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Cholera vibrio

Medical expert of the article

Internist, infectious disease specialist
, medical expert
Last reviewed: 04.07.2025

According to the WHO, cholera is an infectious disease characterized by acute, severe, dehydrating diarrhea with stools in the form of rice water, which is a consequence of infection with Vibrio cholerae. Due to the fact that it is characterized by a pronounced ability to spread widely in epidemics, a severe course and a high mortality rate, cholera is considered a particularly dangerous infection.

The historical homeland of cholera is India, or more precisely, the delta of the Ganges and Brahmaputra rivers (now East India and Bangladesh), where it has existed since time immemorial (cholera epidemics in this region were observed as early as 500 BC). The long existence of an endemic focus of cholera here is explained by many reasons. The cholera vibrio can not only survive in water for a long time, but also reproduce in it under favorable conditions - temperatures above 12 °C, the presence of organic matter. All these conditions are evident in India: a tropical climate (average annual temperature from 25 to 29 °C), abundant rainfall and swampiness, high population density, especially in the delta of the Ganges River, a large amount of organic matter in the water, continuous year-round water pollution with sewage and excrement, a low material standard of living and unique religious and cult rites of the population.

In the history of cholera epidemics, four periods can be distinguished.

Period I - until 1817, when cholera was concentrated only in East and South Asia, mainly in India, and did not spread beyond its borders.

II period - from 1817 to 1926. With the establishment of broad economic and other ties between India and European and other countries, cholera went beyond India and, spreading along the routes of economic and religious ties, caused 6 pandemics that took millions of human lives. Russia was the first of the European countries where cholera penetrated. From 1823 to 1926, Russia experienced 57 cholera years. During this time, more than 5.6 million people fell ill with cholera and 2.14 million people died from it ("40%).

III period - from 1926 to 1961 Cholera returned to its main endemic focus, and a period of relative well-being began. It seemed that with the development of modern systems for cleaning drinking water, removing and disinfecting wastewater, and developing special anti-cholera measures, including the creation of a quarantine service, the countries of the world would be reliably protected from another cholera invasion.

The fourth period began in 1961 and continues to this day. The seventh pandemic began not in India, but in Indonesia, quickly spread to the Philippines, China, the Indochina countries, and then to other countries in Asia, Africa, and Europe. The peculiarities of this pandemic include the fact that, firstly, it was caused by a special variant of the cholera vibrio - V. cholerae eltor, which until 1961 was not even officially recognized as the causative agent of cholera; secondly, in terms of duration, it surpassed all previous pandemics; thirdly, it occurred in two waves, the first of which lasted until 1990, and the second began in 1991 and covered many countries in South and North America, including the United States, which had not seen a cholera epidemic since 1866. From 1961 to 1996, 3,943,239 people fell ill with cholera in 146 countries.

The causative agent of cholera, Vibrio cholerae, was discovered in 1883 during the fifth pandemic by R. Koch, but the vibrio was first discovered in the feces of patients with diarrhea in 1854 by F. Pacini.

V. cholerae belongs to the Vibrionaceae family, which includes several genera (Vibrio, Aeromonas, Plesiomonas, Photobacterium). The genus Vibrio has more than 25 species since 1985, of which the most important for humans are V. cholerae, V. parahaemolyticus, V. alginolyticus, V. vulnificus and V. fluvialis.

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Key features of the genus Vibrio

Short, non-spore- and capsule-forming, curved or straight gram-negative rods, 0.5 µm in diameter and 1.5-3.0 µm in length, motile (V. cholerae is monotrichous, some species have two or more polar flagella); grow well and quickly on regular media, are chemoorganotrophs, and ferment carbohydrates to produce acid without gas (glucose is fermented via the Embden-Meyerhof pathway). Oxidase-positive, form indole, reduce nitrates to nitrites (V. cholerae gives a positive nitrosoindole reaction), break down gelatin, often give a positive Voges-Proskauer reaction (i.e., form acetylmethylcarbinol), have no urease, do not form H2S, have lysine and ornithine decarboxylases, but do not have arginine dihydrolase. A characteristic feature of the genus Vibrio is the sensitivity of most bacterial strains to the drug 0/129 (2,4-diamino-6,7-diazopropylpteridine), while representatives of the families Pseudomonadaceae and Enterobacteriaceae are resistant to this drug. Vibrios are aerobes and facultative anaerobes, the temperature optimum for growth is 18-37 C, pH 8.6-9.0 (grow in the pH range of 6.0-9.6), some species (halophiles) do not grow in the absence of NaCl. The G + C content in DNA is 40-50 mol % (for V. cholerae about 47 mol %). Biochemical tests are used to differentiate within the Vibrionaceae family from the morphologically similar genera Aeromonas and Plesiomonas, as well as to distinguish from the Enterobacteriaceae family.

