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Vibrio cholerae O139 synonym Bengal is closely related to Vibrio cholerae El Tor but has important differences

American Society for Microbiology
Infection and Immunity
Authors:
Judith A Johnson at University of Florida
Judith A Johnson
CA Salles
CA Salles
CA Salles
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Pinaki Panigrahi at Georgetown University
Pinaki Panigrahi
M. John Albert at College of Medicine, Kuwait University
M. John Albert
  • College of Medicine, Kuwait University
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Abstract and Figures

Although Vibrio cholerae O139 synonym Bengal strains, from the current epidemics in India and Bangladesh, are closely related to seventh-pandemic strains, as shown by multilocus enzyme electrophoresis, Bengal strains are encapsulated and portions of the O1 antigen biosynthetic complex genes found in O1 strains are altered or lacking. Encapsulated Bengal strains showed resistance to killing by normal human serum. The presence of the capsule suggests the potential for bloodstream invasion in susceptible hosts and has profound implications for vaccine development.
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INFECTION
AND
IMMUNITY,
May
1994,
p.
2108-2110
0019-9567/94/$04.00+0
Copyright
©
1994,
American
Society
for
Microbiology
Vibrio
cholerae
0139
Synonym
Bengal
Is
Closely
Related
to
Vibrio
cholerae
El
Tor
but
Has
Important
Differences
JUDITH
A.
JOHNSON,l12.3*
CARLOS
A.
SALLES,4
PINAKI
PANIGRAHI,
1'35
M.
JOHN
ALBERT
6
ANITA
C.
WRIGHT,3
ROBERT
J.
JOHNSON,1'2
AND
J.
GLENN
MORRIS,
JR.1'3
Veterans
Administration
Medical
Center
of
Baltimore'
and
Department
of
Pathology,2
Department
of
Medicine
and
Center
for
Vaccine
Development,3
and
Department
of
Pediatrics,5
University
of
Maryland
at
Baltimore,
Baltimore,
Matyland
21201;
Department
of
Biochemistry
and
Molecular
Biology,
Instituto
Oswaldo
Cruz,
FIOCRUZ,
Rio
de
Janeiro,
Brazil4;
and
Department
of
Laboratory
Research,
Laboratory
Sciences
Division,
International
Centre
for
Diarrhoeal
Diseases
Research,
Bangladesh,
Dhaka,
Bangladesh6
Received
29
November
1993/Returned
for
modification
19
January
1994/Accepted
1
February
1994
Although
Vibrio
cholerae
0139
synonym
Bengal
strains,
from
the
current
epidemics
in
India
and
Bangladesh,
are
closely
related
to
seventh-pandemic
strains,
as
shown
by
multilocus
enzyme
electrophoresis,
Bengal
strains
are
encapsulated
and
portions
of
the
01
antigen
biosynthetic
complex
genes
found
in
01
strains
are
altered
or
lacking.
Encapsulated
Bengal
strains
showed
resistance
to
killing
by
normal
human
serum.
The
presence
of
the
capsule
suggests
the
potential
for
bloodstream
invasion
in
susceptible
hosts
and
has
profound
implications
for
vaccine
development.
Vibrio
cholerae
strains
of
0
group
1
(01
strains)
have
traditionally
been
classified
as
the
etiologic
agent
for
cholera,
a
well-recognized
cause
of
morbidity
and
mortality
throughout
the
world:
to
date
there
have
been
seven
recorded
pandemics
of
this
severe
dehydrating
diarrheal
disease.
V.
cholerae
of
0
groups
other
than
1
(non-O1,
or
nonagglutinating,
V
cholerae)
can
also
cause
gastrointestinal
disease
(6)
as'
well
as
extrain-
testinal
infections
such
as
wound
infections
and
septicemia
(9).
Until
recently
it
was
believed
that
only
01
strains
had
epidemic
potential,
with
isolation
of
non-O1
strains
being
restricted
to
sporadic
cases.
Late
in
1992,
large
outbreaks
of
cholera-like
disease
occurred
in
southern
and
eastern
India
and
southern
Bangladesh
(1),
with
subsequent
spread
into
other
parts
of
Asia.
The
causative
agent
was
a
toxigenic
strain
of
the
previ-
ously
unidentified
serovar
0139
(V
cholerae
0139
synonym
Bengal);
these
strains
did
not
agglutinate
with
either
poly-
clonal
or
monoclonal
antisera
directed
against
the
V.
cholerae
01
antigen.
