MICROBIOLOGY PPT LECTURE NOTES | Karya Tulis Ilmiah

Vibrio
• Vibrio cholerae -gastroenteritis
• Vibrio parahaemolyticus -gastroenteritis, wound
infection, bacteremia
• Vibrio vulnificus -wound infection, bacteremia

Vibrio sp.
Gram-negative rods
Curves or comma shaped
Non-spore forming
Highly motile-single polar flagella
Associated with salt water
Oxidase positive
Facultative anaerobe
Tolerate alkaline conditions to
pH9.0
Readily cultivated, Simple
nutritional requirements

Vibrio cholerae
• Antigenic structure

– Common heat-labile flagellar H antigen
– O lipopolysaccharide confers serologic
specificity
• More than 150 O antigen serogroups
• Only O-1 and 0139 serogroups cause Asiatic
cholera
Three serotypes; Ogawa, Inaba, Hikojima
Two biovars; classic and El Tor

• 2 biotypes of serogroup O-1
Classical biotype
El Tor biotype.
• Serogroup 139

V. cholerae - Transmission
feces

water
– fresh
– salt

food

Vibrio cholerae
• Epidemiology
– Epidemic cholera-spread by
contaminated water under conditions of
poor sanitation
– Endemic-consumption of raw seafood
– Copepods

Vibrio cholerae
• Pathogenesis
– Ingest 108-1010 organisms
– Non invasive infection of small intestine
– Organisms secrete enterotoxin
– Watery diarrhea

Virulence factors of V.cholerae O1 and O139
Virulence factor

Biological effect

Cholera toxin

Hypersecretic of electrolytes and water

Coregulated pilus

Adherence to mucosal cells adhesin

Accessory colonization factor

adhesin

Hemagglutination protease

Releases bacteria from mucosal cells

Zona occludens

Exotoxin

Accessory cholera enterotoxin

Exotoxin

Flagellum

Motility

Siderophores

Iron sequestration

Cholera toxin
• Enterotoxin-cholera toxin-CtxAB
–
–
–

–
–

Encoded by a prophage
Molecular mass of 84,000 daltons
A subunit-ADP-ribosylating toxin
B subunit-bind GM1-gangliosides on enterocytes
A subunit ADP ribosylates Gs-alpha which regulates
activation of adenlyate cyclase
– Result is persistent increase in cAMP levels
– Hyper secretion of Na, Cl, K, bicarbonate and H20

Vibrio cholerae-Clinical
manifestations
– Asymptomatic colonization to fatal diarrhea
– Onset 2-3 days after ingestion
– Abrupt onset of watery diarrhea and
vomiting
– Rice water stools
– Severe fluid and electrolyte loss-dehydration,

metabolic acidosis, hypovolemic shock, renal
failure
– Death 60% if untreated, 1% if treated for
fluid loss

Pathogenicity of V. cholera
• Dehydration and death
• Massive secretion of ions/water into
gut lumen

Immunity
• Strong immunity after recovery, SIgA

Bacteriological Diagnosis

• Specimens: stool, vomitus.
• Stained smear
• Culture: alkaline peptone
water of agar plate, and
TCBS agar plate.

• Quick immunological
methods:
immunofluorescent “ball”
test; PCR.

Vibrio-Prevention and Control
• Improved sanitation

• Fluid and electrolyte
replacement
• Antibiotic prophylaxis
• Improved food handling

Vibrio parahemolyticus
• One kind of halophilic vibrios; optimal NaCl
concentration contained in culture media is 3.5%;
hemolysin related to its pathogenicity, can be detected
by human or rabbit RBC test (Kanagawa test); cause
food poisoning in human beings.
• raw sea-food

• Clinical manifestations
– Self-limiting diarrhea to mild cholera-like illness
– 24 hours after ingestion-explosive water diarrhea
• Headache, abdominal cramps, nausea, vomiting, low
grade fever for 72 hours or more
• Uneventful recovery
• Wound infections in people exposed to seawatercontaining vibrios