The cholera vibrio differs from the Pseudomonadaceae family in that it ferments glucose only via the Embden-Meyerhof pathway (without the participation of O2), while the former consume glucose only in the presence of O2. This difference between them is easily revealed on the Hugh-Leifson medium. The medium contains nutrient agar, glucose and an indicator. The sowing is done in two columns with the Hugh-Leifson medium, one of which is filled with petroleum jelly (to create anaerobic conditions). In the case of the growth of the cholera vibrio, the color of the medium changes in both test tubes, in the case of the growth of pseudomonads - only in the test tube without petroleum jelly (aerobic growth conditions).

The cholera vibrio is very undemanding to nutrient media. It reproduces well and quickly in 1% alkaline (pH 8.6-9.0) peptone water (PV) containing 0.5-1.0% NaCl, outpacing the growth of other bacteria. To suppress the growth of Proteus, it is recommended to add potassium tellurite (in a final dilution of 1:100,000) to 1% PV. 1% PV is the best enrichment medium for the cholera vibrio. During growth, it forms a delicate, loose, grayish film on the surface of the PV after 6-8 hours, which is easily destroyed when shaken and falls to the bottom in the form of flakes, the PV becomes moderately cloudy. Various selective media have been proposed for the isolation of the cholera vibrio: alkaline agar, bile-salt agar, alkaline albuminate, alkaline agar with blood, lactose-sucrose and other media. The best is the TCBS (thiosulfate citrate-bromothymol sucrose agar) medium and its modifications. However, alkaline MPA is most often used, on which the cholera vibrio forms smooth, glassy-transparent, bluish-tinted, disc-shaped colonies of viscous consistency.

When sown by injection into a column of gelatin, the vibrio, after 2 days at a temperature of 22-23 C, causes liquefaction from the surface in the form of a bubble, then a funnel-shaped one, and finally, layer-by-layer.

In milk, the vibrio quickly multiplies, causing coagulation after 24-48 hours, and then peptonization of the milk occurs, and after 3-4 days the vibrio dies due to a shift in the pH of the milk to the acidic side.

B. Heiberg, based on their ability to ferment mannose, sucrose and arabinose, divided all vibrios (cholera and cholera-like) into a number of groups, the number of which now amounts to 8.

Vibrio cholerae belongs to the first group of Heiberg.

Vibrios similar in morphological, cultural and biochemical features to the cholera vibrio were and are called differently: paracholera, cholera-like, NAG-vibrios (non-agglutinating vibrios); vibrios not belonging to the O1 group. The last name most accurately emphasizes their relationship to the cholera vibrio. As established by A. Gardner and K. Venkat-Raman, cholera and cholera-like vibrios have a common H-antigen, but differ in O-antigens. According to the O-antigen, cholera and cholera-like vibrios are currently divided into 139 O-serogroups, but their number is constantly expanding. The cholera vibrio belongs to the O1 group. It has a common A-antigen and two type-specific antigens - B and C, by which three serotypes of V. cholerae are distinguished - the Ogawa serotype (AB), the Inaba serotype (AC) and the Hikoshima serotype (ABC). The cholera vibrio in the dissociation stage has an OR-antigen. In this regard, O-serum, OR-serum and type-specific sera Inaba and Ogawa are used to identify V. cholerae.

