. The two groups discussed here are enteropathogenic (EPEC) and
enterohemorrhagic (EHEC).
acquired via horizontal transfer either by plasmids or phages.
8 In S. Typhimurium, at least 60 genes
are required for virulence,
52 and the two SPIs are known to contain at least 42 of these genes. By
comparison of the 16S and 23S rRNA sequence data, the salmonellae have been shown to be closely
related to E. coli and shigellae, with the monophasic salmonellae serovars being adapted to mammals
and the diphasic to reptiles.
21 Regarding their evolution, up to 35 kilobases (kb) of the DNA that
encompasses the SPI region of Salmonella at centisome 63 may have been acquired as a block
from another microorganism as they evolved toward becoming pathogens.
48 This is supported by
the observation that S. enterica and E. coli contain a high incidence of mutator phenotypes that lead
to increased mutation rates and enhanced recombination among the diverse species.
70
A 29-kDa polypeptide enterotoxin has been demonstrated in S. Typhimurium that has the following
features: it cross-reacts with cholera toxin, it activates adenylate cyclase, its preferred host cell receptor
is ganglioside GM 1 , and it is positive in the ileal loop test.
75 This suggests that the toxins could play a
role in causing the diarrheal part of the salmonellae syndrome, but their role in intracellular invasion
and the subsequent pathogenesis is unclear. Production of other cytotoxic proteins has also been
reported in nontyphoid salmonellae.
28
Virulent strains of S. enterica initiate infection in nonphagocytic cells by attaching to the intestinal
mucosa with the aid of fimbrial adhesins encoded by a gene on SPI-1.
96 This is followed by the penetration of the intestinal mucosa, mainly at the lymphoid follicles of Peyer’s patches. Their initial site of
infection is the ileum of the small intestine. Once inside, they invade the M cells of Peyer’s patches
60
From the vesicles of these cells, they enter the lysosome. Virulent strains of S. enterica secrete into
the cytoplasm a protein (SpiC) that prevents the fusion of vesicles with lysosomes. S. Typhimurium
contains fimbriae that selectively adhere to M cells, and although they can enter any intestinal epithelial cell type, M cells are preferred. Their entry into nonphagocytic cells is aided by a type III
(also known as “contact”) secretion system. As Gal´ an
48 has noted, this entry mechanism involves
a rather intimate interaction between the bacterium and host cells that results in “cross-talk.” As a
consequence, cytoskeletal rearrangements, membrane ruffling, and bacterial uptake by macropinocytosis take place. The migration of neutrophils across the epithelial cells occurs and cytokines (e.g.,
interleukin-8) are produced. Once inside these cells, they remain inside membrane-bound vacuoles
during their entire intracellular stage.
84 Following multiplication, the cells ultimately burst and the
pathogen is spread. The entry of salmonellae into macrophages is accompanied also by membrane
ruffling and macropinocytosis.
84 Once inside, they are found inside the membrane-bound phagosomes,
which become enlarged. Salmonella Typhimurium induces apoptosis in macrophages. For a review of
Salmonellae Enteritis, see reference 99.
The nontyphoid salmonellae serovars differ in their degree of human pathogenicity with S. Pullorum
and S. Gallinarium being among the least pathogenic, and S. Choleraesuis, S. Dublin, and S. Enteritidis
being the most pathogenic. Salmonella serovar Choleraesuis is isolated from blood more often than
from stools of victims, and it, along with Salmonella serovar Dublin, is associated with higher mortality
than other serovars.
87 In the case of S. Choleraesuis, intestinal involvement and excretion are rare but
septicemia is common. In one study of 19 cases of salmonellosis caused by this serovar, all victims had
septicemia.
3 Just what sets these serovars apart from the more commonly occurring S. Typhimurium
relative to the locus of enterocyte effacement (LEE) and secretion system is unclear.
Escherichia coli
The disease-causing strains of this organism are placed in 5–6 virulence or pathogenicity groups and
they are discussed in Chapter 27. The two groups discussed here are enteropathogenic (EPEC) and
enterohemorrhagic (EHEC).