In
the
Bangladeshi
studies,
the
incidence
of
disease
was
as
high
in
adults
as
in
children,
suggesting
that
prior
immunity
to
V
cholerae
01
El
Tor
was
not
protective
against
0139
infection
(1).
The
appearance
of
epidemic
non-O1
disease
raises
basic
questions
about
the
degree
of
relatedness
between
0139
iso-
lates
and
epidemic
01
strains:
do
0139
strains
represent
a
simple
mutation
altering
the
0
antigen
of
the
current
pandemic
El
Tor
strain,
as
has
been
proposed
by
Hall
et
al.
(1)?;
are
they
a
distantly
related
non-O1
strain
(with
non-O1
characteristics,
such
as
encapsulation
[5])
that
has
acquired
virulence
factors?;
or
do
they
lie
somewhere
between
these
extremes?
An
under-
standing
of
these
relationships
is
critical
as
we
begin
to
design
vaccines
which
may
be
effective
against
what
appears
to
be
the
etiologic
agent
of
the
eighth
cholera
pandemic.
To
assess
the
phylogenetic
relationship
between
Bengal
strains
and
other
V
cholerae,
we
analyzed
three
Bengal
strains
from
the
Bangladeshi
epidemic
(strains
A11837,
A11841,
and
A11852)
by
multilocus
enzyme
electrophoresis.
These
strains,
*
Corresponding
author.
Mailing
address:
Molecular
Diagnostics
Laboratory,
VAMC
Baltimore,
Room
4D-148,
10
N.
Greene
St.,
Baltimore,
MD
21201.
Phone:
(410)
605-7000,
ext.
5338.
Fax:
(410)
605-7911.
and
control
strains
from
our
collection
of
V
cholerae,
were
confirmed
to
be
V
cholerae
by
API
20E,
with
the
presence
of
cholera
toxin
genes
confirmed
by
using
CTAP,
a
23-base
alkaline
phosphatase-labeled
oligonucleotide
probe
developed
in
our
laboratory
(12).
In
the
enzyme
electrophoretic
typing
system
previously
described
by
Salles
and
colleagues
(10),
all
three
0139
strains
were
classified
as
being
in
zymovar
14.
V
cholerae
01
El
Tor
isolated
during
the
seventh
pandemic
in
Asia
and
01
El
Tor
strains
from
the
recent
South
American
epidemics
are
also
classified
as
zymovar
14
in
this
system.
Epidemic
V.
cholerae
01
strains
having
a
classical
biotype
belong
to
zymovar
13.
The
El
Tor
strain
endemic
to
the
U.S.
Gulf
Coast
forms
a
third
zymovar,
71,
which
differs
in
one
locus
from
14.
Environmental,
nontoxigenic
01
strains
are
generally
not
closely
related
to
epidemic
strains.
Other
non-O1
strains
occupy
over
100
zymovars,
with
a
species
diversity
which
approaches
that
seen
in
Escherichia
coli.
Our
zymovar
data
confirm
previous
reports
suggesting
that
Bengal
strains
are
very
closely
related
to
epidemic
V
cholerae
01
El
Tor.
0139
isolates
do
not
react
with
polyclonal
Inaba-
or
Ogawa-
specific
sera
or
monoclonal
antibodies
specific
for
A,
B,
and
C
antigens,
suggesting
that
the
01-antigen
may
be
missing
or
altered.
The
change
is
not
simply
loss
of
the
0
antigen,
as
0139
strains
are
typeable
and
virulent
and
do
not
produce
rough
colonies.
However,
small
changes
in
the
structure
of
the
0-specific
carbohydrate
might
be
sufficient
to
change
its
anti-
genicity.
To
further
examine
this
question,
eight
strains
(AI1837,
A11838,
A11841,
A11852,
A11854,
A11855,
A14260,
and
A14450)
from
the
Bangladeshi
epidemic,
E.
coli
DH5cx,
and
a
collection
of
01
and
non-O1
V
cholerae
strains
were
probed
for
rJbR
and
rfbS,
the
two
penultimate
genes
in
the
01
antigen
synthesis
operon.
A
region
encoding
01
antigen
biosynthesis
has
been
cloned
and
sequenced
for
El
Tor
and
classical
biotype
strains
(11).
Probes
O1SAP
(GGATTGGT
CACTTGATACCGC)
and
O1RAP
(GGTGAACGCTCTT
GCTACAGC),
specific
for
rJbS
and
rflR,
respectively,
were
derived
from
this
sequence
information,
and
alkaline
phos-
phatase
was
attached
to
a
5'
amino
nucleotide.
