VIBRIO - I

Gram negative rods

Vibrionaceae
The name “vibrio” is derived from
characteristic vibratory motility.
(vibrare= to vibrate)
General charcters of Vibrionaceae

• Gram negative, curved, comma shaped bacilli

• Motile by single polar flagella
• Non spore forming
• Non capsulated
• Most vibrios have relatively simple growth factor
requirements and grow well in alkaline pH
• Facultative anaerobes
• Vibrios are capable of both respiratory & fermentative
metabolism i.e. O+/F+.
• Oxidase and catalase positive
• Natural inhabitants of aquatic environment
 General Characteristics of Vibrio,
Aeromonas and Plesiomonas
 These three genera are distantly related and classified in
family vibrionaceae at one time but molecular biology
techniques showed that these genera are different &
included in three separate families.
 Similarities to Enterobacteriaceae
 Gram-negative
 Facultative anaerobes
 Fermentative bacilli
 Differences from Enterobacteriaceae
 Polar flagella
 Oxidase positive
Discovery
• Filippo Pacini (1812-
1883)
– 1854: Cholera reaches
Florence, Italy. Pacini
discovers causative agent
– Publishes “Microscopical
Observations and
Pathological Deductions on
Cholera”
– 1965: Bacterium named
Vibrio cholerae Pacini 1854
Discovery
• Robert Koch (1843-
1910)

• 1884: Rediscovers
Vibrio cholerae
 BACKGROUND
Cholera, is a Greek word, which means the
gutter of the roof. It is caused by bacteria:
Vibrio cholerae, which was discovered in 1884
by Robert Koch during a diarrheal outbreak in
Egypt.
The genus as 40 species to which 12 are
responsible for intestinal and extra intestinal
infections in man. Most commonly isolated from
clinical specimens are- V. cholerae, V.
parahemolyticus, V. vulnificus, V. mimicus & V.
alginoliticus.
 V. CHOLERAE
V. cholerae has 2 major biotypes: classical
and El Tor, which was first isolated in Egypt in
1905. Currently, El Tor is the predominant
cholera pathogen worldwide.
The organism is a comma-shaped, gram-
negative, short, curved, cylindrical rods, aerobic
bacillus whose size varies from 1-3 um in length
by 0.5-0.8 um, with rounded or pointed ends
It is actively motile with a single polar
flagellum. The motility is of the darting type
under a microscope suggest a ‘swarm of gnats’
(swarm= group, Gnat= winged insects- flea,
mosq).
 Vibrio cholerae (gram stain)

In stained film of mucous flakes of acute cases of cholera-

the organism seen to be arranged in parallel rows described
by Koch as having ‘fish in stream’ appearance.
 Culture characters
• The chorea vibrio is aerobe, growth is scanty and slow
anaerobically.
• Grows within a temperature range of 16-400C, optimum
370C, better in alkaline medium between 7.4-9.6 (optimum
Ph-8.2).
• It requires presence of 0.5-1 % sodium chloride for optimal
growth & grows in ordinary medium.
• 1. Nutrient agar:- moist, translucent, round 1-2mm
in diameter with a bluish tinge in transmitted light.
2.Mackoney agar:-non-lactose fermenter, becomes
reddish due to late lactose fermentation.
3.Blood-agar:- surrounded by zone of greening which later
becomes clear due to haemodigestion .
4.Gelatin stab:-infundibuliform (funnel shaped) or
napiform liquifaction in 3 days incubation at 220C .
5.Alkaline-peptone water (pH- 8.6):- within 6 hrs-
surface pellicle, with continued incubation powdery deposit.
Special media for cultivation of Vibrio

• 1. Holding & transport media:-

a) V.R. media:- 20 gram common salt,5gm
peptone in 1litre D.W. with pH 8.6-8.8.
dispensed in 10-15 ml amt. in screw bottle.
1-3 ml faeces is added or rectal swab is placed.
stable & viable for several weeks.
b) Carry-Blair media-buffered solution of
sod.chloride, sod.thioglycolate, disodium
phosphate, calcium chloride, ph-8.4 .
suitable for salmonella , shigella & vibrio.
 ENRICHMENT MEDIA
• Alkaline peptone water-1% peptone and 1%
sodium chloride, ph-8.6.
• Monsur’s taurocholate-tellurite peptone water
at pH- 9.2

