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EPIDEMIOLOGY & TREATMENT AND


BACTERIA PATHOGENESIS LABORATORY IDENTIFICATION
TAXONOMY PREVENTION
General Characteristics Epidemiology of • Incubation period: 2-3 days • Transport medium - Cary-Blair • Untreated: 60%
• Similarities to Enterobacteriaceae Vibrio spp. • High infectious dose: >108 CFU semi-solid agar fatality
o Gram-negative • Vibrio spp. o 103 -105 CFU with achlorhydria or • Enrichment medium - • Treated: <1%
o Facultative anaerobes (including V. hypochlorhydria (lack of or reduced stomach acid) alkaline peptone broth fatality
o Fermentative bacilli cholerae) grow • Abrupt onset of vomiting and life-threatening watery o Vibrios survive • Rehydration &
• Differences from Enterobacteriaceae in estuarine diarrhea (15-20 liters/day) and replicate at supportive therapy
o Polar flagella and marine • As more fluid is lost, feces-streaked stool changes to high pH o Oral
o Oxidase positive environments rice-water stools: o Other organisms  Sodium
worldwide o Colorless are killed or do chloride (3.5
• Formerly classified together as Vibrionaceae
o Primarily found in water sources • All Vibrio spp. o Odorless not multiply g/L)
o Cause gastrointestinal disease can survive o No protein • Selective/differential  Potassium
o Shown not closely related by molecular and replicate o Speckled with mucus culture medium - TCBS agar chloride (1.5
in • Cholera toxin leads to profuse loss of fluids and g/L)
methods o V. cholerae grow
contaminated electrolytes (sodium, potassium, bicarbonate)  Rice flour (30-
as yellow
Morphology and Physiology waters with o Hypokalemia (low levels of K in blood) 80g/L)
colonies
increased o Cardiac arrhythmia and renal failure  Trisodium
• Comma-shaped (vibrioid) bacilli • Biochemical and serological
salinity and at • Cholera toxin blocks uptake of sodium & chloride from citrate (2.9 g/L)
• V. cholerae, V. parahaemolyticus, V. vulnificus temperatures tests
o Intravenous (IV)
lumen of small intestine
are most significant human pathogens of 10-30oC • Death attributable to: • Doxycycline or
• Broad temperature & pH range for growth on media • Pathogenic o Hypovolemic shock (due to abnormally low tetracycline (Tet
o 18-37°C Vibrio spp. volume of circulating fluid (plasma) in the body) resistance may be
o pH 7.0 - 9.0 (useful for enrichment) appear to form o Metabolic acidosis (pH shifts toward acid side due developing) of
• Grow on variety of simple media including: symbiotic (?) to loss of bicarbonate buffering capacity) secondary value
o MacConkey’s agar associations • Water purification,
o TCBS (Thiosulfate Citrate Bile salts Sucrose) with chitinous Virulence Factors Associated with Vibrio cholerae sanitation & sewage
agar shellfish which O1 and O139 treatment
serve as an
• V. cholerae grow without salt
important and
• Vaccines
o Most other vibrios are halophilic only recently
recognized
Vibrio spp. Associated with Human Disease reservoir
• Asymptomatic
ally infected
humans also
serve as an
important
reservoir in
regions where
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cholera is
endemic Cholera Toxin (A2-5B)(Vibrio cholerae)
• Chromosomally-encoded; Lysogenic phage
Taxonomy of conversion; Highly conserved genetic sequence
Vibrio cholerae • Structurally & functionally similar to ETEC LT
• >200 • B-subunit binds to GM1 ganglioside receptors in
serogroups small intestine
based on
somatic O-
• Reduction of disulfide bond in A-subunit activates A1
antigen fragment that ADP-ribosylates guanosine
triphosphate (GTP)-binding protein (Gs) by
• O1 and O139 transferring ADP-ribose from nicotinamide adenine
serogroups dinucleotide (NAD)
are responsible
for classic
• ADP-ribosylated GTP-binding protein activates adenyl
epidemic cyclase leading to an increased cyclic AMP (cAMP)
cholera level and hypersecretion of fluids and
electrolytes
• O1 serogroup
subdivided Mechanism of Action of Cholera Toxin
into
• Two biotypes:
El Tor and
classical (or
cholerae)
• Three
serotypes:
ogawa, inaba,
hikojima
• Some O1
strains do not
produce cholera
1
enterotoxin
2
(atypical or
nontoxigenic
O1 V. cholerae)
• Other strains
are identical to
O1 strains but
do not
agglutinate in
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O1 antiserum
(non-cholera
(NCV) or non-
agglutinating(N
AG) vibrios)
(non-O1
V.cholerae)
• Several phage
types

Epidemiology of
Vibrio cholera
• Cholera 3 4
recognized for
more than two
millennia with
sporadic
disease and
epidemics
• Endemic in
regions of
Southern and
Southeastern
Asia; origin of
pandemic
cholera
outbreaks
• Generally in 5
NOTE: In step #4, uptake of Na+ and Cl- from the lumen
communities
is also blocked. HCO3- = bicarbonate which provides
with poor
buffering capacity.
sanitation
• Seven
pandemics
(possible
beginning of
8th) since 1817
attributable to
increased world
travel
• Cholera spread
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by
contaminated
water and
food
• Human
carriers and
environmenta
l reservoirs

Recent Cholera
Pandemics
• 7th pandemic:
o V.
cholerae
O1
biotype El
Tor
o Began in
Asia in
1961
o Spread to
other
continents
in 1970s
and 1980s
o Spread to
Peru in
1991 and
then to
most of
South &
Central
America
and to U.S.
& Canada
o By 1995 in
the
Americas,
>106
cases; 104

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dead
• 8th pandemic
(??)
o V.
cholerae
O139
Bengal is
first non-O1
strain
capable of
causing
epidemic
cholera
o Began in
India in
1992 and
spread to
Asia,
Europe and
U.S.
o Disease in
humans
previously
infected
with O1
strain, thus
no cross-
protective
immunity

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Summary of Vibrio parahemolyticus Infection

Summary of Vibrio vulnificus Infection

Virulence Factors Associated with Non-cholera Vibrios

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