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Vibrio cholerae
Buga Rudolf
HTC LECTURE SERIES
.
1
Introduction
•Family of affiliation – Vibrionaceae
•Other species:
oV. alginolyticus,
oV. mimicus,
oV. parahaemolyticus,
o V. vulnificus,etc.
2
Microscopy
•Curved gram negative bacilli (coma shaped).
•Highly motile with single polar flagellum.
3
Diagnosis
•Specimen:
• Severe watery diarrhoea
• Rectal swab
1. Wet mount examination:
o Characteristic darting motility
o Motility is stopped by addition of specific anti-
somatic antibody
2. Gram stain – Curved gram –ve bacilli.
4
Diagnosis…
3. Culture
oTCBS (selective medium)
o Yellow colonies (V. parahaemolyticus –
green colonies) after 24 hour incubation
o Alkaline peptone water (pH 8.6) (enrichment
medium)
4. Fluorescent Ab test
5. PCR
5
Diagnosis…
6. Identification:
• Gram stain
• Oxidase test (+positive, (pick colonies purity plate not
from TCBS)
• Serotyping:
oPoly O1 and 0139
o Mono – Inaba, Ogawa and Hikojima
6
Differential characters
Biotype El Tor Classical
Serotypes
Ogawa Inaba Hikojima Ogawa Inaba Hikojima
Antigens A,B A,C A,B,C A,B A,C A,B,C
7
Viability
•Tolerate alkaline
•Sensitive to acid
8
Clinical manifestation
•Cholera is a potentially epidemic and life
threatening secretory diarrhoea
•Characterised by mucous, voluminous watery
diarrhoea/stools
•Often accompanied by vomiting resulting in
hypovolemic shock and acidosis
•Mild infections can be caused
9
Pathogenesis
•Cholera transmission is by the faecal
oral route
•Sensitive to acid and most die on the
stomach
•Organisms adhere to and colonize the
small bowel
•Secrete potent enterotoxin CT
(choleragen), made of ‘A’’ and ‘B’
subunits 10
Pathogenesis…
•B’ subunit is for attachment to the plasma membrane of
the intestinal cells
•Released, enzymatically active ‘A’ subunit causes a
rise in cyclic adenosine 5-monophosphate (cAMP)
production
•High level of intracellular cAMP causes massive
secretion of electrolytes and water into the intestinal
lumen
11
Host defenses
•Non – specific defenses
• gastric acid
• mucous secretions
• intestinal motility
•Breast feeding protects infants in endemic areas
from the disease
•IgA and IgG antibodies act against the somatic Ag,
outer membrane protein and/or the enterotoxin and
other products of the V.cholerae
12
Epidemiology
•Endemic or epidemic in areas with poor sanitation
•Sporadic or limited outbreaks in developed countries
•In coastal regions, it may persist in shellfish and
planktons
•Long term convalescent carriers are rare
•Enteritis due to the halophile V. parahaemolyticus is
associated with raw or improperly cooked sea foods
13
Antibiotics/Control
•Sanitation effective but not feasible in endemic areas
•No effective vaccine
•Health education
•Antimicrobial agents:
• Tetracycline
• Cotrimaxazol
• Naladixic Acid
• Cipro
• Erythromycine
• Cephalosporins
14

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Vibrio cholerae.ppt

  • 1. Vibrio cholerae Buga Rudolf HTC LECTURE SERIES . 1
  • 2. Introduction •Family of affiliation – Vibrionaceae •Other species: oV. alginolyticus, oV. mimicus, oV. parahaemolyticus, o V. vulnificus,etc. 2
  • 3. Microscopy •Curved gram negative bacilli (coma shaped). •Highly motile with single polar flagellum. 3
  • 4. Diagnosis •Specimen: • Severe watery diarrhoea • Rectal swab 1. Wet mount examination: o Characteristic darting motility o Motility is stopped by addition of specific anti- somatic antibody 2. Gram stain – Curved gram –ve bacilli. 4
  • 5. Diagnosis… 3. Culture oTCBS (selective medium) o Yellow colonies (V. parahaemolyticus – green colonies) after 24 hour incubation o Alkaline peptone water (pH 8.6) (enrichment medium) 4. Fluorescent Ab test 5. PCR 5
  • 6. Diagnosis… 6. Identification: • Gram stain • Oxidase test (+positive, (pick colonies purity plate not from TCBS) • Serotyping: oPoly O1 and 0139 o Mono – Inaba, Ogawa and Hikojima 6
  • 7. Differential characters Biotype El Tor Classical Serotypes Ogawa Inaba Hikojima Ogawa Inaba Hikojima Antigens A,B A,C A,B,C A,B A,C A,B,C 7
  • 9. Clinical manifestation •Cholera is a potentially epidemic and life threatening secretory diarrhoea •Characterised by mucous, voluminous watery diarrhoea/stools •Often accompanied by vomiting resulting in hypovolemic shock and acidosis •Mild infections can be caused 9
  • 10. Pathogenesis •Cholera transmission is by the faecal oral route •Sensitive to acid and most die on the stomach •Organisms adhere to and colonize the small bowel •Secrete potent enterotoxin CT (choleragen), made of ‘A’’ and ‘B’ subunits 10
  • 11. Pathogenesis… •B’ subunit is for attachment to the plasma membrane of the intestinal cells •Released, enzymatically active ‘A’ subunit causes a rise in cyclic adenosine 5-monophosphate (cAMP) production •High level of intracellular cAMP causes massive secretion of electrolytes and water into the intestinal lumen 11
  • 12. Host defenses •Non – specific defenses • gastric acid • mucous secretions • intestinal motility •Breast feeding protects infants in endemic areas from the disease •IgA and IgG antibodies act against the somatic Ag, outer membrane protein and/or the enterotoxin and other products of the V.cholerae 12
  • 13. Epidemiology •Endemic or epidemic in areas with poor sanitation •Sporadic or limited outbreaks in developed countries •In coastal regions, it may persist in shellfish and planktons •Long term convalescent carriers are rare •Enteritis due to the halophile V. parahaemolyticus is associated with raw or improperly cooked sea foods 13
  • 14. Antibiotics/Control •Sanitation effective but not feasible in endemic areas •No effective vaccine •Health education •Antimicrobial agents: • Tetracycline • Cotrimaxazol • Naladixic Acid • Cipro • Erythromycine • Cephalosporins 14