PLATING MEDIA
1. Alkaline bile salt agar (BSA)-ph-8.2 is a
simple media, widely used, colonies are
similar to those on nutrient agar.
2. Monsur’s gelatin taurocholate trypticase
tellurite agar (G.T.T.A)-ph-8.5, useful for
cholera and other vibrios isolation from stool.
After 24 hours colonies-small 1-2 mm in
diameter, translucent, with greyish black
centre and a turbid halo around due to
hydrolysis & denaturation of gelatin.
• Thiosulphate citrate bile salt sucrose agar (T.C.B.S.)
(pH-8.6)- mostly used as selective media,
commercially available and widely used media.
Bromothymol blue is used as an indicator . The
colonies of V. cholerae are yellow due to sucrose
fermentation and blue-green of V. parahemolyticus
due to non- sucrose fermenters.
 Identification
• 1-STRING TEST
• 2-IMViC Reaction
• 3-Nitrate reduction- +ve
• 4-Catalase+ve,Oxidase+ve,Urease-ve
• 5-Decarboxylase test-Ly+ve, Or+ve, Arg-ve
• 6-Sugar fermentation-glu+ve, suc+ve,
manitol+ve, mal+ve, manno+ve with acid &
no gas, Arb & Dul –ve
• String test- a loopful of growth is mixed
with a drop of 0.5% sodium deoxycholate
in saline on a slide. In positive test the
suspension loses it’s turbidity, becomes
mucoid and forms a “string” when the
loop is drawn slowly away the test is used
to separate vibrio species from Aeromonas
spp. & P. shigelloides (D/D).
Biochemical reactions
1.Carbohydrate metabolism is fermentative,
producing acid but no gas. Cholera vibrio
ferments glucose, mannitol, maltose, mannose
and sucrose.
2.Cholera-red reaction- V. cholerae is strongly
indole positive and reduces nitrates to nitrites,
when a few drops of concentrated sulphuric acid
is added to a 24 hrs peptone water culture- a
reddish pink color is developed due to formation
of nitroso- indole.
3. It is catalase & oxidase positive, MR & urease
negative.
4. Decarboxylates lysine & ornithine but
does not utilize arginine.
5. Gelatin is liquefied- funnel shaped or
“napi form” in 3 days at 220C.
6.Vogus-Proskauer reaction and hemolysis
of sheep RBC’s are positive in ElTor
biotype. Negative in classical biotype.
Resistance
They are killed-
• By heating at 56ºC for 30 min.,within few seconds
at boiling,quickly on dry fomites and in sewage
polluted water,in Gange’s water due to large
amount of vibriophages present,by disinfectants,
in few minutes on exposure to gastric juices.
They survives-
• For 1-2 weeks in clean, nonacid fresh or sea
water, few months in sterile sea water- survival in
nature,few days on moist foods, vegetables, fish and
cooked foods, for a week in refrigerator.
Antigens- Its antigenic structure consists of a
flagellar H antigen and a somatic O antigen.
It is the differentiation of the latter that
allows for separation into pathogenic and
nonpathogenic strains.

1. “H” flagellar antigen- heat labile, shared by

many vibrios and non- protective.
2. “O” antigen- it is lipopolysaccharide, endotoxin
and specific serologically. Antibodies against it
are protective.
.
Classification-
(a) Heiberg (1934)- classified vibrios into 6 groups
based on the fermentation of mannose, sucrose and
arabinose. 2 more groups were added later. Cholera
vibrios belongs to group one, which is mannose and
sucrose positive (acid only)
Group Mannose Sucrose Arabinose
fermentatio
n
I A A -
II - A -
III A A A
IV - A A
V A - -
VI - - -
VII A - A
VIII - - A
(b) Serological classification –by Gardner and
venkatraman (1935) –the cholera vibrio and the
similar vibrio possessing a common flagellar antigen
(H) were classified into group A vibrios and the rest
as group B vibrios comprising of biochemically and
antigenically heterogenous collection.
Group A vibrios based on somatic (O) antigen are
classigied into serogroups also called O serogroups or
serovars into more than 200. All isolates from
epidemic cholera till 1992 belong to serogroup O1 and
agglutinated by group O1 antiserum and reffered to as
“agglutinable vibrios”.
Other vibrios which were not agglutinated by O1
antiserum were called “Non agglutinable or NAG
vibrios”.
Gardener and Vanketraman Classification
Updated (1935)

