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Vibrio cholera
Abrar pathan
Morphology
and
Identification
V cholerae is a comma-shaped,
curved rod 2–4 μm long.
It is actively motile by means of a
polar flagellum.
On prolonged cultivation, vibrios may
become straight rods that resemble
the gram-negative enteric bacteria.
Culture
• V cholerae produces convex, smooth, round colonies
that are opaque and granular in transmitted light.
• V cholerae grows well on thiosulfate-citrate-bile-
sucrose (TCBS) agar, a media selective for vibrios, on
which it produces yellow colonies (sucrose
fermented) that are readily visible against the dark-
green background of the agar.
• Vibrios are oxidase positive, which diff erentiates
them from enteric gram-negative bacteria.
• Vibrios grow at a very high pH (8.5–9.5) and are
rapidly killed by acid. Cultures containing fermentable
carbohydrates therefore quickly become sterile.
Growth
Characteristics
V cholerae
regularly ferments
sucrose and
mannose but not
arabinose.
Antigenic Structure
and Biologic Classifi
cation
• Many vibrios share a single heat-
labile fl agellar H antigen.
• Antigens to H antigen are probably
not involved in protection of
susceptible hosts.
• V cholerae has O
lipopolysaccharides that confer
serologic specificity.
Pathogenesis and Pathology
• V cholerae is pathogenic only for humans. A person with normal
gastric acidity may have to ingest as many as 10 raised to 10 or more
V cholerae to become infected
• When the vehicle is water because the organisms are susceptible to
acid. When the vehicle is food, as few as 102 –104 organisms are
necessary because of the buffering capacity of food.
• Any medication or condition that decreases stomach acidity makes a
person more susceptible to infection with V cholerae.
Clinical Findings
• About 50% of infections are asymptomatic.
• The incubation period is 12 hours–3 days for persons who develop
symptoms, depending largely on the size of the inoculum ingested.
• There is a sudden onset of nausea and vomiting and profuse diarrhea
with abdominal cramps.
• Stools, which resemble “rice water,” contain mucus, epithelial cells,
and large number of bacterium.
• There is rapid loss of fluid and electrolytes, which leads to profound
dehydration, circulatory collapse, and anuria.
Diagnostic
Laboratory
Tests
Immunity
• Gastric acid provides some protection against cholera vibrios. An attack of
cholera is followed by immunity to reinfection, but the duration and degree
of immunity are not known.
• In experimental animals, specific IgA antibodies occur in the lumen of the
intestine.
• Similar antibodies in serum develop after infection but last only a few
months.
• Vibriocidal antibodies in serum (titer ≥1:20) have been associated with
protection against colonization and disease.
• The presence of antitoxin antibodies has not been associated with
protection.
Treatment

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Vibrio cholera.pptx

  • 2.
  • 3. Morphology and Identification V cholerae is a comma-shaped, curved rod 2–4 μm long. It is actively motile by means of a polar flagellum. On prolonged cultivation, vibrios may become straight rods that resemble the gram-negative enteric bacteria.
  • 4. Culture • V cholerae produces convex, smooth, round colonies that are opaque and granular in transmitted light. • V cholerae grows well on thiosulfate-citrate-bile- sucrose (TCBS) agar, a media selective for vibrios, on which it produces yellow colonies (sucrose fermented) that are readily visible against the dark- green background of the agar. • Vibrios are oxidase positive, which diff erentiates them from enteric gram-negative bacteria. • Vibrios grow at a very high pH (8.5–9.5) and are rapidly killed by acid. Cultures containing fermentable carbohydrates therefore quickly become sterile.
  • 6. Antigenic Structure and Biologic Classifi cation • Many vibrios share a single heat- labile fl agellar H antigen. • Antigens to H antigen are probably not involved in protection of susceptible hosts. • V cholerae has O lipopolysaccharides that confer serologic specificity.
  • 7. Pathogenesis and Pathology • V cholerae is pathogenic only for humans. A person with normal gastric acidity may have to ingest as many as 10 raised to 10 or more V cholerae to become infected • When the vehicle is water because the organisms are susceptible to acid. When the vehicle is food, as few as 102 –104 organisms are necessary because of the buffering capacity of food. • Any medication or condition that decreases stomach acidity makes a person more susceptible to infection with V cholerae.
  • 8. Clinical Findings • About 50% of infections are asymptomatic. • The incubation period is 12 hours–3 days for persons who develop symptoms, depending largely on the size of the inoculum ingested. • There is a sudden onset of nausea and vomiting and profuse diarrhea with abdominal cramps. • Stools, which resemble “rice water,” contain mucus, epithelial cells, and large number of bacterium. • There is rapid loss of fluid and electrolytes, which leads to profound dehydration, circulatory collapse, and anuria.
  • 10. Immunity • Gastric acid provides some protection against cholera vibrios. An attack of cholera is followed by immunity to reinfection, but the duration and degree of immunity are not known. • In experimental animals, specific IgA antibodies occur in the lumen of the intestine. • Similar antibodies in serum develop after infection but last only a few months. • Vibriocidal antibodies in serum (titer ≥1:20) have been associated with protection against colonization and disease. • The presence of antitoxin antibodies has not been associated with protection.