Table of contents :

Homo-restricted^ref. > 139 O Ag serotypes grouped into 6 serogroups. Alkalophiles (pH 7÷9). Not invasive : just in gut lumen or adhesed to gut lining epithelium.

• Group 1  = Vibrio cholerae O1 (properly said cholera vibrio; almost always fall into the Heiberg I fermentation pattern (sucrose and mannose but not arabinose)).

Proteomics : virulence factors : sensing its changing environment is key when making the transition from an aquatic lifestyle to one more suited to a human host. An inverse correlation between motility and virulence gene expression has been reported, with the NADH:ubiquinone oxidoreductase system which powers motility by generating a sodium-motive force, playing a pivotal role. Bile inhibits activity of the transcription factor ToxT, a protein responsible for direct activation of numerous virulence gene promoters.Components of an acid-tolerance response system and quorum sensing also have a role in regulation of virulence gene expression. V. cholerae O139 O-antigen polysaccharide is essential for Ca²⁺-dependent biofilm development in seawater => impact of estuarine ion flux on the microbial ecology of the estuary
• hemagglutinin

The presence or absence of hemolysis in V. cholerae does not necessarily distinguish pathogenic strains of the organism from nonpathogenic ones. The classical biotype of the cholera bacillus is nonhemolytic and certainly can cause overt cholera. Hemolysis can be found in the El Tor biotype and, historically, this has been used to distinguish the biotypes. Strains of El Tor that do not produce hemolysis have been reported, and some strains of both O1 and O139 V. cholerae which are not hemolytic initially can be hemolytic after serial passage through rabbit ideal loops. The usefulness of hemolysis as a virulence factor is unclear, since nonhemolytic strains produce fluid accumulation in the rabbit gut, and hemolytic strains do not necessarily produce a secretory response^ref
• accessory colonization factor (acf)
• mucinase or hemagglutinin protease (hap) that degrades different types of protein including fibronectin, lactoferrin and cholera toxin itself, contributing to detachment rather than attachment. Possibly the vibrios would need to detach from cells that are being sloughed off of the mucosa in order to reattach to newly formed mucosal cells.
• neuraminidase degrades plasma membraner gangliosides in small bowel enterocytes to the monosialosyl form, creating the GM₁ ganglioside.
• Vibrio cholerae acquired genetic elements in such a sequence : regulatory factors => TCP bacteriophage insertion site => TCP bacteriophage genome, that encodes for a protein (TCP) which is both a type IV fimbria and the receptor for a second bacteriophage (CTXf) => CTXf genome, whose ctxAB operon encodes the AB₅ cholera enterotoxin (CT / CTx) / choleragen. The GM₁ ganglioside on jejunum enterocytes and M cells acts as a receptor for the p11.6^B subunits (a.k.a. choleragenoid). The p29^A subunit divides itself (through disulfide bond reduction) into p5.5^A2 and p23.5^A1 fragments : the latter catalyzes ADP-ribosylation on a Arg residue (glycosidic bond) in Ga_s subunits (helped by c-ARF), causing irreversible activation of adenylyl cyclase. This results in excessive secretion of Na⁺ and Cl^- by enterocytes, which, recalling H₂O for osmotic gradient, cause lavish diarrhea. CT also induces secretion of VIP from neurons in the myoenteric plexus, which in turns further stimulates secretions in enterocytes. LD₅₀ = 20 pg in humans. After Koch thought he had established Vibrio cholerae as the cause of cholera a sceptical colleague drank a culture without ill effect : if drinking water is kept free of the V cholerae infected with the phage all is well, just as phage and bacterium live harmlessly together in zooplankton infested coastal waters of the Pacific
• toxin coregulated pili (Tcp) (a colonization factor) : the ctx operon and the tcp operon are part of a regulon, the expression of which is controlled by the same environmental signals. The proteins involved in control of this regulon expression have been identified as ToxR, ToxS and ToxT. It is expressed before cholera toxin
• zonula occludens toxin (Zot)
• accessory cholera enterotoxin (Ace)
• a single protein required for efficient intestinal colonization mediates attachment to both zooplankton and human epithelial cells by binding to a sugar present on both surfaces^ref
Serovars according to O antigens :
• Ogawa (A and B Ags)
• Inaba (A and C Ags)
• Hikojima (A, B and C Ags : relatively rare)
Biovars :
• cholerae (classical; produce CT-1) : sensitive to group IV phage and bacteriophage IV labile when outside host => only direct transmission; considered extinct, reappeared in Bangladesh in 1982; cases:carriers ratio 1:2-4.
