Foodborne Gastroenteritis Caused by Vibrio, Yersinia, and Campylobacter Species 663
highest numbers of both 01 and non-01 strains occurred in August and November.
38 Neither the fecal
coliform nor the total coliform index was an adequate indicator of the presence of V. cholerae, but the
former was more useful than the latter. Along the Santa Cruz coast of, California, the highest numbers
of non-01 strains occurred during the summer months and were associated with high coliform counts.
70
Both 01 and non-01 strains have been recovered from aquatic birds in Colorado,
96 and both types have
been shown to be endemic in the Texas gulf as evidenced by antibody titers in human subjects.
59
V. cholerae 01 El Tor synthesizes a 82-kDa preprotoxin and secretes it into culture media, where
it is further processed into a 65-kDa active cytolysin.
139 Non-01 strains produce a cytotoxin and a
hemolysin with a molecular weight of 60 kDa, which is immunologically related to the hemolysin of
the El Tor strain. The OmpU outer membrane protein has been shown to be an adherence factor of
V. cholerae, which may facilitate adherence to small intestines. Monoclonal antibodies raised to OmpU
protected HeLa, HEp-2, Caco-2, and Henle 407 epithelial cells from invasion by viable organisms.
118
From a patient with travelers’ diarrhea a strain of 01 was isolated from which the STa (NAG-STa)
gene was cloned.
95 The NAG-STa was chromosomal, and the toxin had a molecular weight of 8815.
The NAG-STa shared 50% and 46% homology to E. coli STh and STp, respectively.
95 NAG-ST is
methanol soluble, active in the infant mouse model, and similar to the ST of Citrobacter freundii.
126
Monoclonal antibodies to NAG-ST cross-react with the ST of Yersinia enterocolitica. Further,
V. mimicus ST and Y. enterocolitica ST are neutralized by monoclonal antibodies to NAG-ST but not
E. coli STh or STp.
126
In a study of the survival of V. cholerae El Tor serotype Inaba in several foods, it was found that
in meats with an inoculum of 2 × 10
3 /g, cells remained viable for up to 90 days at −5
◦ C and for up
to 300 days at −25
◦ C.
36 The organism was not detected in milk after 34 days at −5
◦ C and 150 days
at −25
◦ C with an inoculum of 2 × 10
4 /ml. In milk at 7
◦ C, it survived 32 days on average but only
18–20 days in other foods. The virulence mechanisms of V. cholerae are discussed in Chapter 22.
Vibrio vulnificus
This organism is found in seawater and some seafoods. It is isolated more often from oysters and
clams than from crustacean shellfish products. It has been isolated from seawater from the coast of
Miami, Florida, to Cape Cod, Massachusetts, with most (84%) isolated from clams. Upon injection into
mice, 82% of tested strains were lethal. V. vulnificus, along with other vibrios, have been recovered from
mussels, clams, and oysters in Hong Kong at rates between 6% and 9%.
34 In a study of the estuarine
waters of eastern North Carolina, V. vulnificus was isolated only when the water temperatures were
between 15
◦ C and 22
◦ C.
103
Following the warm summer of 1994 in Denmark during which 11 clinical cases of V. vulnificus
were reported, a study was undertaken to determine the prevalence of the organism in Danish waters.
56
Upon testing suspect colonies with a DNA probe, from 0.8 to 19 colony-forming units (cfu) per liter
were found in water between June and mid-September, and 0.04 to >11 cfu/g in sediment samples
from July to mid-November. A strong correlation was found between the presence of V. vulnificus and
water temperature. The organism was found in 7 of 17 mussels examined from 1 of 13 locations, and
also from wild fish. Biotype 1 constituted 99.6% of 706 V. vulnificus isolates.
56 Like V. alginolyticus
(see below), V. vulnificus causes soft-tissue infections and primary septicemia in humans, especially in
the immunocompromised and those with cirrhosis. The fatality rate for those with septicemia is more
than 50%, and more than 90% among those who become hypotensive.
139 These organisms are highly
invasive, and they produce a cytotoxin with a molecular weight of about 56 kDa that is toxic to CHO
cells and lytic to erythrocytes. However, the cytolysin appears not to be a critical virulence factor.