Strains
were
grown
overnight
on
L
agar,
and
colony
blots
were
prepared
on
Whatman
541
filters
and
hybridized
with
the
probes.
Both
01
antigen
probes
hybridized
with
40
strains
of
01
V
cholerae,
2108
Vol.
62,
No.
5
NOTES
2109
FIG.
1.
Polycationic
ferritin-stained
thin
sections
of
AI1855.
Magnification
x
38,000.
including
El
Tor
and
classical
biotypes
of
both
Inaba
and
Ogawa
serotypes.
In
contrast,
O1RAP
and
OISAP
failed
to
hybridize
with
the
eight
V.
cholerae
Bengal
strains
or
40
other
non-O1
strains,
including
three
cholera
toxin-producing
strains,
suggesting
that
at
least
two
genes
in
the
biosynthetic
pathway
for
the
01
antigen
are
missing
or
altered.
Further
studies
are
clearly
needed
to
define
the
genetic
relationship
between
the
01
and
0139
antigen
biosynthetic
pathways,
particularly
in
light
of
the
apparent
close
genetic
relationship
between
these
two
serovars.
As
we
have
previously
reported,
a
majority
of
non-01
V.
cholerae
strains
are
able
to
produce
a
polysaccharide
capsule
(4,
5).
Strains
are
able
to
shift
between
an
encapsulated
form
with
an
opaque
colonial
morphology
and
an
unencapsulated
or
minimally
encapsulated
form
with
a
translucent
colonial
mor-
phology;
the
degree
of
opacity
correlates
with
the
amount
of
capsular
material
which
can
be
extracted
from
the
cells
(4).
Encapsulation
is
associated
with
resistance
to
the
bactericidal
activity
of
normal
human
serum
and
with
increased
virulence
in
animal
models
(5).
It
has
been
hypothesized
that
the
ability
of
non-01
strains
to
cause
invasive
disease
is
related
to
capsule
expression.
V.
cholerae
01
is
not
similarly
encapsulated
and,
with
very
rare
exceptions,
is
not
invasive.
To
determine
whether
Bengal
strains
shared
the
ability
of
other
non-01
strains
to
express
a
capsule,
overnight
cultures
on
L
agar
were
evaluated
visually
for
opaque
versus
translucent
colony
morphology
and
phase
shifting.
All
eight
0139
strains
had
a
moderately
opaque
colony
morphology
on
initial
streaks;
translucent
sectors
and
colonies
appeared
after
subculturing.
Similar
changes
in
colony
morphology
were
not
seen
when
more
than
100
01
strains
from
clinical
and
environmental
sources
were
examined.
Two
Bengal
strains
(AI1855
and
A11841)
were
prepared
by
standard
methods,
stained
with
polycationic
fer-
ritin,
thin
sectioned
and
examined
by
electron
microscopy
(5).
Both
were
surrounded
by
a
relatively
thin
electron-dense
cap-
sule
(the
photomicrograph
for
strain
Al
1855
is
shown
in
Fig.
1).
Capsular
material,
extracted
and
purified
as
previously
de-
scribed
(8),
was
identified
as
an
animo
sugar-containing
polysac-
charide
by
high-performance
anion-exchange
chromatography
and
magnetic
nuclear
resonance
analysis
(la).
The
50%
lethal
dose
(LD5,,)
after
intradermal
injection
in
mice
was
only
marginally
lower
for
Bengal
strains
than
for
V.
cholerae
01
El
Tor
Ogawa
N16961,
a
highly
virulent
clinical
strain
used
extensively
in
prior
volunteer
studies
(LD50s,
1.5
x
10'
[geometric
mean
of
the
LD50s
of
three
0139
strains]
versus
5
x
10'
[strain
N16961]).
However,
in
contrast
to
findings
with
both
classical
and
El
Tor
01
strains,
which
were
not
isolated
from
blood,
V.
cholerae
could
be
isolated
from
the
blood
of
VOL.
62,
1994
I
2110
NOTES
mice
given
high
doses
of
0139
or
control
encapsulated
non-01
strains.
The
improved
ability
of
0139
isolates
to
survive
in
the
blood
may
be
due
to
increased
resistance
to
complement-mediated
killing.
Like
other
encapsulated
non-01
strains
(5),
Bengal
isolates
showed
a
drop
in
viable
counts
of
less
than
1.5
log1o
following
a
30-min
incubation
in
65%
normal
human
serum,
compared
with
a
circa
5-log
drop
for
classical
or
El
Tor
01
strains.