• eltor (isolated in El Tor quarantine station for pilgrims in the Sinai peninsula) : most strains produce CT-2 but the Gulf Coast strains produce CT-1. Resistant to bacteriophage IV and polymixin B. They produce an hemagglutinin (for chicken RBCs) and an hemolysin (for goat or sheep RBCs in Greig test : however, during the most recent pandemic, most (except for the recent isolates from Texas and Louisiana) don't express it); cases:carriers  ratio 1:30-100; longer latency and less severe infections (paracholera). More stable when outside host => also indirect transmission. The presence or absence of hemolysis in V. cholerae does not necessarily distinguish pathogenic strains of the organism from nonpathogenic ones. The classical biotype of the cholera bacillus is nonhemolytic and certainly can cause overt cholera. Hemolysis can be found in the El Tor biotype and, historically, this has been used to distinguish the biotypes. Strains of El Tor that do not produce hemolysis have been reported, and some strains of both O1 and O139 V. cholerae which are not hemolytic initially can be hemolytic after serial passage through rabbit ideal loops. The usefulness of hemolysis as a virulence factor is unclear, since nonhemolytic strains produce fluid accumulation in the rabbit gut, and hemolytic strains do not necessarily produce a secretory response^ref
Epidemiology : estuarine environments. Cholera was originally an endemic disease localized within the delta region of the River Ganges. As the Indian trade with Western European countries increased from 1817, cholera spread all over the world, bringing as many as 6 pandemics before 1923. No other pandemic of such classical cholera has
ever broken out since.
• 1817-1823 : first pandemic by classical biovar emerged in India. The first pandemic of what the British and the Americans called Asiatic cholera (or cholera morbus) reached Southeast Asia, East Africa, the Middle East, and the Caucasus, but petered out in 1823
• 1829-1851 : second pandemic by classical biovar. A second pandemic, between 1826 and 1837, also originated in India, but this time it took a devastating toll on both Europe and America, arriving in Britain in the autumn of 1831 and in America the following year. By 1833, twenty thousand people had died of cholera in England and Wales, with London especially hard hit
• 1852-1859 : third pandemic by classical biovar. A third pandemic swept England and Wales in 1848-49 (more than fifty thousand dead) and again in 1854, when thirty thousand died in London alone.
• 1854 : before acceptance of the "germ theory" John Snow stopped an epidemic in Soho, London by the simple expedient of removing the handle of the "Broad Street pump" (a contaminated water supply)
• 1863-1879 : forth pandemic by classical biovar. When cholera returned to London in 1866, its toll was much smaller, and the main outbreak was traced to a section of Bazalgette’s system which had yet to be completed. In many people’s opinion, Snow, who had died in 1858, now stood vindicated.