UP TO 200
NOW
 NAG vibrios are mostly non – pathogenic,commensals
and isolated from the environment but can cause a
cholera like disease, agglutinated by their specific
antisera . The serogroup O139 identified in 1992 from
India (Chennai) causes epidemics of cholera and
possibly 8th pandemic. Therefore O1 and O139 are
responsible for epidemics and pandemics worldwide.
Biotypes of O1 V. Cholerae – 2 Biotypes differentiated
by biochemical and other test, agglutinated by O1
antisera.
Classical vibrio cholerae
Eltor vibrio cholerae
The Eltor vibrios were isolated by Gottschlich (1905)
from 6 Haj pilgrims at the Tor quarantine station on
the sinai penninsula (Egypt)
• These are identical except in biochemical and other
tests to classical cholera vibrios
SEROTYPES – based on minor surface antigenic
characters , both biotypes were classified further into
3 serotypes
Ogawa – agglutinated by its own antisera
Inaba – agglutinated by its own antisera
Hikojima – agglutinated by both antisera
• Strains of V.cholerae 0 1 may be further subdivided on
the basis of their O (A,B & C) antigens into 3 subtypes
– SEROTYPE O ANTIGENS
Ogawa AB
Inaba AC
Hikojima ABC
• V. cholerae O139 From Chennai it spreads to
rest of India, Bangladesh, South east Asia ,
China, Pakistan & parts of Europe and this may
be the start of 8th pandemic ? .
• It is non agglutinable to O1 and other available
antisera , therefore assigned to a new serotype
O139 Bengal, resembling to Eltor biotype
closely & replaced it gradually as well as coexist
in endemic areas.
• It is more invasive capsulated and causes
bacteremia
• O-1 strain vaccines could not protect against
O139 cholera
• It can be agglutinated by O139 antisera.
PHAGE TYPING
Strains of classical biotype of V.cholerae 01 can be
divided into 5 types by means of 3 phages (I-III) &
(IV) phage lyses all classical but not El Tor strains.
Phage type Sensitivity To Phase group

I II III IV
1 + + + +
2 _ + + +
3 + - + +
4 _ - + +
5 + + - +
PHAGE TYPING (ElTor)
• On basis of lysis of 4,phages ,El Tor
strains can be divided into 6 types . All
these strains are lysed by fifth (V) phage.
PHAGE SENSITIVITY TO PHASE GROUP