There
has
already
been
one
case
report
of
septicemia
due
to
an
0139
strain
(3);
in
keeping
with
observations
with
other
non-01
isolates
(9),
sepsis
occurred
in
a
patient
with
underly-
ing
liver
disease.
The
0139
strains
which
we
have
examined
do
not
have
the
thick
capsules
usually
associated
with
non-01
V.
cholerae
blood
isolates
(4),
suggesting
that
the
risk
of
dissem-
inated
disease
in
infected
persons
is
relatively
low.
Nonethe-
less,
these
observations
indicate
that
disseminated
disease
can
occur;
if
0139
strains
follow
the
pattern
of other
non-01
strains,
the
risk
of
dissemination
will
be
greatest
in
persons
with
chronic
underlying
illnesses
(9).
This
risk
raises
theoreti-
cal
questions
about
the
advisability
of
administering
oral
attenuated
vaccines
that
still
carry
the
capsule
to
persons
who
may
have
underlying
illnesses.
The
presence
of
the
capsule
may
also
have
an
effect
on
antigen
recognition:
in
volunteer
studies
with
other
non-01
strains,
the
presence
of
a
capsule
appeared
to
mask
certain
critical
surface
antigens,
with
a
resulting
decrease
in
host
immunologic
response
(7).
The
presence
of
a
capsule
and
the
apparent
absence
of
some
01
biosynthetic
genes
suggest
that
the
appearance
of
0139
strains
is
due
to
more
than
a
simple
point
mutation
in
the
0-antigen
biosynthetic
complex.
Further
work
is
needed
to
determine
whether
these
are
the
only
significant
genetic
and
phenotypic
differences
and
what
role
these
differences,
espe-
cially
the
presence
of
the
capsule
on
Bengal
strains,
play
in
pathogenesis
and
the
immune
response
elicited
by
these
isolates.
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... Like PAIs and conjugative transposons, they encode an integrase and excisionase that mediates mobility, chromosomal attachment sites (att), an origin of transfer (oriT), and genes encoding conjugal transfer proteins (Botelho et al. 2020). V. cholerae strains from the seventh pandemic display enhanced levels of resistance to sulfamethoxazole, trimethoprim, streptomycin, and furazolidone (Johnson et al. 1994;Nair et al. 1994;. Resistance to three of these antibiotics, the former two being some of the most widely used, is due to the acquisition of the ICE element SXT. ...
... Detailed molecular epidemiological analyses indicate that O139 strains are closely related to O1 El Tor strains in terms of virulence potential and disease severity ( (Berche et al. 1994;Bhattacharya et al. 1993;Faruque et al. 2003), Morris et al. 1995). However, unlike the wbe locus of O1 strains, the wbf locus of O139 strains encodes a capsule (O-antigen capsule) and a modified core polysaccharide of the LPS that resulted in the seroconversion (Johnson et al. 1994;. Since the emergence of V. cholerae O139, several new genetic and phenotypic variants have emerged, including new ribotypes, CTX genotypes, and altered antibiotic resistance (Faruque et al. 1997(Faruque et al. , 1999Mitra et al. 1996). ...
Cholera Dynamics and the Emergence of Pandemic Vibrio cholerae
Chapter
  • Feb 2023
  • ADV EXP MED BIOL
Cholera is a severe diarrheal disease caused by the aquatic bacterium Vibrio cholerae. Interestingly, to date, only one major clade has emerged to cause pandemic disease in humans: the clade that encompasses the strains from the O1 and O139 serogroups. In this chapter, we provide a comprehensive perspective on the virulence factors and mobile genetic elements (MGEs) associated with the emergence of pandemic V. cholerae strains and highlight novel findings such as specific genomic background or interactions between MGEs that explain their confined distribution. Finally, we discuss pandemic cholera dynamics contextualizing them within the evolution of the bacterium.Keywords Vibrio cholerae CholeraPathogen emergenceCholera pandemicsPathogen evolution
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... V ibrio cholerae es un bacilo gramnegativo causante del cólera, un tipo de diarrea secretora que se ha asociado a grandes brotes epidémicos a lo largo de la historia, particularmente los serogrupos O-1 y O-139, los cuales tienen la capacidad de producir toxinas [1][2][3][4] . ...