• 1881-1896 : fifth pandemic by classical biovar
• 1883 : first isolation of the "Kommabacillus" by Robert Koch
• 1899-1923 : sixth pandemic by classical biovar
• 1961 : seventh pandemic begun in Sulawesi (Celebes), Indonesia and is still acting, sustained by eltor biovar. Because humans are the only reservoirs, survival of the cholera vibrios during interepidemic periods probably depends on a relatively constant availability of low-level undiagnosed cases and transiently infected, asymptomatic individuals. Long-term carriers have been reported but are extremely rare. The classic case occurred in the Philippines, where "cholera Dolores" harbored cholera vibrios in her gall-bladder for 12 years : no secondary cases had been associated with her well-marked strain. Recent studies, however, have suggested that cholera vibrios can persist for some time in shellfish, algae or plankton in coastal regions of infected areas and it has been claimed that they can exist in a "viable but nonculturable state". It has spread to
• neighboring Southeast Asia
• Japan^ref has reported secondary cases : although cholera cases in Japan used to be restricted to returnees from cholera-endemic areas, infections among people who never experienced overseas travel have increased noticeably in recent years. With cholera being endemic in the country, there was an outbreak in Arida City, Wakayama Prefecture in 1977, of which the source of infection was ascribed to a returnee from the Philippines. Another outbreak occurred in 1978, presumably due to consumption of lobsters of Indonesian origin served at a wedding parlor at Ikenohata, Tokyo. In 1989, there was an outbreak, which began in Nagoya, involving patients living in 7 different prefectures, and, in 1991, another outbreak occurred in Tokyo Metropolis. As an imported incident worth special mention, many cholera patients appeared among travelers to Bali Island in 1995. Cases of cholera infection exploded in as many as 37 different prefectures involving 296 cases^ref. Cholera cases in 1996 numbered 62, comprising 49 (79%t) imported cases and 13 (21%) domestic cases without history of overseas travel; the total number of cases was markedly less than that of 1995 (377). The difference may be attributed to the markedly decreased number of cases (3) of Bali returnees. Cholera cases numbered 101 in 1997. Out of these cases, 36 -- with no history of overseas travel -- were living in 17 different prefectures^ref accounting for 36% of the total number of cases in 1997. The largest number of cases was found in August 1997, and the next largest in July 1997, showing an incidence pattern similar to that of Vibrio parahaemolyticus food poisoning^ref. On the other hand, the imported cases numbered largest, at 16, in April 1997. This was due to outbreaks involving 11 patients in 2 groups of sightseeing tours to Thailand. The ages of the patients without history of overseas travel ranged from 13 to 86 years (average 60 years), of which those aged over 60 years accounted for about 51%. The ages of the patients who had history of overseas travel ranged from 6 to 72 years (average 46 years), and those > 60 years accounted for only about 17%. The cases without history of overseas travel were mostly older people, but no case was found among their family members. 34 strains of Vibrio cholerae O1 isolated from cases with no history of overseas travel in 1997 were analyzed for phage type, drug sensitivity, and genotype by pulsed-field gel electrophoresis (PFGE) after digestion with NotI restriction enzyme. Identical, or very similar, patterns were obtained with all strains. The patterns were identical to those of the strains prevailing recently in Southeast Asia, and different from those of the strains responsible for the past domestic outbreaks. It was difficult to identify the route of infection from these analytical results. V. cholerae O139 was 1st isolated from a traveler to India in Saitama Prefecture in April 1993 and from a Nepalese visitor to Nagano Prefecture in July of the same year^ref. These cases both developed severe cholera symptoms, but the case in Tochigi Prefecture in October 1993, returning from India, showed only mild diarrhea. The other 4 cases reported during February to April 1994 were infected in Thailand. V. cholerae O139 was isolated from 2 cases returning from the Indian subcontinent in August 1993 and also from other 2 cases returning from India and China in October 1994. There were no reports of cases of V. cholerae O139 infection for some time following the above-mentioned cases, but, in September 1997, infection was found in a returnee (a 24-year-old male) from Nepal
• Singapore : in 1993, 12 persons were infected with cholera after eating inadequately cooked mussels harvested near a sewage discharge site. The 1999 Singapore outbreak affected at least 8 individuals at a wedding reception and was related to a banana flavored drink in which contaminated ice was used. There have been imported cases of V. cholerae infection in 2000 and 2002. In May 2004 an 89-year-old man died, among 9 people infected, and authorities are trying to trace the source of the disease
• Indian Subcontinent :
• Bangladesh : the annual case rate exceeds 2 per 1000 population
• Near East
• Africa was reached in 1970 : African countries reporting outbreaks of cholera or acute watery diarrhea to the WHO 2003 and 2006


• Malawi recorded its 1st case of infection in 1973 with about 35 000 infections and since then the epidemic has been claiming a lot of lives in the country. In 1998/99 cholera attacked 3000 people, while 2000 lives were lost in 2001/02. In 2004, the country registered about 12 040 cases of cholera.
