532 Modern Food Microbiology
Overall, the full significance of the acid tolerance response and other sigma factors in foodborne
bacterial infections is not fully understood. However, enough information has been presented for some
pathogens to suggest the need for more research in this area.
PATHOGENESIS
When one looks at the many different types of causative organisms, it should not be surprising
that there are many mechanisms that lead to the initiation and course of foodborne illness. The
flat- and roundworms are contracted by ingesting infected meat or fish, and upon entry into the
gastrointestinal (GI) tract, different paths are taken by these organisms, including passage to the liver,
to skeletal muscles, or simply remaining in the GI tract. The foodborne protozoa remain in the gut
with the notable exception of Toxoplasma gondii, which can cross the placental barrier and inflict
severe damage to a fetus. The phytoplankton toxins and mycotoxins are ingested preformed, and these
chemical compounds have affinities for specific tissue or cell targets (e.g., aflatoxins for DNA). The
pathogenic mechanisms of the foodborne bacteria are more involved, and they are discussed below.
Additional information on each group noted can be found in the respective chapters that follow. A
glossary of relevant terminology is presented in Exhibit 3.
Gram-Positive Bacteria
In general, Gram-positive pathogens produce exocellular substances that typically account for most,
if not all, of the virulence factors for this group and this is typified by Staphylococcus aureus. Virulent
strains are known to produce a number of exotoxic factors that are absent in avirulent strains. In the
case of the gastroenteritis syndrome presented in Chapter 23, the enterotoxins constitute the only
agents of importance. Regardless of the number and type of other extracellular products that may
be elaborated, enterotoxin-negative strains do not cause the gastroenteritis syndrome. What is known
about the mode of action of staphylococcal enterotoxins is presented in Chapter 23.
Like the gastroenteritis-causing strains of the staphylococci, foodborne diseases caused by Clostridium botulinum, C. perfringens, and Bacillus cereus are also due to exotoxins. The only toxin of importance in botulism is a potent neurotoxin, which is elaborated by cells growing in susceptible foods.
The C. perfringens enterotoxin (CPE) is a spore-associated protein that is produced during sporulation
of bacterial cells in the GI tract. The emetic toxin of B. cereus is an exotoxin, but the toxic components
that cause the diarrheal syndrome are not as well understood. More on what is known about the mode
of action of these toxins is presented in Chapter 24.
It was widely assumed for many decades that a bacterium causing foodborne gastroenteritis “must”
produce an enterotoxin in the manner of the staphylococci, and reasons for this view can be ascribed
to this bacterium as being the prototype of foodborne disease organisms. Also, with the exception
of neurotoxigenic strains of C. botulinum, S. aureus was the first foodborne pathogen whose mode
of pathogenicity was established. First studied by Denys in 1894 and next by Barber in 1914, who
produced in himself the symptoms of foodborne disease, it was proven conclusively by Dack et al.
in 1930
29 when they showed that all symptoms of the disease could be produced by feeding a culture filtrate of S. aureus (to volunteer graduate students at that time!). This neat and crisp prototype
has been sought for all foodborne pathogens and, in a sense, led to what in retrospect appears to
have been undue efforts to find an enterotoxin in all foodborne pathogens, including the Gram negatives.
Overall, the full significance of the acid tolerance response and other sigma factors in foodborne
bacterial infections is not fully understood. However, enough information has been presented for some
pathogens to suggest the need for more research in this area.
PATHOGENESIS
When one looks at the many different types of causative organisms, it should not be surprising
that there are many mechanisms that lead to the initiation and course of foodborne illness. The
flat- and roundworms are contracted by ingesting infected meat or fish, and upon entry into the
gastrointestinal (GI) tract, different paths are taken by these organisms, including passage to the liver,
to skeletal muscles, or simply remaining in the GI tract. The foodborne protozoa remain in the gut
with the notable exception of Toxoplasma gondii, which can cross the placental barrier and inflict
severe damage to a fetus. The phytoplankton toxins and mycotoxins are ingested preformed, and these
chemical compounds have affinities for specific tissue or cell targets (e.g., aflatoxins for DNA). The
pathogenic mechanisms of the foodborne bacteria are more involved, and they are discussed below.
Additional information on each group noted can be found in the respective chapters that follow. A
glossary of relevant terminology is presented in Exhibit 3.
Gram-Positive Bacteria
In general, Gram-positive pathogens produce exocellular substances that typically account for most,
if not all, of the virulence factors for this group and this is typified by Staphylococcus aureus. Virulent
strains are known to produce a number of exotoxic factors that are absent in avirulent strains. In the
case of the gastroenteritis syndrome presented in Chapter 23, the enterotoxins constitute the only
agents of importance. Regardless of the number and type of other extracellular products that may
be elaborated, enterotoxin-negative strains do not cause the gastroenteritis syndrome. What is known
about the mode of action of staphylococcal enterotoxins is presented in Chapter 23.
Like the gastroenteritis-causing strains of the staphylococci, foodborne diseases caused by Clostridium botulinum, C. perfringens, and Bacillus cereus are also due to exotoxins. The only toxin of importance in botulism is a potent neurotoxin, which is elaborated by cells growing in susceptible foods.
The C. perfringens enterotoxin (CPE) is a spore-associated protein that is produced during sporulation
of bacterial cells in the GI tract. The emetic toxin of B. cereus is an exotoxin, but the toxic components
that cause the diarrheal syndrome are not as well understood. More on what is known about the mode
of action of these toxins is presented in Chapter 24.
It was widely assumed for many decades that a bacterium causing foodborne gastroenteritis “must”
produce an enterotoxin in the manner of the staphylococci, and reasons for this view can be ascribed
to this bacterium as being the prototype of foodborne disease organisms. Also, with the exception
of neurotoxigenic strains of C. botulinum, S. aureus was the first foodborne pathogen whose mode
of pathogenicity was established. First studied by Denys in 1894 and next by Barber in 1914, who
produced in himself the symptoms of foodborne disease, it was proven conclusively by Dack et al.
in 1930
29 when they showed that all symptoms of the disease could be produced by feeding a culture filtrate of S. aureus (to volunteer graduate students at that time!). This neat and crisp prototype
has been sought for all foodborne pathogens and, in a sense, led to what in retrospect appears to
have been undue efforts to find an enterotoxin in all foodborne pathogens, including the Gram negatives.