Bacteriemia por Vibrio cholerae no-O1/no-O139 que porta una región homóloga a la isla de patogenicidad VpaI-7
Article
Full-text available
  • Jun 2019
  • REV CHIL INFECTOL
Bacteremia caused by Vibrio cholerae non-O1/non-O139 carrying a region homologous to pathogenicity island VpaI-7 We report a case of V. cholerae non-O1 / non-O139 bacteremia in an 81-year-old woman with abdominal pain, fever, vomiting, liquid stools, choluria and jaundice, while visiting a rural area without access to potable water. The identification was made by the MALDI-TOF mass spectrometry technique and subsequently the non-toxigenic non-O1 / non-139 strain was confirmed in the national reference laboratory. The molecular characterization demonstrated the absence of the cholera toxin gene (CTX), and the TCP pilus, however, presented 5 of 6 virulence genes present in an island of homologous pathogenicity named VPaI-7 of V. parahaemolyticus (vcs N2 +, vcs C2 +, vcs V2 +, toxR-, vspD +, T vopF +) and in addition it was positive for hylAy rtxA virulence genes recognized outside the island. This is the first case reported in Chile of a clinical strain of V. cholerae non-O1, non-O139 isolated from blood culture that carries in its genome a homologous segment of the pathogenicity island named VPaI-7 of V. parahaemolyticus, which codifies for a type III secretion system (TTSS) that probably contributes to his virulence.
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... induces a different pattern of response from that seen after V cholerae O1 infection. 33 Our results showed that inflammatory responses in duodenal tissues of O139 patients were upregulated, as in O1 infected patients. However, a difference was seen only in the kinetics of the response in O139 patients. ...
Acute dehydrating disease caused by Vibrio cholerae serogroups O1 and O139 induce increases in innate cells and inflammatory mediators at the mucosal surface of the gut
Article
Full-text available
  • Jan 2004
The general concept is that as Vibrio cholerae is not invasive, it mediates a non-inflammatory type of infection. This is being re-evaluated based on available data that natural cholera infection or cholera toxin induces a Th2-type of immune profile and stimulates the humoral immune response, innate cells, and mediators in the host. To perform a comprehensive analyses of the inflammatory components, we studied mucosal biopsies from patients, both adults and children with acute watery diarrhoea caused by V cholerae O1 and O139. Patients with cholera, adults (n = 30) and children (n = 18), as well as healthy controls (n = 24) were studied. Histochemical, immunohistochemical, and ultrastructural studies were carried out to elucidate the contribution of the different factors using paraffin and frozen duodenal and/or rectal sections as appropriate. Samples were collected during the acute stage and during early and/or late convalescence. Following natural cholera infection, patients responded with increases in neutrophil polymorphs during the acute stage (p<0.001) compared with healthy controls whereas mucosal mast cells (MMC) (p = 0.008) and eosinophils (p = 0.034) increased in the gut during convalescence. Electron microscopic analyses of duodenal biopsies from adult patients showed increased piecemeal degranulation in both MMC and eosinophils and accumulation of lipid bodies in MMC. Duodenal biopsies from V cholerae O1 infected patients showed upregulation of myeloperoxidase, lactoferrin, PGHS-1, SCF, tryptase, tumour necrosis factor alpha, alpha-defensin, and eotaxin during the acute stage and chymase, interleukin 3 and major basic protein during convalescence. We have shown that innate cells and their mediators are upregulated in acute watery diarrhoea. These cells and factors of the innate arm may be important in the host's defence against cholera. Such effects may need to be simulated in a vaccine to achieve long lasting protection from cholera.
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... The ongoing 7th pandemic was first evolved on the island of Sulawesi in Indonesia in 1961 (Karaolis et al., 1995). All of the seven cholera pandemics are caused by the O1 serotype of V. cholerae, except the spatial emergences of O139 Bengal in eastern part of India and Bangladesh in 1992 (Johnson et al., 1994). Interestingly, all of these pathogenic strains harbored VPI-1 as well as CTX in their chromosomes (Li et al., 2003). ...
Vibrio Pathogenicity Island-1: The Master Determinant of Cholera Pathogenesis
Article
Full-text available
  • Oct 2020
Cholera is an acute secretory diarrhoeal disease caused by the bacterium Vibrio cholerae. The key determinants of cholera pathogenicity, cholera toxin (CT), and toxin co-regulated pilus (TCP) are part of the genome of two horizontally acquired Mobile Genetic Elements (MGEs), CTXΦ, and Vibrio pathogenicity island 1 (VPI-1), respectively. Besides, V. cholerae genome harbors several others MGEs that provide antimicrobial resistance, metabolic functions, and other fitness traits. VPI-1, one of the most well characterized genomic island (GI), deserved a special attention, because (i) it encodes many of the virulence factors that facilitate development of cholera (ii) it is essential for the acquisition of CTXΦ and production of CT, and (iii) it is crucial for colonization of V. cholerae in the host intestine. Nevertheless, VPI-1 is ubiquitously present in all the epidemic V. cholerae strains. Therefore, to understand the role of MGEs in the evolution of cholera pathogen from a natural aquatic habitat, it is important to understand the VPI-1 encoded functions, their acquisition and possible mode of dissemination. In this review, we have therefore discussed our present understanding of the different functions of VPI-1 those are associated with virulence, important for toxin production and essential for the disease development.