I II III IV V
1 + + + + +
2 + + + _ +
3 + + _ + +
4 + + _ _ +
5 + _ _ _ +
6 _ + _ _ +
VIBRIO II
• Cholera is an acute diarrheal disease caused by
cholera vibrio. In severe form, it presents as-
Profused diarrhea and
copious effortless vomiting
• This may lead to hypovolemic shock and death
in less than 24 hours.
• In treated cases the disease may last for 4-6
days, patient may pass a total volume of liquid
stool equal to twice his body weight. Therefore
cholera is a dramatic and terrifying illness.
• The incubation period < 24 hours- 5 days, the
symptoms are mild with ElTor biotype.
• The severity varies widely from rapidly fatal
disease to a transient asymptomatic colonization.
About 60% infections by classical vibrio & 75%
with ElTor remain asymptomatic.
• All the clinical feature of severe cholera results
from the massive loss of fluid & electrolytes.
• The stool is typically a colorless watery fluid with
flecks of mucous, resembling water in which rice
has been washed- rice water stools. The stool is
odorless, rich in bicarbonates, isotonic electrolyte
solution with little protein.
• It leads to decreased extracellular fluid volume,
hemoconcentration, hypokalemia, acidosis and
shock.
 Complication are-
• Muscular cramps, renal failure, pulmonary
oedema, cardiac arrhythmias and paralytic ilius
i.e., profound dehydration, circulatory collapse
and anuria.
• Mortality- 25-50% in untreated cases.
 Death attributable to:
 Hypovolemic shock (due to abnormally low
volume of circulating fluid (plasma) in the body.
 Metabolic acidosis (pH shifts toward acid side
due to loss of bicarbonate buffering capacity)
• ZIMBABWE: At a cholera
treatment center in the
town of Chegutu in
Mashonaland West
Province, a girl receives
intravenous fluids through a
drip into her arm.
Intravenous administration
of rehydration solution is
needed in severe cholera
cases to replace the fluids
lost through diarrhea and
vomiting. A large hole is cut
into her portable bed, with
a bucket placed
underneath, for patients
who are too weak to walk
to a proper latrine
• Above: A Cholera patient under intensive care at
HLSS' Owinykibul Army Barack Cholera Treatment
Centre, Eastern Equatoria State in 2014
 History & Epidemiology
Cholera is an epidemic and endemic disease,
exclusively a human disease, spread by contaminated
food and vegetables by feces of carriers or patients.
Its homeland is large deltaic area of Ganges &
Brahmaputra in Bengal, where the disease is known
from ancient times. In Kolkata peak is in hot dry season
& ends with the onset of monsoon but extends to
neighboring states during rainy season.
Cholera is notifiable disease, about 30 lakhs cases
occur annually and 2 lakhs are reported to WHO,
resulting in more than 1 lakh deaths annually.
•Till in the early 19th century cholera was confined to India,
periodically causing large epidemics in different parts. From
1817-1923 cholera spread from Bengal in 6 separate
pandemics, involving most parts of the world.
About 8 pandemics occurred to date -
1. 1817-`23: First Pandemic
2. 1829-`51: Second Pandemic
3. 1852-`60: Third Pandemic (Pacini)
4. 1863-`79: Fourth Pandemic
5. 1881-`96: Fifth Pandemic (Koch).
6. 1899-`1923: Sixth Pandemic
7. 1961- still on: Seventh Pandemic
8. 1992-?: Eighth Pandemic
7th pandemic started for the first time outside India in
Celebes, Sulawesi (Indonesia) by another biotype ElTor.
In the 8th pandemic? Cholera returned to India, caused
by NAG O139 Bengal, discovered in Chennai.
Pathogenesis
Enters orally via contaminated water or food.
Vibrios are highly susceptible to acids in stomach
& small doses do not cause infection.
High infectious dose: >108 bacilli but much lower
dose 103 -105 bacilli with achlorhydria or
hypochlorhydria, meditation or surgery (partial
gastrectomy) predisposes to cholera.
The vibrio begin to multiply in alkaline
environment in jejunum, adheres with epithelial
cells with the help of enzymes, fimbria such as
“toxin corregulated pilus (TCP)” & colonize. Then
remain attach to epithelial surface but do not
damage or invade. The changes are biochemical
due to secretion of cholera toxin.
 Cholera toxin- it is an enterotoxin, produced when vibrio
multiplies on epithelial cell surface. It is similar to heat
labile toxin (LT) of E. coli in structure, chemically,
antigenically & in biological properties but 100 times
more potent.
 It is determined by filamentous phage integrated with the
bacterial chromosome, replicates as a plasmid and can
be transmitted to a nontoxigenic strain. Several genes
are involved in the virulence of V. cholerae O1-
Ctx A, Ctx B- for 2 subunits of cholera toxin,
Tcp- toxin corregulated pilus.
Gene complex,
acf- accessory colonization factor,
Hap- hemagglutination protease &
Neuraminidase
These genes are controlled by regulatory genes- Tox R.
Mechanism:- Molecular weight is 84,000, consist of one A and
five B subunits. B- subunit (binding)- binds to the ganglioside
GM1 receptors on the epithelial cells and promotes entry of
subunit A into the epithelial cells (jejunal).
A- subunit (active)- after entry divides into A1 & A2
fragments.
A2- Links the biologically active A1 to the B
subunit.
A1 fragments- enters the cell and activates
adenyl cyclase
- The enterotoxin causes the transfer of adenosine
diphosphate ribose (ADP ribose) from NAD (nicotinamide
adenine dinucleotide) to a regulatory protein, which is a part
of adenylate cyclase enzyme responsible for the generation of
intracellular cAMP (cyclic adenosine monophosphate).
This result into irreversible activation of adenylate cyclase and
overproduction of cAMP.
-It cause inhibition of uptake of Na+ & Cl- ions by cells lining
the villi and hyper secretion of Cl- & HCo3- ions, which blocks
uptake of water & passive outflow of water across mucosal
cells, leading to serious loss of water & electrolytes
-A1 fragment causes-
-Prolonged activation of adenylate cyclase & accumulation
of c-AMP leading to outpouring of large quantities of
water & electrolytes in lumen & the consequent watery
diarrhea.
-It is isotonic with plasma but contains much more of K+ &
HCo3-.
-All clinical manifestations & complications are due to
massive water & electrolyte depletion.
 1 2
Mechanism
of Action of
Cholera
Toxin

