524 Modern Food Microbiology
2. It needs to attach to or colonize the intestinal walls in such way that it can increase in numbers.
The mucus layer that covers the intestinal mucosa is regarded as being the first line of defense
encountered by enteric pathogens.
24 But, in the case of Listeria monocytogenes, it has been
suggested that it overcomes the mucus barrier by removing mucus through the aid of listeriolysin
O (LLO).
24 With a pathogen such as C. perfringens, it appears that it does not need to attach to
intestinal tissues.
3. It must possess the capacity to defend itself against host defense mechanisms such as gutassociated lymphoid tissue.
4. It must be able to compete with the large heterogeneous microbiota of the gut. This is the gist of
competitive exclusion in that the harmless biota, once attached to all available sites on the intestinal walls, will exclude pathogens (see Chapter 26). Also, the gastrointestinal tract is a low-O 2 environment where the predominant organisms are anaerobes, but it has been observed that growth
of S. Typhimurium in such environments actually induces its ability to enter mammalian cells.
60
5. Once attached, the organisms need to be able to either elaborate toxic products (e.g., Vibrio
cholerae non-01) or cross the epithelial wall and enter phagocytic or somatic cells (e.g., L.
monocytogenes).
The inability of most microorganisms to meet the above requirements in all probability is the reason
why they have not been demonstrated to be foodborne pathogens. The attachment sites and mechanisms
are important virulence factors for foodborne pathogens, and this aspect is discussed further below.
Attachment Sites
A diagram of the human digestive system is presented in Figure 22–3, and a list of pathogens that can
adhere to or enter at each site is presented in Exhibit 22–2. Helicobacter is listed since it is apparently
the only bacterium that colonizes stomach walls. The obligate anaerobe, Sarcina ventriculi, is known
to grow in the human stomach but it is not a foodborne pathogen. Whether H. pylori is a foodborne
pathogen is yet to be proven. The pH of the stomach during food intake is in the 3.0–5.0 range but it
may be as low as 1.5 during fasting.
QUORUM SENSING
This is one of the demonstrated means by which cell-to-cell communication occurs between bacteria. It allows for the expression of certain physiologic and phenotypic functions based on population
density, and it is more fully described and illustrated below. It is presented here because of its demonstrated occurrence in the virulence of some bacteria, and its apparent involvement in other infections.
The prototype system for quorum sensing is LuxI-LuxR, first described in Vibrio fisheri around
1970 (lux = luminescence gene). How quorum sensing works is depicted in Figure 22–4.
35 On the
left side of Figure 22–4 is a V. fischeri cell that is secreting autoinducer (AI) molecules made by LuxI
autoinducer synthase. With low cell numbers, the AI continues to be produced with no evidence of
cell-to-cell communication in effect. After a certain high level (a quorum) is attained, AI re-enters
the producing and closely related cells. As the AI reenters, it binds to the LuxR protein, which is a
transcriptional activator, on the right side of Figure 22–4, and gene expression is activated. Some of
the phenotypic expressions that have been demonstrated to occur in various organisms are listed in
Table 22–1. If the cell on the left side of Figure 22–4 is assumed to be V. fischeri, it is non-luminescent
2. It needs to attach to or colonize the intestinal walls in such way that it can increase in numbers.
The mucus layer that covers the intestinal mucosa is regarded as being the first line of defense
encountered by enteric pathogens.
24 But, in the case of Listeria monocytogenes, it has been
suggested that it overcomes the mucus barrier by removing mucus through the aid of listeriolysin
O (LLO).
24 With a pathogen such as C. perfringens, it appears that it does not need to attach to
intestinal tissues.
3. It must possess the capacity to defend itself against host defense mechanisms such as gutassociated lymphoid tissue.
4. It must be able to compete with the large heterogeneous microbiota of the gut. This is the gist of
competitive exclusion in that the harmless biota, once attached to all available sites on the intestinal walls, will exclude pathogens (see Chapter 26). Also, the gastrointestinal tract is a low-O 2 environment where the predominant organisms are anaerobes, but it has been observed that growth
of S. Typhimurium in such environments actually induces its ability to enter mammalian cells.
60
5. Once attached, the organisms need to be able to either elaborate toxic products (e.g., Vibrio
cholerae non-01) or cross the epithelial wall and enter phagocytic or somatic cells (e.g., L.
monocytogenes).
The inability of most microorganisms to meet the above requirements in all probability is the reason
why they have not been demonstrated to be foodborne pathogens. The attachment sites and mechanisms
are important virulence factors for foodborne pathogens, and this aspect is discussed further below.
Attachment Sites
A diagram of the human digestive system is presented in Figure 22–3, and a list of pathogens that can
adhere to or enter at each site is presented in Exhibit 22–2. Helicobacter is listed since it is apparently
the only bacterium that colonizes stomach walls. The obligate anaerobe, Sarcina ventriculi, is known
to grow in the human stomach but it is not a foodborne pathogen. Whether H. pylori is a foodborne
pathogen is yet to be proven. The pH of the stomach during food intake is in the 3.0–5.0 range but it
may be as low as 1.5 during fasting.
QUORUM SENSING
This is one of the demonstrated means by which cell-to-cell communication occurs between bacteria. It allows for the expression of certain physiologic and phenotypic functions based on population
density, and it is more fully described and illustrated below. It is presented here because of its demonstrated occurrence in the virulence of some bacteria, and its apparent involvement in other infections.
The prototype system for quorum sensing is LuxI-LuxR, first described in Vibrio fisheri around
1970 (lux = luminescence gene). How quorum sensing works is depicted in Figure 22–4.
35 On the
left side of Figure 22–4 is a V. fischeri cell that is secreting autoinducer (AI) molecules made by LuxI
autoinducer synthase. With low cell numbers, the AI continues to be produced with no evidence of
cell-to-cell communication in effect. After a certain high level (a quorum) is attained, AI re-enters
the producing and closely related cells. As the AI reenters, it binds to the LuxR protein, which is a
transcriptional activator, on the right side of Figure 22–4, and gene expression is activated. Some of
the phenotypic expressions that have been demonstrated to occur in various organisms are listed in
Table 22–1. If the cell on the left side of Figure 22–4 is assumed to be V. fischeri, it is non-luminescent