Vibrio vulnificus (page 2)
(This chapter has 3 pages)
© Kenneth Todar, PhD
Wound infections result from contaminating an existing open wound
seawater harboring the organism, or by cutting part of the body on
fish, fishhooks, etc., followed by contamination with the organism.
Also, people who consume foods contaminated with this organism are
to gastroenteritis, which usually develops within 16 hours of eating
contaminated food. They experience vomiting, diarrhea, and abdominal
Many patients develop distinctive bullous skin lesions.
The bacterium invades directly from the GI tract or broken skin to
bacteremia and septicemia. Invasion is characterized by the occurrence
of blister-like skin lesions or bullae, and rapidly-spreading necrosis
resembling necrotizing fasciitis.
skin lesions associated with Vibrio vulnificus infection on the
leg in a 75-year-old patient with liver cirrhosis in whom septic shock
and bacteremia developed. B V. vulnificus bacteremia developed
day after a fish bone injury on the fourth finger of the left hand
in a 45-year-old patient with uremia. C. Gram-negative curved
isolated from a blood sample of the 45-year-old patient with
from Hsueh, et al. Vibrio vulnificus in Taiwan. CDC Emerging
Diseases Volume 10, Number 8, August 2004.
Determinants of Virulence
Attempts to associate phenotypic or genotypic characteristics of Vibrio
vulnificus with strain virulence have been largely unsuccessful. V.
vulnificus exhibits considerable strain-to-strain variation in
More than 100 strains of the bacterium have been identified, and it is
possible that many thousands more exist. The bacterium also exhibits a
large number of potential determinants of virulence, on the order of V.
cholerae and Pseudomonas aeruginosa combined, but their
in disease has not been elucidated.
There are at least three ways that Vibrio vulnificus strains
have been divided into two "biotypes", one of which is pathogenic for
and the other of which is found in shellfish or fish, or is
free-living. One way is based on the difference in a 17-bp nucleotide
16S rRNA gene. By this criterion two major groups of V.
been identified, designated types A and B. The majority of
isolates are type A, and there is a positive correlation between the
B genotype and the cause of human disease. Similarly, a homogeneous LPS
type is found in vibrios that live in associations with eels (biotype
and distinct heterogenous LPS types are observed in clinical
(Biotype 1). The presence of a capsule occurs in virulent
noncapsulated strains are nonvirulent. The significance of these
is not known, and they do not explain how the bacteria are able to
from free-swimming and colonizing oysters to colonizing human tissues.
Generalized Stress Response
Many of the heat shock proteins produced by V. vulnificus, such
as the chaperonins DnaK and GroEL, and the proteases, Clp and
are induced by environmental changes other than increased temperature,
such as ethanol, heavy metals or oxidizing agents, high osmolarity,
starvation, exposure to low temperature, or interaction with eucaryotic
hosts. This is thought to be a generalized stress response in the
bacterium. Through a process termed cross protection, this
improves the bacterium's thermotolerance, salt tolerance, tolerance to
heavy metals and UV exposure, and starvation survival. The generalized
stress response may be critical for bacterial adaptation to changes in
the environment and is a major link between bacterial ecology
Stress is also thought to cause genomic differences observed among
of V. vulnificus. Genomic differences may be the result
gene rearrangements in the bacterium. Since the bacterium may exist in
a rapidly changing ecosystem where major alterations in temperature,
concentration, UV irradiation, and nutrient availability are routinely
encountered, it is possible that such gene rearrangements may increase
the chances of survival of the bacterium when it moves from water to
Expression of a polysaccharide capsule is necessary for virulence of
vulnificus. The noncapsulated form is nonvirulent. Under
conditions, acapsular variants arise at a fairly high frequency
with certain environmental stresses dramatically increasing this switch
rate. Once such noncapsulated (translucent) colonies arise, they
do not appear able to revert back to the capsule-expressing (opaque)
The mechanism of this capsule switching has not been explained.
Type IV pili (fimbriae) are required for virulence. Type IV pili are
N-methylphenylalanine pili, characteristic of vibrios, that allow the
to adhere to epithelial cells. The receptor has not yet been
The N-methylphenylalanine pili of Vibrio cholerae apparently
acid (sialic acid) as a receptor.
Figure 3. Electron micrograph
of Vibrio vulnificus. The arrows mark fimbriae (pili) of the
The laboratory of Dr. Mark Strom at the
NOAA Northwest Fisheries Science Center is
studying how the adhesins of the bacterium, which include fimbriae and
other cell surface components, influence the course of mammalian
and infection, as well as the organism's ability to colonize and
As a Gram negative bacterium, V. vulnificus lipopolysaccharide
(endotoxin) is expected to play a role in fever and septic shock
on by infection. On the basis of lipopolysaccharide (LPS) antigens, the
species can be organized into three biotypes. Biotype 1 is the
human pathogen; biotype 2 is associated with eels; and biotype 3 was
isolated from fish handlers in Israel. Biotype 2 consists of a
type of LPS, and although Biotype 1 was originally divided into 5
antigenic subgroups, other subgroups are known to exist. Biotype 1 is
invariably associated with human disease, and one particular LPS type
is significantly more prevalent among clinical strains. This suggests
either the presence of this LPS type itself causes increased virulence,
or that the LPS type is a marker of more virulent strains.
Besides attachment ability, capsule switching, LPS, and the ability
to undergo the stress response, other properties of V. vulnificus
that have been considered as determinants of virulence include
of alternate (stress) sigma factors, SSR repeats, motility, quorum
production of a siderophore and a hemolysin (cytolysin), and numerous
enzymes, including proteases, collagenase, mucinase, esterase,
hyaluronidase, DNAase and sulfatase.
A recently identified determinant of virulence in Vibrio
is the member of the RTX family of toxins produced by a limited group
Gram-negative pathogens. RTX toxins cause pore formation in red blood
necrotic death of Hep2 cells, and depolymerization of actin in HeLa
For an excellent review of the virulence of Vibrio vulnificus
et al. Molecular Pathogenesis of Vibrio vulnificus