In 1992-1993, a large cholera epidemic began in Bangladesh, India, China, Malaysia and other countries, the causative agent of which was a new, previously unknown serovar of the Vibrio cholerae species. It differs from V. cholerae O1 by antigenic features: it has the 0139 antigen and a polysaccharide capsule and is not agglutinated by any other O-sera. All its other morphological and biological properties, including the ability to cause cholera, i.e., to synthesize the exotoxin-cholerogen, turned out to be similar to the properties of V. cholerae O1. Consequently, a new causative agent of cholera, V. cholerae 0139, apparently arose as a result of a mutation that changed the O-antigen. It was named V. cholerae 0139 bengal.

The question of the relationship of the so-called cholera-like vibrios to V. cholerae has long been unclear. However, a comparison of V. cholerae and cholera-like (NAG-vibrios) by more than 70 features revealed their similarity of 90%, and the degree of DNA homology of V. cholerae and the studied NAG-vibrios is 70-100%. Therefore, cholera-like vibrios are combined into one species with the cholera vibrio, from which they differ mainly in their O-antigens, in connection with which they are called vibrios of the non-01-group - V. cholerae non-01.

The V. cholerae species is divided into 4 biotypes: V. cholerae, V. eltor, V. proteus and V. albensis. The nature of the El Tor vibrio has been debated for many years. This vibrio was isolated in 1906 by F. Gottschlich at the El Tor quarantine station from the body of a pilgrim who died of dysentery. F. Gottschlich isolated several such strains. They were no different from the cholera vibrio in all their properties and were agglutinated by cholera O-serum. However, since there was no cholera among the pilgrims at that time, and long-term carriage of the cholera vibrio was considered unlikely, the question of the possible etiologic role of V. eltor in cholera remained controversial for a long time. In addition, the El Tor vibrio, unlike V. cholerae, had a hemolytic effect. However, in 1937, this vibrio caused a large and severe cholera epidemic on the island of Sulawesi (Indonesia) with a mortality rate of over 60%. Finally, in 1961, it became the culprit of the 7th pandemic, and in 1962 the question of its cholera nature was finally resolved. The differences between V. cholerae and V. eltor concern only some characteristics. In all other properties, V. eltor is not fundamentally different from V. cholerae. In addition, it has now been established that the V. proteus biotype (V.finklerpriori) includes the entire group of vibrios, except for the 01 group (and now 0139), previously called NAG vibrios. The V. albensis biotype was isolated from the Elbe River and has the ability to phosphoresce, but having lost it, it is no different from V. proteus. Based on these data, the Vibrio cholerae species is currently divided into 4 biotypes: V. cholerae 01 cholerae, V. cholerae eltor, V. cholerae 0139 bengal and V. cholerae non 01. The first three belong to two serovars 01 and 0139. The last biovar includes the previous biotypes V. proteus and V. albensis and is represented by many other serovars of vibrios that are not agglutinated by 01 and 0139 sera, i.e. NAG vibrios.

Pathogenicity factors of cholera vibrio

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Chemotaxis of Vibrio cholerae

With the help of these properties, the vibrio interacts with epithelial cells. In cholera vibrio mutants (who have lost the ability to chemotaxis), virulence is significantly reduced, in Mob mutants (who have lost mobility) it either completely disappears or decreases sharply.

Adhesion and colonization factors by which the vibrio adheres to the microvilli and colonizes the mucous membrane of the small intestine. Adhesion factors include mucinase, soluble hemagglutinin/protease, neuraminidase, etc. They promote adhesion and colonization by destroying substances that are part of the mucus. Soluble hemagglutinin/protease promotes the separation of vibrios from epithelial cell receptors and their exit from the intestine into the external environment, ensuring their epidemic spread. Neuraminidase strengthens the bond between choleragen and epithelial cells and facilitates the penetration of the toxin into the cells, which increases the severity of diarrhea.

Cholera toxin is a choleragen.

So-called new toxins that are capable of causing diarrhea, but have no genetic or immunological relationship with choleragen.

Dermoneurotic and hemorrhagic factors. The nature of these toxic factors and their role in the pathogenesis of cholera have not been sufficiently studied.