• Guinea Bissau : 26,000 cases and > 400 deaths in 2005
• Angola has largely been spared cholera outbreaks since 1995. That may have lessened the population's immunity and helps explain the rapid spread of the disease since the first case was reported on 13 Feb 2006, recording 554 deaths and 12 052 cases in just over 2 months. Angola had reported 46,758 cases of cholera, including 1893 deaths, as of June 19, 2006^ref. The outbreak has affected 14 of 18 provinces, but nearly half the cases were reported in the coastal capital, Luanda, and another 17% in Benguela provinces. The overall case fatality rate is about 4%, although in some provinces, it has reached 30%^ref
• Tanzania : the last severe outbreak recorded in 1997, when more than 1100 people were taken ill by the disease and at least 124 died in Zanzibar, which has a population of 1 million
• Ghana : no case in 2005
• Northern Europe
• North America
• USA : in 1978, an outbreak of about 12 cases in Louisiana : in that outbreak, sewage was infected, and infected shellfish apparently were involved. Interestingly, the hemolytic vibrio strain implicated was identical to one that caused an unexplained isolated case in Texas in 1973. WHO recorded about 124,000 in 2002, and 3,800 deaths. In USA shell fish is usually implicated in autochthonous cases (most often Gulf Coast) :
• no cases were reported during 1911 to 1965; 136 during 1965 to 1991 (3 fatal) - 93 of these locally-acquired. 26 (9 imported, 0 fatal) in 1991; 103 (100 imported, 1 fatal) in 1992 - including 64 from California and 75 passengers
• on an airline flight from South America; 22 (19 imported) during 1993 (including one infection by V. cholerae O139 from India); 47 (45 imported - 2 V. cholerae 0139) in 1994; 23 (imported, nonfatal) in 1995; 4 (0 fatal) in 1996; 3 first half of 1997.
• 6 cases (imported) of V. cholerae O139 infection were reported during 1992 to 1994.
In the USA, epidemic cholera has not occurred during the past 100 years. Although small outbreaks have been identified, most cases have been sporadic. During 1996-2005, a total of 64 cases of toxigenic V. cholerae O1 were reported to CDC from USA states and territories. In 35 (55%) cases, cholera infection was acquired during foreign travel. For the remaining 29 (45%) cases, infection was acquired in the USA. 7 (24%) of these 29 cases were attributed to consumption of Gulf Coast seafood (such as crabs, shrimp, or oysters); 22 (76%) others could not be attributed to consumption of Gulf Coast seafood. Among the 22 cases not associated with either foreign travel or Gulf Coast seafood, 13 were associated with consumption of seafood from areas other than the Gulf Coast, and 9 exposures were undetermined. 13 of the cases occurred in states outside of the Gulf Coast, 8 occurred in USA territories (7 in Guam and 1 in the Mariana Islands), and 1 case occurred in Louisiana. 7 of the 11 USA cholera cases in 2005 were reported during Oct-Dec 2005, after Hurricanes Katrina and Rita. In addition to the 2 Louisiana cases described in this report, 2 cases occurred in Guam, and 3 others were attributed to foreign travel. The number and sources of these 7 cases are consistent with reports of cholera in previous years^ref. No evidence suggests increased risk for cholera among Gulf Coast residents or consumers of Gulf Coast seafood after the hurricanes. Illness in the 2 Louisiana residents was attributed to shellfish that was not prepared or handled properly, perhaps because of difficult living conditions after the hurricanes. Boiling shellfish for > 10 minutes is recommended to render the V. cholerae organism nonviable and then placing the shellfish into clean serving dishes to prevent recontamination^ref (Wachsmuth IK, Blake PA, Olsvik O, eds. Vibrio cholerae and cholera: molecular to global perspectives. Washington, DC: American Society for Microbiology, 1994)^ref.