NOTE: In step #4,

3 4
uptake of Na+ and Cl-
from the lumen is also
blocked.
HCO3- = bicarbonate
which provides
buffering capacity.
Mechanism of Action of Cholera Toxin
•The enterotoxin acts locally & does not invade the
intestinal wall. As a result few WBC & no RBC are found
in the stool.
Fluid loss originates in the duodenum and upper
jejunum; the ileum is less affected.
The large volume of fluid produced in the upper
intestine, however, overwhelms the absorptive capacity
of the lower bowel, which results in severe diarrhea.
To understand the mechanism of cholera toxin, De &
Chatterjee (1953) 1st demonstrated that injection of
cholera culture or filtrate into the ligated ileal loop in
rabbit caused fluid accumulation & ballooning.
Laboratory Diagnosis- required to confirm the diagnosis
1. Specimen-
a)Stool- Most useful specimen, should be collected before
administration of antibiotics, from pan is not
recommended.
b)Collection using rubber catheter- a lubricated catheter is
introduced into the rectum (no. 24-26) & letting the
liquid stool flow directly into a sterile screw caped
container.
c) Rectal swab- can be used, provided made with good
quality cotton wool, absorbing atleast 0.1-0.2 ml of
fluid. Useful in convalescent with no longer watery
diarrhea, moistened with transport media before
sampling. Vomitus is not used.
2) Transport- when delay in processing, following media
can be used- (1-3ml stool in 10-15 ml media).
a) Venkatraman- Ram Krishnan (VR) medium- crude
see salt 20 cm + peptone 5 gm in 1 liter D.W at pH
8.6- 8.8.
b) Alkaline salt transport media- VR media + boric
acid, NaoH & KCl at pH 9.2.
c) Cary- Blair's media- also useful for salmonella &
shigella. Buffered solution of NaoH, sodium
thioglycolate, Di- sodium phosphate & Calcium
chloride at a pH- 8.4.
d) Autoclaved see water- when other media are not
available.
e) Strips of blotting paper may be soaked in watery
stool & sent in plastic envelops if transport media are
not available.
f) Alkaline peptone water or Monsur’s media.
3) Direct Microscopy-
Gram staining- of mucous flakes shows short,
comma-shaped bacilli. Gram negative rods arranged
in parallel rows, described by Koch as “fish in
stream” appearance.
Motility- by hanging drop method- darting motility,
also known as shooting star or “swarm of gnats”
motility.
D/D- Campylobacter, Aeromonas & Pseudomonas.
-Motility after adding antisera- V. cholera becomes
non- motile when a drop of watery stool is added
with flagellar (H) antiserum. It differentiates it from
other actively motile bacteria. It is simple, quick &
reliable method which confirms the diagnosis.
4) Culture:-
-
-NA- produces glistening, translucent colonies with a
bluish tinge in transmitted light.
- uniform turbidity with pellicle in peptone water.
- Hemodigestion- non- specific killing of blood cells
by metabolites of bacteria. On BA-main inoculation
turns green but no change around single colonies.
-Enrichment broth- inoculation after 4-6 hrs. on
plate- APW at pH-8.6
-Plating on MCA & TCBS.
5) Biochemical tests-
-Catalase & oxidase positive-.
-No3 reduction test is positive,TSI- A/A, gas is
absent, indole+ urease negative, citrate variable.
-Positive cholera red reaction, string test, MR test &
VP- positive in ElTor.
-Decarboxylation test is- vibrio utilizes lysine &
ornithine.
-Aeromonas- only arginine
-Plesiomonas- utilizes all three.
 Slide agglutination:-
• Colonies of vibrios should be picked with a straight wire