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The Role of Nutrients and Nutritional Signals in the Pathogenesis of Vibrio cholerae
Chapter
  • Feb 2023
  • ADV EXP MED BIOL
Vibrio cholerae, the agent of cholera, is a natural inhabitant of aquatic environments. Over the past decades, the importance of specific nutrients and micronutrients in the environmental survival, host colonization, and pathogenesis of this species has become increasingly clear. For instance, V. cholerae has evolved ingenious mechanisms that allow the bacterium to colonize and establish a niche in the intestine of human hosts, where it competes with commensals (gut microbiota) and other pathogenic bacteria for available nutrients. Here, we discuss the carbon and energy sources utilized by V. cholerae and what is known about the role of nutrition in V. cholerae colonization. We examine how nutritional signals affect virulence gene regulation and how interactions with intestinal commensal species can affect intestinal colonization.Keywords Vibrio cholerae Carbon utilizationNutrient uptakeHost colonizationHost–pathogen interaction
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PRESIDENT'S ADDRESS: A LIFE WITH CHOLERA
Article
  • Jan 2022
  • Trans Am Clin Climatol Assoc
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Large epidemic of cholera-like disease in Bangladesh caused by Vibrio cholerae O139 synonym Bengal
Data
Full-text available
  • Jan 1993
Abstract Epidemics of cholera caused by Vibrio cholerae O1 occur regularly in Bangladesh, but until lately V cholerae non-O1 has been associated only with sporadic cases of diarrhoeal disease in many parts of the world, including Bangladesh. We describe a large epidemic of cholera-like disease in Bangladesh that is due to a V cholerae non-O1. The epidemic began in December, 1992, in southern Bangladesh and spread throughout the country. By the end of March 107,297 cases of diarrhoea and 1473 deaths had been reported. The disease is indistinguishable from cholera in clinical features and response to treatment, but most of the cases are in adults, which suggests that the population has no previous immunological experience of the organism. At two centres 375 (40%) of 938 and 236 (48%) of 492 rectal swabs were positive for V cholerae non-O1, as were 5 of 54 surface water samples. 55 isolates of V cholerae non-O1 were studied in detail. They resembled El Tor vibrios in being resistant to polymyxin B and positive for agglutination of chicken erythrocytes. The strain did not belong to any of the 138 known V cholerae serogroups; so a new serogroup O139, with the suggested name Bengal, is proposed. All the isolates studied produced large amounts of an enterotoxin apparently identical to cholera toxin. This strain seems to have pandemic potential. It is important that other countries in southeast Asia are aware of the strain's potential to cause severe morbidity and mortality.
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Non-O1 Vibrio cholerae NRT36S produces a polysaccharide capsule that determines colony morphology, serum resistance, and virulence in mice
Article
Full-text available
  • Apr 1992
Non-O1 Vibrio cholerae produced two distinct colony types, designated as opaque and translucent. NRT36S, a clinical isolate shown to be virulent in volunteers, produced predominantly opaque colonies, but translucent colonies appeared on subculture. Opaque variants were recovered exclusively following exposure to normal human serum or animal passage. A nonreverting translucent mutant of NRT36S, JVB52, was isolated following mutagenesis with the transposon Tn5 IS50L::phoA (TnphoA). Only translucent colonies were produced by a nonpathogenic environmental isolate, A5. Electron microscopic examination of the opaque form of NRT36S revealed thick, electron-dense, fibrous capsules surrounding polycationic ferritin-stained cells. The ferritin-stained material around translucent NRT36S or A5 was patchy or absent. JVB52 had a thin but contiguous capsular layer. The amount of ferritin-stained capsular material correlated with the amount of surface polysaccharide determined by phenol-sulfuric acid assay: opaque NRT36S had approximately three times as much polysaccharide as translucent NRT36S or A5 and four times as much as JVB52. The encapsulated, opaque variant of NRT36S was protected from serum bactericidal activity, while translucent non-O1 V. cholerae was readily killed. The encapsulated form also had increased virulence in mice. Our data provide the first indication that non-O1 V. cholerae strains can have a polysaccharide capsule. This capsule may be important in protecting the organism from host defenses and may contribute to the ability of some non-O1 V. cholerae strains to cause septicemia in susceptible hosts.