• South America (since 1991)
Although 94% of the 101,383 cholera cases and 99% of the 2345 related deaths registered with the WHO in 2004 occurred in sub-Saharan Africa, these numbers present a misleading picture of the global cholera burden. V. cholerae infects persons in many developing countries, with the highest rates in Asia, but many Asian countries do not report their cases because of the effects on trade and travel, however unwarranted. The true burden is probably several million cases in Asia and Africa, with fewer cases in Latin America. Assuming a case fatality rate of 4 percent (on the basis of treated cases), annual mortality of at least 40,000 to 100,000 is probable, and even this may be an underestimation: since many patients die before reaching a health care facility, the true number of deaths may be much higher. There are about 110,000 to 200,000 cholera cases worldwide each year. Around 5,000 deaths are reported annually. Mozambique as a whole has reported up to 45,000 cases in a single year.
Outbreaks of many infectious diseases, including cholera, malaria and dengue, vary over characteristic periods > 1 year. Evidence that climate variability drives these interannual cycles has been highly controversial, chiefly because it is difficult to isolate the contribution of environmental forcing while taking into account nonlinear epidemiological dynamics generated by mechanisms such as host immunity. A critical interplay of environmental forcing, specifically climate variability, and temporary immunity explains the interannual disease cycles present in a four-decade cholera time series from Matlab, Bangladesh.The transmission rate, the key epidemiological parameter affected by extrinsic forcing, over time for the predominant strain (El Tor) have been reconstructed with a nonlinear population model that permits a contributing effect of intrinsic immunity. Transmission shows clear interannual variability with a strong correspondence to climate patterns at long periods (over 7 years, for monsoon rains and Brahmaputra river discharge) and at shorter periods (under 7 years, for flood extent in Bangladesh, sea surface temperatures in the Bay of Bengal and the El Niño-Southern Oscillation). The importance of the interplay between extrinsic and intrinsic factors in determining disease dynamics is illustrated during refractory periods, when population susceptibility levels are low as the result of immunity and the size of cholera outbreaks only weakly reflects climate forcing^ref.
Transmission :
• orofaecal route after ingestion of > 10¹¹ vibrios (> 10⁴ in individuals with hypochlorhydria or gastroresecated) via feces- or vomitus-contaminated water, raw or under-cooked seafood
• in general, overall disinfection of a residence after discovery of a case of  V. cholerae infection is unnecessary.  The possibility that contaminated food or water remains in the home, however, and this ought to be considered.  Because the organism has a high ID₅₀, spread is not usually from fomites or person-to-person.  Adequate and potable water availability is the most important factor in preventing the spread of cholera
=> (epidemic or Asiatic) cholera : most infections are subclinical, but < 10% infected persons, after an incubation period ranging from 6 hrs. up to 5 days, experience sudden and explosive diarrhea (first fecal, then watery ("rice water" stools) and mucous-flecked due to vibrio aggregates), nausea and vomiting and prostration leading rapidly to fluid and electrolyte depletion (up to 100 motions/die, loss of up to 10% of body H₂O; 5 mg => loss of 1÷6 L H₂O/die ; 25 mg => up to 25 L H₂O/die) => gastrocnemius cramps, dry and cold skin, rarely fever, nausea and vomiting and abdominal pain. It lasts from 12 hrs. up to 7 days. Because the stool can contain 10^7-9 viable vibrios / mL (in asymtomatic individuals < 10⁵ / g stools), such a patient could shed 2^.10¹² vibrios per day into the environment. If untreated, 50-60 % undergo hypovolemic shock (choleric facies), acute tubular necrosis => acute renal failure; if untreated death occurs within 2 hrs - few days.
=> wound infections due to V. cholerae are not as common as the gastrointestinal manifestation. In a table from a report of Vibrio surveillance from the USA, however, 3 (12%) of Gulf Coast isolates of nontoxigenic V. cholerae were reported to cause wound infections and 2 (10%) caused wound infection associated with non-Gulf Coast isolates^ref. In addition, Ko et al^ref reported on non-O1, non-O139 V. cholerae infections from Taiwan and found 4 of 30 patients with wound infections. Of the 4, 3 had necrotizing fasciitis similar to infection by V. vulnificus. All 4 patients had underlying co-morbidities, especially liver disease. In a case report, Farina, et al^ref reported a case of V. cholerae O2 cutaneous infection in a cirrhotic Italian tourist returning from Tunisia. Both of these references cite older cases as well.
