Vibrio parahaemolyticus is part of the normal flora of estuarine and
other coastal areas throughout most of the world. The optimal temperature for
growth of V. parahaemolyticus is 37°C, although it will grow well at
25-44°C (Blake et al., 1980).
In most areas, bacterial densities increase during the warmer months, and as
a result, most outbreaks of V. parahaemolyticus illness in the U.S. occur
during the summer (Watkins and Cabelli, 1985). Seasonal variation of V.
parahaemolyticus in the Gulf of Mexico is not as evident. Studies which
investigated V. parahaemolyticus levels in Galveston Bay blue crabs
(Davis and Sizemore, 1980) and Louisiana oysters (Paille et al., 1987) showed
increased concentrations during the summer months. However, seasonal variation
was not observed in V. parahaemolyticus levels in Galveston Bay oysters
(Thompson and Vanderzant, 1976a).
Pathogenic strains of V. parahaemolyticus cause hemolysis on Wagatsuma
agar (the Kanagawa phenomenon). It has been reported that over 95% of the
isolates from individuals with gastroenteritis are hemolytic, or Kanagawa
positive (Joseph et al., 1983, as cited in Morris and Black, 1985). However,
only 0.18% (Thompson and Vanderzant, 1976b) to 1% (Joseph et al., 1983, as cited
in Morris and Black, 1985) of the environmental isolates are K+. A number of
theories have been suggested to explain the greater proportion of K+ strains
from gastroenteritis isolates than from environmental isolates. It is possible
that the present isolation methods do not favor the detection of K+ strains, and
are therefore underestimating the number of hemolytic strains in the environment
(Hackney et al., 1980). It has been suggested that a small number of pathogenic
strains exist in the environment among a large number of nonpathogenic strains
(Nolan et al., 1984; Thompson and Vanderzant, 1976b). However, a study which
investigated the survival patterns of K- and K+ strains of V.
parahaemolyticus in the environment found no selective advantage of K-
strains in the natural environment (Karunasagar et al., 1987). And finally, the
organisms may acquire the hemolysin(s) in the intestinal tract of humans
(Thompson and Vanderzant, 1976b). However, studies in which human volunteers
ingested K- strains of V. parahaemolyticus did not become ill with
gastroenteritis (Senyal and Sen, 1974, as cited in Thompson and Vanderzant,
The generation time of V. parahaemolyticus has been reported to be as
short as nine minutes under ideal conditions (Katoh, 1965, as cited in Blake et
al., 1980). Barker (1974, as cited in Bachman et al., 1983) calculated that at
this rapid rate of replication, 10 bacteria would lead to 1 million bacteria
within 3 to 4 hours.
V. parahaemolyticus illness has been associated with consuming
contaminated crabs, oysters, shrimp and lobster (Thompson and Vanderzant,
1976a). One outbreak of V. parahaemolyticus gastroenteritis was traced to
depurated oysters (Barrow and Miller, 1969, as cited in Richards, 1988),
supporting the laboratory evidence that vibrio bacteria do not depurate well
(Eyles and Davey, 1984).
V. parahaemolyticus has been isolated from the Atlantic (Watkins and
Cabelli, 1985; Hackney, et al., 1980), Pacific (Nolan et al., 1984) and Gulf
Coasts (Thompson and Vanderzant, 1976a).
Symptoms & Treatment
Gastroenteritis caused by V. parahaemolyticus is generally mild to
moderate in severity. The onset of symptoms is usually within 4 to 96 hours of
consuming contaminated seafood (Morris and Black, 1985). The most commonly
experienced symptoms include: diarrhea, abdominal cramps, nausea, vomiting and
headache. Fever and chills are less frequently reported (Bryan, 1987; Morris and
Black, 1985; Blake et al., 1980). Gastroenteritis caused by V.
parahaemolyticus is usually a self-limited illness, lasting a median of 3
days (Morris and Black, 1985).
Vibrio parahaemolyticus can also cause septicemia, and ear and wound
infections (Blake et al., 1980). The one reported case of septicemia involved an
individual who had a preexisting immunocompromising disease (cirrhosis).
V. parahaemolyticus was first recognized as pathogen in Japan in the
early 1950's (Blake et al., 1980). In 1969, there were several unconfirmed
outbreaks of gastroenteritis in the U.S. that were thought to be caused by V.
parahaemolyticus (USDHEW, 1969, as cited in Thompson and Vanderzant, 1976a).
From 1977 to 1981 there were nine outbreaks of seafood-borne V.
parahaemolyticus illness reported to the CDC (USFDA, 1984).
Detection & Protection
Traditional indicator species do not accurately detect the presence of V.
parahaemolyticus, since it is a naturally occurring bacterium (Hackney et
al., 1980; Thompson and Vanderzant, 1976a). Illness can be prevented by
thoroughly cooking shellfish and by bandaging open wounds to prevent exposure to
Vibrio vulnificus, originally thought to be V.
parahaemolyticus, is a naturally occurring, lactose fermenting bacterium. It
requires salt and is commonly isolated at salinities of 7-16 ppt (Kelly, 1982).
Sampling in the Gulf of Mexico showed that the organism is seldom found in water
temperature <25°C, and that the incidence of recovery increases steadily as
water temperatures rise. Highest densities in the Gulf are found after water
temperatures exceed 25°C for several months. Laboratory studies demonstrate an
optimal growth temperature of 37°C (Kelly, 1982).
Cases of V. vulnificus sepsis have been associated with the
consumption of oysters and blue crabs (Blake et al., 1980).
Vibrio vulnificus is primarily found in the Gulf of Mexico (Kelly,
1982), but has also been isolated from the Atlantic (Oliver et al., 1983, as
cited in O'Neill et al., in press) and Pacific Oceans (Kaysner et al., 1987, as
cited in O'Neill et al., in press). In the Gulf, cell densities are highest
during the warmer months, usually April through October (Blake, 1983; Kelly,
1982). The organism has been recovered from shellfish harvested as far north as
Maine (O'Neill, et al., in press).
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