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Serotype conversion in Vibrio-Cholerae O1
Article
Full-text available
  • May 1992
Vibrio cholerae O1 exists as two major serotypes, Inaba and Ogawa, which are associated with the O antigen of the lipopolysaccharide and are capable of unequal reciprocal interconversion. The 20-kilobase rfb regions encoding O-antigen biosynthesis in strains 569B (Inaba) and O17 (Ogawa) have been cloned in Escherichia coli K-12 and the nucleotide sequences have been determined. Besides several base substitutions and a small deletion in the 569B sequence relative to O17, there is a single nucleotide change resulting in a TGA stop codon within the gene for the 32-kDa RfbT protein. We have demonstrated that rfbT is responsible for serotype conversion (Inaba to Ogawa). The construction of a specific rfbT mutation in the Ogawa strain O17, and the ability of the gene from O17 to complement Inaba strains to Ogawa, confirmed rfbT as the gene required for the Ogawa serotype. By Southern hybridization and sequencing of PCR products of a number of strains, we have shown that the changes observed in one Inaba strain (569B) are not conserved in other Inaba strains. This may explain why some Inaba strains are able to convert to Ogawa whereas others are not. The protein encoded by rfbT has been identified and expressed in E. coli K-12 using a phage T7 expression system. Amino-terminal analysis of partially purified protein has identified the translational start of the protein. Primer extension studies have enabled the 5' end of the mRNA to be defined. It exists as a separate transcript from the rest of the rfb region, and the distinctive G + C content of rfbT suggests that it has been acquired from a non-Vibrio source.
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Development and testing of a nonradioactive DNA oligonucleotide probe that is specific for Vibrio cholerae cholera toxin
Article
Full-text available
  • Oct 1992
An alkaline phosphatase-labeled oligonucleotide DNA probe (CTAP) that was specific for the cholera toxin gene (ctxA) was identified. All cholera toxin-producing strains of Vibrio cholerae, regardless of serotype, hybridized with the CTAP probe, while nontoxigenic strains from either environmental sources or from deletion or substitution mutations did not hybridize. Unlike the whole-gene probes for either ctxA or for the heat-labile toxin or Escherichia coli (eltA), this 23-base sequence did not hybridize with E. coli or with vibrios other than V. cholerae that produce related toxins. By using CTAP to identify colonies grown on nonselective medium, V. cholerae was enumerated at concentrations of 10(3) to 10(7)/g from stool samples of volunteers who had ingested V. cholerae O1 strain 569B. CTAP provides a specific and sensitive tool for diagnosis and environmental monitoring of cholera toxin-producing V. cholerae.
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Purification and determination of the structure of capsular polysaccharide of Vibrio vulnificus M06-24
Article
Full-text available
  • May 1992
Virulence of Vibrio vulnificus has been strongly associated with encapsulation and an opaque colony morphology. Capsular polysaccharide was purified from a whole-cell, phosphate-buffered saline-extracted preparation of the opaque, virulent phase of V. vulnificus M06-24 (M06-24/O) by dialysis, centrifugation, enzymatic digestion, and phenol-chloroform extraction. Nuclear magnetic resonance spectroscopic analysis of the purified polysaccharide showed that the polymer was composed of a repeating structure with four sugar residues per repeating subunit: three residues of 2-acetamido-2,6-dideoxyhexopyranose in the alpha-gluco configuration (QuiNAc) and an additional residue of 2-acetamido hexouronate in the alpha-galactopyranose configuration (GalNAcA). The complete carbohydrate structure of the polysaccharide was determined by heteronuclear nuclear magnetic resonance spectroscopy and by high-performance anion-exchange chromatography. The 1H and 13C nuclear magnetic resonance spectra were completely assigned, and vicinal coupling relationships were used to establish the stereochemistry of each sugar residue, its anomeric configuration, and the positions of the glycosidic linkages. The complete structure is: [----3) QuipNAc alpha-(1----3)-GalpNAcA alpha-(1----3)-QuipNAc alpha-(1----]n QuipNAc alpha-(1----4)-increases The polysaccharide was produced by a translucent phase variant of M06-24 (M06-24/T) but not by a translucent, acapsular transposon mutant (CVD752). Antibodies to the polysaccharide were demonstrable in serum from rabbits inoculated with M06-24/O.