=> immunoproliferative small intestinal disease (IPSID) ?
Laboratory examinations :
• colloidal-gold based colorimetric immunoassay Cholera sensitive membrane antigen rapid test (SMART) (New Horizons Diagnostics Corporation, Columbia, Md.) for the direct detection of V. cholerae O1 in clinical specimens, and this test takes only 15 min to complete. The test uses a MAb specific to the A factor of V. cholerae O1 lipopolysaccharide (2) and a high-titer polyclonal anti-V. cholerae O1 antibody. The principle of the test is as follows. A specimen suspected of containing V. cholerae O1 is reacted with the colloidal-gold-labeled MAb. If V. cholerae O1 is present in the specimen, it complexes to the V. cholerae O1 MAb. The complex diffuses and is captured and concentrated by the polyclonal antibody-coated solid-phase matrix. It then appears to the naked eye as a pink-to-red test spot developing from the deposition of colloidal gold. In the absence of V.

cholerae O1, the complex does not form and hence no pink/to-red color appears in the test spot
• Bengal SMART^ref, modeled after Cholera SMART (New Horizons Diagnostics Corporation), was developed for the detection of V. cholerae O139 synonym Bengal. In the development of the Bengal SMART kit, MAb ICL12 and a rabbit polyclonal serum against V. cholerae O139 were used
• Medicos Dip Stick
• the monoclonal antibody-based Institut Pasteur (IP) dipstick test is the most appropriate rapid diagnostic assay for the detection of V. cholerae O1 in locations where the skill level of personnel may be low, such as remote areas or refugee camp settings. High cost may limit the utility of any diagnostic test in the developing world^ref. A sample of positive fecal samples should be sent to a reference laboratory for antibiotic-sensitivity testing, since the detection of antibiotic-resistant cholera is critical. Resistant strains are very common, and treatment protocols should be adjusted accordingly. At present, V. cholerae strains in Bangladesh are nearly all resistant to tetracycline, trimethoprim–sulfamethoxazole, and erythromycin; though the strains are still sensitive to ciprofloxacin, the minimal inhibitory concentration is increasing, and we are using azithromycin or multiple doses of ciprofloxacin. Patients with cholera recover even without an antibiotic if hydration is maintained, but antibiotics should be used for severely and moderately dehydrated patients to reduce purging and minimize the supply and logistical requirements for caring for a large patient population. During an epidemic in a resource-poor country, antibiotics save lives. They should not be used prophylactically, however, since such use encourages the spread of resistant strains.
Therapy :
• fluid and electrolyte replacement : Ringer's lactate initially for severe cases, then oral rehydration salts (ORS : Na⁺Cl^- 3.5 g, K⁺Cl^- 1.5 g, Na⁺HCO₃^- 2.5 g (or trisodium citrate 2.9 g) and Glc 20.0 g dissolved in 1 L of water)
• antidiarrhoic drugs
• CFTR inhibitors
• antibacterials : tetracycline 500 mg po qid for 3 days or furazolidone 400 mg daily for 3 days or a single dose of 300 mg doxycycline. They halve lasting of diarrhoea. Single-dose azithromycin was effective in the treatment of severe cholera in adults. The lack of efficacy of ciprofloxacin (each given in a single 1-g dose of 2 500-mg tablets) may result from its diminished activity against V. cholerae O1 strains currently circulating in Bangladesh^ref.
Secretory IgA, as well as IgG and IgM in serum exudate, can be detected in the intestinal mucosa of immune individuals : they bring about protective immunity by immobilizing vibrio flagella and blocking attachment to the intestinal epithelium.
Prevention :
• many villagers rely on rivers, lakes, and ponds for household water - especially because many drilled wells have become contaminated with arsenic.
• boiling is the most effective way to purify water, but in some countries wood for fuel is scarce.
• folding a sari cloth (the traditional cotton garment worn by women in India and Bangladesh) to give > 4 (ideally 8) layers filters out virtually all the bacteria. The bacteria are tiny and would on their own be impossible to strain out with a simple filter. But they hang onto the egg-cases and mouths of Copepoda (copepods : microscopic crustaceans a thousand times larger than the bacteria). A rise in water temperature results in a plankton bloomwhichauses a growth spurt of copepods, each of which can carry up to 10,000 cholera bacteria. Old, cheap sari cloth makes a better filter than new, expensive cloth : the threads become smushy and loose, as a result the pore size becomes even smaller.
