Vibrio cholerae cholerae classical biotype; Vibrio cholerae El Tor biotype; serogroups O1 and O139 -Bengal- and Vibrio cholerae NAG (Non-O1, Non-O139) Identification; Toxin production

Cholera is a diarrheal disease caused by severe massive luminal secretion of electrolytes and water from enterocytes, with increase in intracellular cAMP concentration (cyclic adenosine monophosphate) -induced Vibrio cholerae toxin. This bacterium is mainly transmitted through contaminated water or food (seafood eaten raw or undercooked, contaminated vegetables, etc.), or other items contaminated with it.

They have known seven cholera pandemics in the world. The last, which began in 1961 is still developing. Vibrio cholerae cholera (Vibrio cholerae classical) and Vibrio cholerae biotype El Tor (so called because it was first described station forty El Tor, in the Sinai Peninsula): the bacteria causing two biotypes differ. These biotypes can differentiate themselves by their hemolytic capability and hemagglutination and by their sensitivity to some antimicrobial or bacteriophages. Within the species Vibrio cholerae serogroups may be differentiated according to the antigenicity of the lipopolysaccharide -antigen O- (LPS). Have differentiated over 206 different serogroups of Vibrio cholerae according to the antigenicity O. Of these, until 1991, only 138 different serogroups was found, but in October 1992, an epidemic of cholera - like disease (Cholera-like occurred ) in the Bay of Bengal, which hit the port city of Madras in southern India. In December of that year it spread to the southern coast of Bangladesh and then the whole country. Producing strain belonged to none of the 138 known hitherto serogroups, and was assigned the serogroup O139 (Bengal). Vibrio cholerae O139 causes a disease similar to that generated by Vibrio cholerae El Tor involved in the seventh pandemic. This strain was extended between 1993 and 1994, then he seemed to have disappeared, but reappeared in 1996 in Calcutta and other parts of India. Of the more than 200 serogroups or different, which have been linked to cholera, with potential to cause pandemics or major outbreaks are serogroups O1 and O139. All strains of Vibrio cholerae serogroups not correspond whose serogroups O1 to or O139, called Vibrio cholerae strains NAG or Vibrio cholerae non-O1; non-O139. These strains exist in aquatic environments, and its epidemiological significance is different from having serogroups O1 and O139, since only been implicated as causing human diarrhea boxes in many countries. These strains have been subdivided into two groups by some: enteropathogenic and non-enteropathogenic. These serogroups found O6, O14, O10 (India), O10 and O12 (Peru), O37 (Sudan), O141 (many regions).

Corresponding to serogroup O1 strains they can be differentiated into two serotypes, Ogawa and Inaba, Ogawa serotype being the most prevalent in the current pandemic.

The high pathogenicity of Vibrio cholerae of serogroups O1 and O139 is mainly due to production of cholera toxin (CT), an enterotoxin encoded by the ctxAB genes. These genes are from the CTX? bacteriophage lysogen filamentous.

In addition to cholera toxin, other virulence factors:

    • TCP (coregulated pilus Toxin) which participates in the process of colonization of the intestinal tract, and it is the receiver using the CTX? bacteriophage to infect bacteria and insert its genome with the gene encoding cholera toxin. The genes required for biosynthesis of TCP are associated in the genomic region called VPI (Vibrio Pathogenicity Island) of Vibrio cholerae classical and El Tor biotypes. However, these genes, and ctxAB gene are absent in strains of Vibrio cholerae NAG (non-O1, non-O139).
    • Cholera enterotoxin accessory (ace gene: accesory cholerae enterotoxin).
    • Occlusive zonular toxin (zot gene: zonula occludens toxin).
    • ToxR (Toxin Regulatory Protein) which corregula expression of CT and TCP.
    • Other factors that facilitate adhesion and colonization: hemagglutinin mannose resistant mucosa (Mannose-fucose resistant cell-associated hemaglutinnin); Mannose sensitive hemagglutinin (Mannose-sensitive hemagglutinin), and outer membrane proteins (Outer Membrane Protein).


  • Vibrio cholerae NAG (non-O1, non-O139). These environmental vibrios lack toxin - coding genes on its chromosome, but can capture virulence genes through mobile genetic elements and become toxigenic. Pathogenic factors might include:
      • Thermostable enterotoxin (NAG-ST: Heat-Stable Toxin).
      • Hemolysin (hlyA: hemolysin gene).
      • Protease (HAPA: Protease gene).
      • Actin crosslinking cytotoxin (rtxaC: Cytotoxic actin cross-linking repeats toxic gene).
      • Sialidase (nanh: Silalidase gene).
      • Type 3 secretion system (TTSS: Type three secretion system).
      • Type 6 secretion system (TSSS: Type six secretion system).
      • Occasionally found CT toxin producing strains (ctxA gene), and TCP (coregulated pilus Toxin).

Tests in IVAMI:

  • Microbiological identification of Vibrio cholerae by metabolic tests.
  • Identification of Vibrio cholerae biotype cholerae (classical) and El Tor biotype of Vibrio cholerae by conventional tests.
  • Identification of serogroups O1 and O139 by molecular testing.
  • Identification of Vibrio cholerae NAG (non-O1, non-O139), using conventional molecular testing.
  • Detection of toxin production ctxA, zot and ace, and TCP colonization factor by molecular methods.
  • Detecting thermostable enterotoxin production by strains of Vibrio cholerae NAG.

Test samples

  • Isolates cultured

Delivery term

  • 24 to 48 hours (if available before preliminary information will be communicated).

Cost of testing