Foodborne Gastroenteritis Caused by Vibrio, Yersinia, and Campylobacter Species 671
and the finding that C. jejuni can penetrate HeLa cells.
80 However, C. jejuni is not invasive by either
the Sereny or the Anton assay.
Caco-2 cells are invaded by an energy-dependent invasion mechanism, not by endocytosis.
109 Several sequelae are associated with campylobacteriosis, including Guillain–Barr´ e syndrome (GBS: for a
review, see reference 116). It is estimated that about one-third of patients with GBS develop symptoms
1–3 weeks after C. jejuni enteritis. In the Penner serotyping scheme, over 48 serotypes of C. jejuni
are recognized, and serotype 19 is one that appears to be associated with GBS. This strain has an
oligosaccharide structure that is identical to the terminal tetrasaccharide of host ganglioside GM 1 .
Because the gangliosides are surface components of nerve tissue, antibodies to the oligosaccharide
structure of C. jejuni would exhibit antineural effects.
142
Plasmids have been demonstrated in C. jejuni cells. Of 17 strains studied, 11 were found to carry
plasmids ranging from 1.6 to 70 MDa, but their role and function in disease are unclear.
A serotyping scheme has been developed for C. jejuni. From chickens and humans, 82% and 98%,
respectively, of isolates belonged to biovar 1.
113
Overall, the specific modes of Campylobacter pathogenesis are still unclear. In one review, it is
noted that motility and invasion play a role in pathogenesis, and that the roles of the toxins are far
from clear.
71
Enteritis Syndrome and Prevalence
From the first U.S. outbreak of C. jejuni traced to a water supply,
29 in which about 2,000 individuals
contracted infections, the symptoms (and percentages of individuals affected) were as follows: abdominal pain or cramps (88), diarrhea (83), malaise (76), headache (54), and fever (52). Symptoms lasted
from 1 to 4 days. In the more severe cases, bloody stools may occur, and the diarrhea may resemble
ulcerative colitis, whereas the abdominal pain may mimic acute appendicitis.
15 The incubation period
for enteritis is highly variable. It is usually 48–82 hours but may be as long as 7–10 days or more.
Diarrhea may last 2–7 days, and the organisms may be shed for more than 2 months after symptoms
subside.
Clinical laboratory isolates of Campylobacter in the United States for 1996–1998 exceeded
salmonellae isolates (Figure 28–1). The isolates were from clinical laboratories in selected cities
of five states This is the FoodNet Surveillance Network
24 described in Chapter 22. It should be noted
that the numbers do not represent isolations from actual foodborne illness. It is assumed that the organisms noted were contracted from foods even though this connection is not demonstrated. In the case of
Campylobacter, it is assumed that about 90% are of food origin. While this surveillance method might
be a valid indicator of actual foodborne cases, it is unprecedented. It is unusual that such a fragile and
environmentally sensitive organism should be the leading cause of foodborne illness. It is interesting
to note that the largest recorded outbreak of Campylobacter enteritis, as noted above, was traced to
the water supply of a Vermont town where about 2,000 persons were infected.
29
PREVENTION
V. parahaemolyticus, Y. enterocolitica, and C. jejuni are all heat-sensitive bacteria that are destroyed
by milk pasteurization temperatures. The avoidance of raw seafood products and care in preventing
cross-contamination with contaminated raw materials will eliminate or drastically reduce the incidence
of foodborne gastroenteritis caused by V. parahaemolyticus and Y. enterocolitica. To prevent wound
and the finding that C. jejuni can penetrate HeLa cells.
80 However, C. jejuni is not invasive by either
the Sereny or the Anton assay.
Caco-2 cells are invaded by an energy-dependent invasion mechanism, not by endocytosis.
109 Several sequelae are associated with campylobacteriosis, including Guillain–Barr´ e syndrome (GBS: for a
review, see reference 116). It is estimated that about one-third of patients with GBS develop symptoms
1–3 weeks after C. jejuni enteritis. In the Penner serotyping scheme, over 48 serotypes of C. jejuni
are recognized, and serotype 19 is one that appears to be associated with GBS. This strain has an
oligosaccharide structure that is identical to the terminal tetrasaccharide of host ganglioside GM 1 .
Because the gangliosides are surface components of nerve tissue, antibodies to the oligosaccharide
structure of C. jejuni would exhibit antineural effects.
142
Plasmids have been demonstrated in C. jejuni cells. Of 17 strains studied, 11 were found to carry
plasmids ranging from 1.6 to 70 MDa, but their role and function in disease are unclear.
A serotyping scheme has been developed for C. jejuni. From chickens and humans, 82% and 98%,
respectively, of isolates belonged to biovar 1.
113
Overall, the specific modes of Campylobacter pathogenesis are still unclear. In one review, it is
noted that motility and invasion play a role in pathogenesis, and that the roles of the toxins are far
from clear.
71
Enteritis Syndrome and Prevalence
From the first U.S. outbreak of C. jejuni traced to a water supply,
29 in which about 2,000 individuals
contracted infections, the symptoms (and percentages of individuals affected) were as follows: abdominal pain or cramps (88), diarrhea (83), malaise (76), headache (54), and fever (52). Symptoms lasted
from 1 to 4 days. In the more severe cases, bloody stools may occur, and the diarrhea may resemble
ulcerative colitis, whereas the abdominal pain may mimic acute appendicitis.
15 The incubation period
for enteritis is highly variable. It is usually 48–82 hours but may be as long as 7–10 days or more.
Diarrhea may last 2–7 days, and the organisms may be shed for more than 2 months after symptoms
subside.
Clinical laboratory isolates of Campylobacter in the United States for 1996–1998 exceeded
salmonellae isolates (Figure 28–1). The isolates were from clinical laboratories in selected cities
of five states This is the FoodNet Surveillance Network
24 described in Chapter 22. It should be noted
that the numbers do not represent isolations from actual foodborne illness. It is assumed that the organisms noted were contracted from foods even though this connection is not demonstrated. In the case of
Campylobacter, it is assumed that about 90% are of food origin. While this surveillance method might
be a valid indicator of actual foodborne cases, it is unprecedented. It is unusual that such a fragile and
environmentally sensitive organism should be the leading cause of foodborne illness. It is interesting
to note that the largest recorded outbreak of Campylobacter enteritis, as noted above, was traced to
the water supply of a Vermont town where about 2,000 persons were infected.
29
PREVENTION
V. parahaemolyticus, Y. enterocolitica, and C. jejuni are all heat-sensitive bacteria that are destroyed
by milk pasteurization temperatures. The avoidance of raw seafood products and care in preventing
cross-contamination with contaminated raw materials will eliminate or drastically reduce the incidence
of foodborne gastroenteritis caused by V. parahaemolyticus and Y. enterocolitica. To prevent wound