• when germicidal rate for Vibrio Cholerae of El-Tor biotype in the 5 different kinds of water bodies reach to 100% in 5 minutes, concentrations of chlorine compound disinfectant, indophor, chlorine dioxide and glutaraldehyde are 25.0-250.0 mg/L, 100.0-250.0 mg/L, 10.0-25.0 mg/L and 100-500 mg/L, respectively. Concentrations of disinfectants needed to disinfected waste water are higher than that to disinfect natural water^ref.
• killed injectable, oral and transgenic, or attenuated vaccines. It is unlikely that cholera could ever be eliminated by the use of vaccines, but that they could reduce the number of cases among high-risk populations. Their effectiveness in the field is assisted greatly by indirect (herd) protection.5 Vaccine strategies work synergistically with safe water and sanitation to reduce risk: vaccinated persons are less likely to become infected and contaminate the environment, and safer water improves vaccine effectiveness by reducing the bacterial inoculum consumed^ref
It is considered by CDC as a category B biological weapon.
• Group 2 = atypical or non-toxigenic Vibrio cholerae O1
=> asymptomatic
• Group 3 = Vibrio cholerae non-O1 (a.k.a. non-cholera vibrio (NCV) or non-agglutinating vibrio (NAV)).
• if CT⁺ => cholera
• Vibrio cholerae O139 (Bengal : capsulated; arose in October 1992 in India and Bangladesh probably from horizontal transfer of CTXf; it may become the cause of the 8^th great pandemic of cholera)
• if NAG-ST⁺ => dysentery
• Vibrio cholerae non-O1/non-O139

Human cases of infection with V. cholerae non-O1, non-O139 serotypes are more often associated with seawater, but can also occur in freshwater^{ref1, ref2, ref3}. Previous studies of surface water contamination carried out in 1994-98 and 2004 in eastern regions of Poland, which border on Ukraine, revealed the presence of V. cholerae non-O1 strains in the water throughout the year, even in winter. Strains isolated from eastern Polish rivers also did not contain cholera toxin genes, but 40% were found to produce heat-stable enterotoxin NAG-ST, with varying haemolytic activity, and toxigenicity was shown in tests on animals^{ref1, ref2} (Pancer K, Stypulkowska-Misiurewicz H: Toxic products of Vibrio cholerae environmental strains isolated in Poland. ETOX?8, Kloster Banz, Niemcy, 29.06.-4.07.1997, Bacterial Protein Toxins, Zbl.Bakteriol. 1998, Suppl.29,473-74). In Europe, infections with V. cholerae non-O1, non-O139 serotypes are rare, and sporadic cases are generally reported. Experimental infections in healthy volunteers and data from gastroenteritis outbreak investigations indicate that the incubation period is 10 hours in volunteers and 12 to 24 hours in outbreaks. The median duration of illness ranges from 12 to 24 hours (Morris JG, Nair GB: "Noncholera" Vibrio infections in Tropical Infectious Diseases ed. RL Guerrant, DH Walker and PF Weller, 1999 Churchill Livingstone). Symptoms of V. cholerae non-O1, non-O139 infection include gastroenteritis if large numbers of the bacteria enter the digestive tract, and wound infections. Septicemia is also a possibility, especially in infected patients who are immunocompromised^{ref1, ref2}. The atypically high temperatures in the summer of 2006 provided conditions favorable for the growth of Vibrio bacteria in the environment. During such a hot summer, routine testing of water samples from bathing beaches should be extended to detect the presence of Vibrio, due to the increased level of bacteria in the water.
• Vibrio cholerae 569B

• Pfeiffer's phenomenon : the lysis of Vibrio cholerae when injected into the peritoneal cavity of an immunized guinea pig; the term is also used to describe the in vitro lysis of cholera vibrios or other bacteria when incubated with specific antibody and complement.

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