137
highest numbers of both 01 and non-01 strains occurred in August and November.
38 Neither the fecal
coliform nor the total coliform index was an adequate indicator of the presence of V. cholerae, but the
former was more useful than the latter. Along the Santa Cruz coast of, California, the highest numbers
of non-01 strains occurred during the summer months and were associated with high coliform counts.
70
Both 01 and non-01 strains have been recovered from aquatic birds in Colorado,
96 and both types have
been shown to be endemic in the Texas gulf as evidenced by antibody titers in human subjects.
59
V. cholerae 01 El Tor synthesizes a 82-kDa preprotoxin and secretes it into culture media, where
it is further processed into a 65-kDa active cytolysin.
139 Non-01 strains produce a cytotoxin and a
hemolysin with a molecular weight of 60 kDa, which is immunologically related to the hemolysin of
the El Tor strain. The OmpU outer membrane protein has been shown to be an adherence factor of
V. cholerae, which may facilitate adherence to small intestines. Monoclonal antibodies raised to OmpU
protected HeLa, HEp-2, Caco-2, and Henle 407 epithelial cells from invasion by viable organisms.
118
From a patient with travelers’ diarrhea a strain of 01 was isolated from which the STa (NAG-STa)
gene was cloned.
95 The NAG-STa was chromosomal, and the toxin had a molecular weight of 8815.
The NAG-STa shared 50% and 46% homology to E. coli STh and STp, respectively.
95 NAG-ST is
methanol soluble, active in the infant mouse model, and similar to the ST of Citrobacter freundii.
126
Monoclonal antibodies to NAG-ST cross-react with the ST of Yersinia enterocolitica. Further,
V. mimicus ST and Y. enterocolitica ST are neutralized by monoclonal antibodies to NAG-ST but not
E. coli STh or STp.
126
In a study of the survival of V. cholerae El Tor serotype Inaba in several foods, it was found that
in meats with an inoculum of 2 × 10
3 /g, cells remained viable for up to 90 days at −5
◦ C and for up
to 300 days at −25
◦ C.
36 The organism was not detected in milk after 34 days at −5
◦ C and 150 days
at −25
◦ C with an inoculum of 2 × 10
4 /ml. In milk at 7
◦ C, it survived 32 days on average but only
18–20 days in other foods. The virulence mechanisms of V. cholerae are discussed in Chapter 22.
Vibrio vulnificus
This organism is found in seawater and some seafoods. It is isolated more often from oysters and
clams than from crustacean shellfish products. It has been isolated from seawater from the coast of
Miami, Florida, to Cape Cod, Massachusetts, with most (84%) isolated from clams. Upon injection into
mice, 82% of tested strains were lethal. V. vulnificus, along with other vibrios, have been recovered from
mussels, clams, and oysters in Hong Kong at rates between 6% and 9%.
34 In a study of the estuarine
waters of eastern North Carolina, V. vulnificus was isolated only when the water temperatures were
between 15
◦ C and 22
◦ C.
103
Following the warm summer of 1994 in Denmark during which 11 clinical cases of V. vulnificus
were reported, a study was undertaken to determine the prevalence of the organism in Danish waters.
56
Upon testing suspect colonies with a DNA probe, from 0.8 to 19 colony-forming units (cfu) per liter
were found in water between June and mid-September, and 0.04 to >11 cfu/g in sediment samples
from July to mid-November. A strong correlation was found between the presence of V. vulnificus and
water temperature. The organism was found in 7 of 17 mussels examined from 1 of 13 locations, and
also from wild fish. Biotype 1 constituted 99.6% of 706 V. vulnificus isolates.
56 Like V. alginolyticus
(see below), V. vulnificus causes soft-tissue infections and primary septicemia in humans, especially in
the immunocompromised and those with cirrhosis. The fatality rate for those with septicemia is more
than 50%, and more than 90% among those who become hypotensive.
139 These organisms are highly
invasive, and they produce a cytotoxin with a molecular weight of about 56 kDa that is toxic to CHO
cells and lytic to erythrocytes. However, the cytolysin appears not to be a critical virulence factor.
137