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Experimental non-O group 1 Vibrio cholerae gastroenteritis in humans
Article
Full-text available
  • Apr 1990
In this study, 27 volunteers received one of three non-O group 1 Vibrio cholerae strains in doses as high as 10(9) CFU. Only one strain (strain C) caused diarrhea: this strain was able to colonize the gastrointestinal tract, and produced a heat-stable enterotoxin (NAG-ST). Diarrhea was not seen with a strain (strain A) that colonized the intestine but did not produce NAG-ST, nor with a strain (strain B) that produced NAG-ST but did not colonize. Persons receiving strain C had diarrhea and abdominal cramps. Diarrheal stool volumes ranged from 154 to 5,397 ml; stool samples from the patient having 5,397 ml of diarrhea were tested and found to contain NAG-ST. The median incubation period for illness was 10 h. There was a suggestion that occurrence of diarrhea was dependent on inoculum size. Immune responses to homologous outer membrane proteins, lipopolysaccharide, and whole-cell lysates were demonstrable with all three strains. Our data demonstrate that V. cholerae of O groups other than 1 are able to cause severe diarrheal disease. However, not all strains are pathogenic for humans: virulence of strain C may be dependent on its ability both to colonize the intestine and to produce a toxin such as NAG-ST.
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LARGE EPIDEMIC OF CHOLERA-LIKE DISEASE IN BANGLADESH CAUSED BY VIBRIO-CHOLERAE 0139 SYNONYM BENGAL
Article
  • Aug 1993
Epidemics of cholera caused by Vibrio cholerae 01 occur regularly in Bangladesh, but until lately V cholerae non-01 has been associated only with sporadic cases of diarrhoeal disease in many parts of the world, including Bangladesh. We describe a large epidemic of cholera-like disease in Bangladesh that is due to a V cholerae non-01. The epidemic began in December, 1992, in southern Bangladesh and spread throughout the country. By the end of March 107 297 cases of diarrhoea and 1473 deaths had been reported. The disease is indistinguishable from cholera in clinical features and response to treatment, but most of the cases are in adults, which suggests that the population has no previous immunological experience of the organism. At two centres 375 (40%) of 938 and 236 (48%) of 492 rectal swabs were positive for V cholerae non-01, as were 5 of 54 surface water samples. 55 isolates of V cholerae non-01 were studied in detail. They resembled El Tor vibrios in being resistant to polymyxin B and positive for agglutination of chicken erythrocytes. The strain did not belong to any of the 138 known V cholerae serogroups; so a new serogroup 0139, with the suggested name Bengal, is proposed. All the isolates studied produced large amounts of an enterotoxin apparently identical to cholera toxin. This strain seems to have pandemic potential. It is important that other countries in southeast Asia are aware of the strain's potential to cause severe morbidity and mortality.
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Identification of Vibrio cholerae by enzyme electrophoresis
Article
  • Jul 1991
Zymovar analysis of 260 strains of Vibrio cholerae plus 3 reference strains of V. mimicus, using 13 structural loci, led to the grouping of strains in 73 zymovars (strain or group of strains sharing the same alleles). Effective separation of strains, distinction of V. cholerae strains from closely related V. mimicus and the detection of 2 vibrio strains, including one with two O1 serovars, in supposedly pure collection cultures, illustrate the potential of zymovar analysis in the identification of V. cholerae isolates. Two El Tor strains from USA, one CT+ and the other CT-, shared the same zymovar 71, while 127 typical El Tor strains belonged to zymovar 14.
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Non-O:l Vibrio cholerae Bacteremia: Case Report and Review
Article
  • Sep 1988
  • Rev Infect Dis
A caseof non-Oil Vibrio cholerae bacteremia and prostatic abscess in a patient with idiopathic aplastic anemia was studied, and the data were compared with those from 23 previously reported cases of non-Oil V. cholerae bacteremia. The case-fatality rate for the 13 cases for which the outcome is known is 61.5070. The majority of known cases have occurred in immunocompromised patients, particularly those with hematologic malignancyor cirrhosis. Host susceptibility is potentially important in this condition. Bacterial products such as a cholera-like toxin and El Tor hemolysin also may playa role in the disease process. The incidence of enteritis due to non-Oil V. cholerae is unclear because of the methods used for routine stool culture; however, the small number of reported isolates from blood is likely to reflect the infrequency of bacteremia, since Vibrio species are readily identifiable on sheep blood agar. While non-Oil V. cholerae is sensitive to most antibiotics in vitro, no data are available on antibiotic efficacy.
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