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Endotoxins of Vibrio cholerae

Lipopolysaccharides of V. cholerae have a strong endotoxic property and cause general intoxication of the body.

The main of the listed pathogenicity factors of the cholera vibrio is the exotoxin choleragen (CTX AB), which determines the pathogenesis of this disease. The cholera molecule consists of two fragments - A and B. Fragment A consists of two peptides - A1 and A2, it has a specific property of cholera toxin and gives it the qualities of a superantigen. Fragment B consists of 5 identical subunits. It performs two functions: 1) recognizes the receptor (monosialoganglioside) of the enterocyte and binds to it; 2) forms an intramembrane hydrophobic channel for the passage of subunit A. Peptide A2 serves to bind fragments A and B. The actual toxic function is performed by peptide Aj (ADP-ribosyltransferase). It interacts with NAD, causing its hydrolysis; The resulting ADP-ribose binds to the regulatory subunit of adenylate cyclase. This leads to inhibition of GTP hydrolysis. The resulting GTP + adenylate cyclase complex causes ATP hydrolysis with the formation of cAMP. (Another pathway for cAMP accumulation is the suppression by choleragen of the enzyme that hydrolyzes cAMP to 5-AMP). Manifestation of the function of the ctxAB gene encoding the synthesis of exotoxin depends on the function of a number of other pathogenicity genes, in particular the tcp genes (encoding the synthesis of toxin-controlled adhesion pili - TCAP), the regulatory genes toxR, toxS and toxT, the hap (soluble hemagglutinin/protease) and neuraminidase (neuraminidase) genes. Therefore, the genetic control of the pathogenicity of V. cholerae is complex.

As it turned out, there are two pathogenicity islands in the V. cholerae chromosome. One of them is the genome of the filamentous moderate converting phage CTXφ, and the other is the genome of the also filamentous moderate converting phage VPIcp. Each of these pathogenicity islands contains cassettes of genes specified in the prophase, which determine the pathogenicity of the cholera pathogen. The CTXφ prophage carries the CTX genes, genes of new toxins zot and ace, the ser gene (adhesin synthesis), and the ortU gene (synthesis of a product with an unknown function). This cassette also includes the nei gene and the RS2 phage region, which codes for replication and integration of the prophage into chromosomes. The zot, ace, and ortU genes are necessary for the formation of phage virions when the prophage is excluded from the chromosome of the pathogen.

The VPIcp prophage carries the tcp genes (encoding the production of pili (TCPA protein)), toxT, toxR, act genes (additional colonization factor, mobility genes (integrases and transposases)). Transcription of virulence genes is regulated by three regulatory genes: toxR, toxS, and toxT. These genes coordinately, at the transcription level, change the activity of more than 20 virulence genes, including the ctxAB, tcp, and other genes. The main regulatory gene is the toxR gene. Its damage or absence leads to avirulence or to a more than 100-fold decrease in the production of cholera toxin CTX and TCPA. Possibly, this is how the coordinated expression of virulence genes is regulated in pathogenicity islands formed by temperate converting phages and in other bacterial species. It has been established that another prophage K139 is present in the chromosome of V. cholerae eltor, but its genome has been little studied.

The hap gene is localized on the chromosome. Thus, the virulence (pathogenicity) and epidemic capacity of V. cholerae are determined by 4 genes: ctxAB, tcp, toxR and hap.

Various methods can be used to detect the ability of V. cholerae to produce choleragen.

Biological test on rabbits. When cholera vibrios are injected intramuscularly into suckling rabbits (aged no more than 2 weeks), they develop a typical cholera syndrome: diarrhea, dehydration and death of the rabbit.

Direct detection of choleragen by PCR, IFM or passive immune hemolysis reaction (cholerogen binds to Gmj of erythrocytes, and they are lysed upon addition of antitoxic antibodies and complement). However, detection of the ability to produce toxin alone is not enough to determine the epidemic danger of such strains. For this, it is necessary to detect the presence of the hap gene, therefore, the best and most reliable way to differentiate toxigenic and epidemic strains of cholera vibrios of serogroups 01 and 0139 is by PCR using specific primers to detect all 4 pathogenicity genes: ctxAB, tcp, toxR and hap.