& tested by slide agglutination with cholera ‘O’ subgroup
I serum, if positive further agglutinate with specific
Ogawa & Inaba sera for serotyping, Hikojima strains will
agglutinate equally well with both Ogawa & Inaba.
• If negative repeat with 5 colonies, as agglutinable & non
O 1 Vibrios co-exist in the same specimen.
• Further test biochemical for classical & ElTor vibrios.
• If not agglutinable by O 1 serum- test with O139 serum
& against H- antiserum to determine non O1 cholera
Vibrios as H- antigen is shared by all cholera vibrios.
7) Serology- complement- dependent vibriocidal test is
useful for assessing the prevalence in an area.
8) Testing water samples- by
i) Enrichment method- 900ml water to 100 ml
tenfold concentrated P.W. at pH 9.2 incubate &
re-enrichment before plating on selective media.
ii) Filtration method- water is passed through
millipore membrane filter & placed on selective
media.
Sewage- should be first diluted in saline, filtered
through gauze & treat as water.
Prophylaxis-
Improvement of sanitation & safe water supply.
Vaccination is most widely used method of
prevention in endemic areas.
a) Parenteral vaccine- killed suspension containing 8000
million V. cholerae per ml with equal no. of Ogawa &
Inaba serotypes given as subcutaneous or
intramuscular injection.
- Protection is 50-60 %.
- Duration is 3-6 months.
Similarly O139 strain vaccine is also prepared.
b) Oral vaccines- recently tried 2 vaccines.
i) Killed oral whole cell vaccines- with or without B-
subunit of cholera toxin.
ii) Live oral vaccines with classical, ElTor & O139 strains
with deleted toxin gene.
An ideal cholera vaccine is yet to be found.
Treatment:-
i) Prompt & adequate replacement of fluid and
electrolytes, orally or by I.V. route.
ii) Antibiotics- to reduce period of Vibrio excretion
& need for parenteral fluids.
National reference centre for cholera is located in-
National Institute of Cholera & Enteric diseases
(NICED), Kolkata.
Cholera III
 Halophilic Vibrios
Those Vibrios which requires sodium chloride in growth
media or natural environment for their growth are know
as Halophilic Vibrios. The halophilic Vibrios which causes
human infection are-
V. parahemolyticus
V. alginolyticus &
V. vulnificus.
Their natural habitat is sea water and marine life thats
why infections are seen by eating raw sea food .
VIBRIO PARAHAEMOLYTICUS
V. parahemolyticus-
- Isolated in 1951 in Japan as the causative agent of an
outbreak of food poisoning after eating sea –fish. It is now
considered as an important cause of food poisoning
throughout the world.
- Found in costal areas in fish, shrimps, crabs and oysters.
In Kolkata found in small pond fish & in 5-10% diarrhoea
cases admitted.
Morphology- resembles to cholera vibrio but differentiated
by-
-being capsulated,
-shows bipolar staining,
-shows pleomorphism-when grown in 3% salt
agar and produces peritrichous flagella on
solid media. (In broth-polar flagella).
Culture characters- can grow only if salt is added into the
media (up to 8 %).
- On TCBS – Green , opaque and raised centre.
- On MC – pale, NLF colonies
- On BA - show Beta hemolysis .
- Do not grow in P.W & on CLED media.
Biochemical Reactions - oxidase, Catalase, nitrate, indole
and citrate are -positive
- Ferments Glucose, mannitol, mannose and arabinose with
acid only.
- Sugars not femented are-Lactose, sucrose, xylose, adonitol,
Inositol, sorbitol And salicin.
-V.P +ve and decarboxylates lysine and ornithine.
