BSCI 424 — PATHOGENIC MICROBIOLOGY — Fall 2000

Vibrio Summary

Morphology & Physiology:

  Gram-negative, facultatively anaerobic comma-shaped bacillus

  Oxidase positive

  Optimal growth: 18-37° C; pH - 7.0, tolerates up to pH 9

  Grows on several different media including MacConkey and TCBS

  V. cholerae grow without salt, but other vibrios are halophilic

Taxonomy:

  Family Vibrionaceae

  139 serogroups of V. cholerae based on O-somatic antigen (O-polysaccharide side chain of lipopolysaccharide)

  O1 and O139 serogroups responsible for classic epidemic cholerax

 O1 serogroup subdivided into two biotypes: el tor and cholerae

 Further subdivided into serotypes: ogawa, inaba, hikojima

 Some O1 strains do not produce cholera enterotoxin (atypical or nontoxigenic O1 V. cholerae)

 Other strains are identical to O1 strains but do not agglutinate in O1 antiserum (non-cholera (NCV) or non-agglutinating (NAG) vibrios) (non-O1 V. cholerae)

  Several phage types (classification method based on susceptibility to different bacteriophages)

  See also Aeromonas and Plesiomonas (both formerly classified as Vibrionaceae)

Clinical Syndromes:

 V. cholerae: cholera (gastroenteritis)

  V. parahaemolyticus: gastroenteritis, wound infections, bacteremia

  V. vulnificus: bacteremia, wound infections, cellulitis (see WebLinked image)

Epidemiology:

  Cholera recognized for more than two millenia

  Sources:

V. cholerae: water, food

V. parahaemolyticus: shellfish, seawater

V. vulnificus: shellfish (particularly raw oysters), seawater 

  V. cholerae endemic in regions of Southern and Southeastern Asia and is responsible for pandemic cholera

  Seven cholera pandemics since 1817 (possibly beginning the eighth pandemic with a V. cholerae O139 Bengal strain that was initially recognized in India in 1992)

  Increase in rapid intercontinental travel via airplane has contributed to spread of disease

  Increase in number of cases seen in the U.S, Central America and S. America following spread of V. cholerae O1 biotype el tor strain associated with seventh pandemic from Asia, Africa, Europe and Oceana to Peru in 1991

Pathogenesis & Immunity:

  Incubation period - hours to days

  Abrupt onset of diarrhea and vomiting

  Cholera toxin leads to increase in cAMP with hypersecretion of fluids and electrolytes and blockage of absorption of electrolytes from the lumen; Fluid loss can approach 15 to 20 liters/day

  Electrolyte imbalance leads to hypovolemic shock and metabolic acidosis and ultimately death

  Untreated cases - 60% fatality

Laboratory Identification:

  Transport medium

  Enrichment - alkaline peptone broth

  Culture - TCBS agar

  Biochemical and serological tests

Treatment, Prevention & Control:

  Rehydration & support - Oral or IV

  Tetracycline

  Sanitary and sewage treatment

  Water purification

  Vaccines not yet totally efficacious
 

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