The ability of V. cholerae other than serogroups 01 or 0139 to cause sporadic or cluster diarrheal diseases in humans may be due either to the presence of LT or ST type enterotoxins, which stimulate the adenylate or guanylate cyclase systems, respectively, or to the presence of only the ctxAB genes but no hap gene.

During the seventh pandemic, V. cholerae strains with varying degrees of virulence were isolated: cholerogenic (virulent), weakly cholerogenic (low-virulence), and non-cholerogenic (non-virulent). Non-cholerogenic V. cholerae, as a rule, exhibit hemolytic activity, are not lysed by the cholera diagnostic phage HDF(5), and do not cause human disease.

For phage typing of V. cholerae 01 (including El Tor) S. Mukherjee proposed sets of phages, which were then supplemented with other phages in Russia. A set of such phages (1-7) allows one to distinguish phage types among V. cholerae 0116. For identification of toxigenic and non-toxigenic V. cholerae El Tor, instead of HDF-3, HDF-4 and HDF-5, phages CTX* (lyse toxigenic El Tor vibrios) and CTX" (lyse non-toxigenic El Tor vibrios) are now proposed in Russia.

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Resistance of cholera pathogens

Cholera vibrios survive well at low temperatures; they remain viable in ice for up to 1 month; in sea water - up to 47 days, in river water - from 3-5 days to several weeks, in boiled mineral water they survive for more than 1 year, in soil - from 8 days to 3 months, in fresh feces - up to 3 days, on boiled products (rice, noodles, meat, porridge, etc.) they survive for 2-5 days, on raw vegetables - 2-4 days, on fruits - 1-2 days, in milk and dairy products - 5 days; when stored in the cold, the survival period increases by 1-3 days; on linen linen contaminated with feces, they survive for up to 2 days, and on damp material - a week. Cholera vibrios die within 5 minutes at a temperature of 80 °C, and instantly at 100 °C; they are highly sensitive to acids; they die within 5-15 minutes under the influence of chloramine and other disinfectants. They are sensitive to drying and direct sunlight, but they survive well and for a long time and even multiply in open water bodies and wastewater rich in organic matter, with an alkaline pH and a temperature above 10-12 °C. They are highly sensitive to chlorine: a dose of active chlorine of 0.3-0.4 mg/l of water in 30 minutes causes reliable disinfection from cholera vibrios.

Vibrios pathogenic to humans that do not belong to the species Vibrio Cholerae

The genus Vibrio includes more than 25 species, of which, in addition to V. cholerae, at least eight are capable of causing disease in humans: V. parahaemolyticus, V. alginolyticus, V. vulnificus, V. fluvialis, V. fumissii, V. mimicus, V. damsela, and V. hollisae. All of these vibrios inhabit seas and bays. Infection occurs either through swimming or through eating seafood. It has been found that cholera and non-cholera vibrios can cause not only gastroenteritis, but also wound infections. This ability has been found in V. cholerae 01 and non-01 groups, V. parahaemolyticus, V. alginolyticus, V. mimicus, V. damsela, and V. vulnificus. They cause inflammatory processes in soft tissues when they are damaged by the shell of marine animals or when in direct contact with infected sea water.

Of the listed pathogenic non-cholera vibrios, the most practical interest are V. parahaemolyticus, V. alginolyticus, V. vulnificus and V. fluvialis.

V. parahaemolyticus - a parahaemolytic vibrio - was first isolated in Japan in 1950 during a large outbreak of food poisoning caused by the consumption of semi-dried sardines (mortality was 7.5%). The causative agent belonged to the genus Vibrio by R. Sakazaki in 1963. He divided the studied strains into 2 species: V. parahaemolyticus and V. alginolyticus. Both species are found in coastal seawater and in its inhabitants, they are halophiles (Greek hals - salt); unlike ordinary vibrios, halophilic ones do not grow on media without NaCl and reproduce well at high concentrations of it. The species affiliation of halophilic vibrios is determined by their ability to ferment sucrose, form acetylmethylcarbinol, and reproduce in PV with 10% NaCl. All these features are inherent in the species V. alginolyticus, but are absent in V. parahaemolyticus.