-Pathogenesis- All strains are not pathogenic. Strains
isolated from environmental sources such as water & sea
food are always non-hemolytic when grown in high salt
BA ( wagatsuma’s agar), while strains from human
patients are always hemolytic. This phenomenon is known
as Kanagawa phenomenon and is due to production of a
heat stable hemolysin. The Kanagawa positive strains are
pathogenic to man, while negative strains are non
pathogenic. Enterotoxin is absent and it cause enteritis by
invasion of the intestinal epithelium.
- The food poisoning is associated with consumption of
marine food while acute diarrhoea is not associated with
food poisoning.
- Faeces contains- cellular exudate and blood.
- A few extraintestinal infections are also seen particularly in
wounds.
Lab. Diagnosis:- The faeces of patients with a history of
consumption of seafood is examined in the same manner as
that for V. cholerae.
- Examination of seafood and seawater for halophilic vibrio
species after enrichment in alkaline peptone water with 1%
sodium chloride.
- The diagnostic features are- being capsulated,
shows bipolar staining,
Green colonies on TCBS &
a positive Kanagawa phenomenon
.
V. vulnificus-
-Second most serious type of infection occur after
V. cholerae (fatality 20-30%). It is a marine,
halophilic vibrio forming green, non-sucrose
fermenting colonies on TCBS.
-VP negative, ferments lactose, can tolerate salt up
to less than 8% and can grow in the presence of
300 unit disk of polymyxin
Pathogenesis & infections- it has 2 biotypes-
- Strain 1- found in shellfish & cause human infections.
- Strain 2- found in Eels.
Has polysaccharide capsule & activates cytokines which
causes septicemia. After ingestion usually oysters,
penetrates the gut mucosa and enters the blood stream
leading to septicemia without GIT symptoms & high
mortality. Infections are most severe with-
- hepatic disease,
-hematopoitic disease,
-chronic renal failure and
-those receiving immunosuppressive
drugs.
It also causes acute diarrhoea after consumption of
shellfish.
- Direct exposures to seawater can lead to a rapidly
progressive wound infection in open wounds.
Diagnosis- stool culture & blood culture when
inoculated on TCBS- shows green colonies because
sucrose is not fermented.
Lactose is fermented.
Treatment – Tetracycline is the drug of choice
Ciprofloxacin is also effective.
V. alginolyticus
is a halophilic vibrio, formerly regarded as biotype of
V. parahemolyticus
- Ferments sucrose so that produces yellow colonies on
TCBS, can tolerate higher salt tolerance up to 10% , VP
positive, swarming is seen on nonselective solid media.
- Associated with infections of eyes, ears and wounds after
exposure to seawater.
- D/D from V. hemolyticus – VP +ve, sucrose +, swarming
and growth in 10% sod. chloride added .
- OTHER VIBRIOS
- V.mimicus – so named because it is closely
related/ resembles cholera vibrio in biochemical
tests.
- Responsible for sporadic cases of diarrhea on
the gulf coast of U.S.A. by eating seafood
especially oysters.
- The disease is self-limiting and clinical
manifestations resemble those caused by V.
parahemolyticus.
- D/D- cannot ferment sucrose- green colonies on
TCBS.
- Other species
V. hollisae, V. fluvialis & V. furnissii are responsible
for causing -Gastro-enteritis,
-Wound infections &
-Bacteremia.
- Single cases of infections are caused/ documented by-
V. metschnikovii –bacteremia
V. cincinnatiensis- meningitis &
V. carchariae- wound infection.