The parahaemolytic vibrio has three types of antigens: heat-labile flagellar H-antigens, heat-stable O-antigens that are not destroyed by heating to 120 °C for 2 hours, and surface K-antigens that are destroyed by heating. Freshly isolated cultures of V. parahaemolyticus have well-defined K-antigens that protect live vibrios from agglutination by homologous O-sera. The H-antigens are the same for all strains, but the H-antigens of monotrichus differ from the H-antigens of peritrichs. According to the O-antigen, V. parahaemolyticus is divided into 14 serogroups. Within the serogroups, vibrios are divided into serotypes according to K-antigens, the total number of which is 61. The antigenic scheme of V. parahaemolyticus has been developed for its strains isolated from humans only.

Pathogenicity of V. parahaemolyticus is associated with its ability to synthesize hemolysin, which has enterotoxic properties. The latter is detected using the Kanagawa method. Its essence lies in the fact that V. parahaemolyticus, pathogenic for humans, causes clear hemolysis on blood agar containing 7% NaCl. On blood agar containing less than 5% NaCl, hemolysis is caused by many strains of V. parahaemolyticus, and on blood agar with 7% NaCl - only strains with enteropathogenic properties. The parahaemolytic vibrio is found on the coasts of the Japanese, Caspian, Black and other seas. It causes foodborne toxic infections and dysentery-like diseases. Infection occurs when eating raw or semi-raw seafood infected with V- parahaemolyticus (sea fish, oysters, crustaceans, etc.).

Among the eight non-cholera vibrios mentioned above, the most pathogenic for humans is V. vulnificus, which was first described in 1976 as Beneckea vulnificus and then reclassified as Vibrio vulnificus in 1980. It is often found in seawater and its inhabitants and causes various human diseases. Strains of V. vulnificus of marine and clinical origin do not differ from each other either phenotypically or genetically.

Wound infections caused by V. vulnificus progress rapidly and lead to the formation of tumors with subsequent tissue necrosis, accompanied by fever, chills, sometimes severe pain, and in some cases requiring amputation.

V. vulnificus has been found to produce exotoxin. Animal experiments have shown that the pathogen causes severe local damage with the development of edema and tissue necrosis, followed by death. The role of exotoxin in the pathogenesis of the disease is being studied.

In addition to wound infections, V. vulnificus can cause pneumonia in drowning victims and endometritis in women after exposure to seawater. The most severe form of infection caused by V. vulnificus is primary septicemia associated with eating raw oysters (and possibly other marine animals). This disease develops very rapidly: the patient develops malaise, fever, chills, and prostration, then severe hypotension, which is the main cause of death (mortality rate is about 50%).

V. fluvialis was first described as a gastroenteritis pathogen in 1981. It belongs to a subgroup of non-cholera pathogenic vibrios that have arginine dihydrolase but no netornithine and lysine decarboxylases (V. fluvialis, V. furnissii, V. damsela, i.e., phenotypically similar to Aeromonas). V. fluvialis is a common causative agent of gastroenteritis, which is accompanied by severe vomiting, diarrhea, abdominal pain, fever, and severe or moderate dehydration. The main pathogenic factor is enterotoxin.

Epidemiology of cholera

The main source of infection is only a person - a patient with cholera or a vibrio carrier, as well as water contaminated with them. No animals in nature get cholera. The route of infection is feco-oral. Routes of infection: a) the main one - through water used for drinking, bathing and household needs; b) contact-household and c) through food. All major epidemics and pandemics of cholera were associated with water. Cholera vibrios have such adaptive mechanisms that ensure the existence of their populations both in the human body and in certain ecosystems of open water bodies. Severe diarrhea, which is caused by the cholera vibrio, leads to cleansing of the intestines from competing bacteria and contributes to the widespread spread of the pathogen in the environment, primarily in wastewater and in open water bodies where they are dumped. A person with cholera excretes the pathogen in huge quantities - from 100 million to 1 billion per 1 ml of feces, a vibrio carrier excretes 100-100,000 vibrios in 1 ml, the infectious dose is about 1 million vibrios. The duration of excretion of the cholera vibrio in healthy carriers is from 7 to 42 days and 7-10 days in those who have recovered. Longer excretion is extremely rare.

A peculiarity of cholera is that after it, as a rule, there is no long-term carriage and no stable endemic foci are formed. However, as already indicated above, due to the pollution of open water bodies with wastewater containing large amounts of organic substances, detergents and table salt, in the summer the cholera vibrio not only survives in them for a long time, but even multiplies.

Of great epidemiological significance is the fact that cholera vibrios of the 01 group, both non-toxigenic and toxigenic, can persist for a long time in various aquatic ecosystems as uncultivated forms. Using the polymerase chain reaction, vct genes of uncultivated forms of V. chokrae were detected in various water bodies in a number of endemic territories of the CIS during negative bacteriological studies.

The endemic focus of the El Tor cholera vibrio is Indonesia, the emergence of this culprit of the seventh pandemic from there is believed to be associated with the expansion of Indonesia's economic ties with the outside world after it gained independence, and the duration and lightning-fast development of the pandemic, especially its second wave, was decisively influenced by the lack of immunity to cholera and various social upheavals in the countries of Asia, Africa and America.

In the event of cholera, a range of anti-epidemic measures are taken, among which the leading and decisive ones are active, timely detection and isolation (hospitalization, treatment) of patients in acute and atypical forms and healthy vibrio carriers; measures are taken to prevent possible routes of infection; special attention is paid to water supply (chlorination of drinking water), compliance with sanitary and hygienic conditions at food enterprises, in children's institutions, public places; strict control, including bacteriological, is carried out over open water bodies, immunization of the population is carried out, etc.

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Symptoms of cholera

The incubation period for cholera varies from several hours to 6 days, most often 2-3 days. Having entered the lumen of the small intestine, cholera vibrios, due to their mobility and chemotaxis to the mucous membrane, are directed to the mucus. In order to penetrate through it, vibrios produce a number of enzymes: neuraminidase, mucinase, proteases, lecithinase, which destroy substances contained in the mucus and facilitate the movement of vibrios to the epithelial cells. By adhesion, vibrios attach to the glycocalyx of the epithelium and, losing mobility, begin to multiply intensively, colonizing the microvilli of the small intestine (see color insert, Fig. 101.2), and simultaneously produce a large amount of exotoxin-cholerogen. Choleragen molecules bind to monosialoganglioside Gni! And penetrate the cell membrane, where they activate the adenylate cyclase system, and the accumulating cAMP causes hypersecretion of fluid, cations and anions Na, HCO, Kl, Cl from enterocytes, which leads to cholera diarrhea, dehydration and desalination of the body. There are three types of the disease:

  • a violent, severe dehydrating diarrheal disease that results in the death of the patient within a few hours;
  • less severe course, or diarrhea without dehydration;
  • asymptomatic course of the disease (carriage of vibrios).

In severe cases of cholera, patients develop diarrhea, stool frequency increases, feces become more abundant, become watery, lose their fecal odor and look like rice broth (a cloudy liquid with mucus residues and epithelial cells floating in it). Then debilitating vomiting occurs, first of the intestinal contents, and then the vomit takes on the appearance of rice broth. The patient's temperature drops below normal, the skin becomes bluish, wrinkled and cold - cholera algid. As a result of dehydration, the blood thickens, cyanosis develops, oxygen starvation, kidney function suffers sharply, convulsions appear, the patient loses consciousness and death occurs. The mortality rate from cholera during the seventh pandemic varied from 1.5% in developed countries to 50% in developing countries.

Post-infectious immunity is strong, long-lasting, and recurrent diseases are rare. Immunity is antitoxic and antimicrobial, caused by antibodies (antitoxins persist longer than antimicrobial antibodies), immune memory cells, and phagocytes.

Laboratory diagnostics of cholera

The main and decisive method of diagnosing cholera is bacteriological. The material for examination from the patient is feces and vomit; feces are examined for carriage of vibrios; a ligated section of the small intestine and gall bladder are taken for examination from persons who died from cholera; from objects of the external environment, water from open reservoirs and wastewater are most often examined.

When conducting a bacteriological study, the following three conditions must be met:

  • sow material from the patient as quickly as possible (cholera vibrio survives in feces for a short period of time);
  • the container in which the material is taken should not be disinfected with chemicals and should not contain traces of them, since the cholera vibrio is very sensitive to them;
  • eliminate the possibility of contamination and infection of others.

The culture is isolated according to the following scheme: sowing on PV, simultaneously on alkaline MPA or any selective medium (TCBS is best). After 6 hours, the film formed on PV is examined, and if necessary, a transfer is made to a second PV (the sowing rate of the cholera vibrio in this case increases by 10%). From PV, a transfer is made to alkaline MPA. Suspicious colonies (glassy-transparent) are transferred to obtain a pure culture, which is identified by morphological, cultural, biochemical properties, motility and finally typed using diagnostic agglutinating sera O-, OR-, Inaba and Ogawa and phages (HDF). Various options for accelerated diagnostics have been proposed, the best of which is the luminescent-serological method. It allows to detect cholera vibrio directly in the test material (or after preliminary cultivation in two test tubes with 1% PV, to one of which the cholera phage is added) within 1.5-2 hours. For accelerated detection of cholera vibrio, the Nizhny Novgorod IEM has proposed a set of paper indicator disks consisting of 13 biochemical tests (oxidase, indole, urease, lactose, glucose, sucrose, mannose, arabinose, mannitol, inositol, arginine, ornithine, lysine), which allow to differentiate representatives of the genus Vibrio from the genera Aeromonas, Plesiomonas, Pseudomonas, Comamonas and from the Enterobacteriaceae family. For rapid detection of cholera vibrio in feces and in environmental objects, RPGA with an antibody diagnosticum can be used. In order to detect non-cultivated forms of cholera vibrio in environmental objects, only the polymerase chain reaction method is used.

In cases where non-Ol-group V. cholerae are isolated, they should be typed using the corresponding agglutinating sera of other serogroups. Isolation of non-Ol-group V. cholerae from a patient with diarrhea (including cholera-like diarrhea) requires the same anti-epidemic measures as in the case of isolation of Ol-group V. cholerae. If necessary, the presence of the pathogenicity genes ctxAB, tcp, toxR and hap is determined in such vibrios using PCR.

Serological diagnostics of cholera is of an auxiliary nature. For this purpose, the agglutination reaction can be used, but it is better to determine the titer of vibriocidal antibodies or antitoxins (antibodies to cholera are determined by enzyme immunoassay or immunofluorescence methods).

Laboratory diagnostics of non-cholera pathogenic vibrios

The main method of diagnosing diseases caused by non-cholera pathogenic vibrios is bacteriological using selective media such as TCBS, MacConkey, etc. The belonging of the isolated culture to the genus Vibrio is determined on the basis of key characteristics of bacteria of this genus.

Treatment of cholera

Treatment of cholera patients should primarily consist of rehydration and restoration of normal water-salt metabolism. For this purpose, it is recommended to use saline solutions, for example, of the following composition: NaCl - 3.5; NaHC03 - 2.5; KCl - 1.5 and glucose - 20.0 g per 1 liter of water. Such pathogenetically substantiated treatment in combination with rational antibiotic therapy allows to reduce the mortality rate in cholera to 1% or less.

Specific prevention of cholera

To create artificial immunity, a cholera vaccine was proposed, including one made from killed Inaba and Ogawa strains; a cholera toxoid for subcutaneous use and an enteral chemical bivalent vaccine consisting of anatoxin and somatic antigens of the Inaba and Ogawa serotypes, since cross-immunity is not formed. However, the duration of post-vaccination immunity is no more than 6-8 months, so vaccinations are carried out only according to epidemiological indications. Antibiotic prophylaxis has proven itself well in cholera foci, in particular tetracycline, to which the cholera vibrio is highly sensitive. Other antibiotics effective against V. cholerae can be used for the same purpose.


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