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PubMed1979

The study of intestinal immunity against V. cholerae: purification of V. cholerae El Tor haemagglutinin and the protective role of its antibody in experimental cholera.

V. cholerae El Tor Ogawa strain O17SR grown on trypticase soy agar were extracted with 0.05 M cyclohexylamino propane sulfonic acid (CAPS) pH 9.5 at 37 degrees C for 1 hour. The bacteria were then removed by centrifugation and millipore filtration. The filtered fluid, after being dialysed against many changes of cold distilled water, was concentrated and passed through Sephadex G200 column. Three protein profiles were eluted out with 0.05 M Tris buffer pH 8.6. The haemagglutinin and the bacterial lipopolysaccharide (LPS) were confined to the first profile. They were subsequently separated by agarose gel electrophoresis. The haemagglutinin was found to be more anodic than the LPS. After homogenization of the gel strips containing the haemagglutinin followed by centrifugation at 9,000 g pure haemagglutinin was obtained in the supernatant. Rabbit aniserum against pure haemagglutinin contained protective antibodies against V. cholerae infection in the baby mouse model. Specific antibodies prepared from this antiserum was as protective as the antibodies directed against whole V. cholerae and heat stable somatic antigens of V. cholerae upon the same weight unit.

Agglutinins↗
PubMed1958

The swine lungworm as a reservoir and intermediate host for hog cholera virus. II. Attempts to demonstrate the presence of hog cholera virus in lungworms derived from swine with cholera.

Suspensions of adult lungworms, procured from swine that were outwardly healthy but derived from eggs passed by swine with hog cholera, induced this disease in a small proportion of swine into which they were injected intramuscularly. This result was achieved in both lungworm-free and lungworm-infested swine, though perhaps slightly more regularly in the lungworm-infested animals. Swine that had had an intramuscular injection of lungworm suspension and that had remained normal, developed hog cholera much more regularly following the ingestion of lungworm larvae of cholera origin than did swine not previously injected with lungworms. The findings described were markedly dependent upon season and were regularly reproducible only during the first 4 or 5 months of the year. The results presented are considered as further evidence that the swine lungworm serves as reservoir and intermediate host for hog cholera virus and that the virus is ordinarily carried by the lungworm in a masked form which must be provoked to pathogenicity by some stress before it can cause obvious disease in swine.

Animals↗
PubMed1992

Evidence that inactivated oral cholera vaccines both prevent and mitigate Vibrio cholerae O1 infections in a cholera-endemic area.

In a randomized, placebo-controlled field trial of B subunit-killed whole cell (BS-WC) and killed whole cell only (WC) inactivated oral cholera vaccines in rural Bangladesh, active surveillance of selected neighborhoods during the first year after vaccination identified 127 Vibrio cholerae O1 infections among 3285 three-dose recipients. For each vaccine, protective efficacy was greater against symptomatic (57%, P < .05 for BS-WC; 58%, P < .05 for WC) than against asymptomatic infections (46%, P < .05 for BS-WC; 32%, P = .09 for WC), and protection against each grade of infection was demonstrable for both the classical and El Tor biotypes. Although vaccine protection against symptomatic infections was evident in both young children and older persons, only persons vaccinated at age > 5 years were protected against asymptomatic infections. These results suggest that the inactivated oral vaccines acted both to protect against intestinal colonization by V. cholerae O1 and to interrupt the pathogenic sequence of established infections.

Adolescent↗
PubMed1991

[Cholera toxin producibility by Vibrio cholerae isolated during the cholera outbreak in the NTT Nagoya Hall].

An outbreak of cholera occurred among guests of the NTT Nagoya Hall in September 1989. Clinical findings showed that all but one were symptomatic infections out of 44 bacteriologically confirmed cases. In relation to the high incidence of symptomatic infections, we examined cholera toxin (CT) producibility of the isolated V. cholerae. 1. Strains of the NTT case produced 16-256 (mean 130) ng of CT per ml in CAYE-L medium at 30 degrees C and 32-256 (mean 142) ng of CT per ml by Polymyxin B treatment. But strains of past case produced 8-256 (mean 34), 8-128 (mean 44) ng of CT per ml, respectively. Strains of the NTT case produced a larger amount of CT than that of the past cases. 2. Strains of the NTT case produced 512-4096 (mean 2100) ng of CT per ml in CAYE-L medium at 37 degrees C and 1024-2048 (mean 1600) ng of CT per ml by Polymyxin B treatment. But strains of the past case produced 8-64 (mean 25), 8-128 (mean 45) ng of CT per ml, respectively. Strains of the NTT case produced a larger an amount of CT than them of past case. We observed the same phenomenon in AKI medium at 37 degrees C. The yield of CT in CAYE-L medium was greater at 37 degrees C than 30 degrees C. 3. Strains of NTT case grew faster than that of the past case in CAYE-L medium at 37 degrees C. But the growth rate was the same as both strains in AKI and CAYE media.(ABSTRACT TRUNCATED AT 250 WORDS)

Cholera↗
PubMed1974

Experimental Cholera in Chinchillas: the Immune Response in Serum and Intestinal Secretions to Vibrio cholerae and Cholera Toxin.

The immune response to Vibrio cholerae and cholera toxin was studied in chinchillas inoculated intra-intestinally with 10(8) viable V. cholerae 596B. Sera and intestinal fluids were collected from animals on days 1, 2, 3, 5, 7, 10, 14, 30, and 60 postinoculation, and antibodies were quantified by various methods. When radiovibriolytic and radiotoxin precipitin tests were used, a significant (fourfold) rise in both antibacterial and antitoxic titers was detected in intestinal fluids on the 2nd day of infection. In contrast, a significant rise in serum antibodies occurred between days 3 and 5. Since the acute phase of the chinchilla disease lasts 1 to 3 days, recovery coincided with rise in intestinal antibody but not with rise in serum antibody. Our results indicate that both antibacterial and antitoxic mechanisms are operative in chinchilla cholera and that the initial and crucial immune response is local in nature.

Journal Article↗
PubMed1997

Conservation of cholera toxin gene in a strain of cholera toxin non-producing Vibrio cholerae O1.

BT23, a Vibrio cholerae O1 E1 Tor isolate, possesses the cholera toxin (CT) gene as determined by PCR. However, CT was not detected in the culture medium by the reversed passive latex agglutination test, nor in the whole cell lysate as examined by Western blotting. The toxin-coregulated pilus (TCP) was not detected by Western blotting. This suggests the presence of defects in the regulatory cascade. toxR, toxS and toxT, members of the regulatory cascade, were examined by PCR. toxR and toxS were conserved but toxT was not. CT and TCP production was complemented by transformation of toxT. The lack of toxT was suspected to be the cause of the undetectable production of CT in strain BT23.

Bacterial Proteins↗
PubMed1984

Protection against experimental cholera in the rat. A study on the formation of antibodies against cholera toxin and desensitization of adenylate cyclase after immunization with cholera toxin.

The importance of antibodies to cholera toxin (CT) versus desensitization of intestinal adenylate cyclase for protection against experimental cholera in the rat was investigated. Animals were immunized five times with CT either perorally or intravenously; antitoxic antibodies were measured in both serum and bile, and intestinal anti-CT-containing plasma cells (ACC) as well as eosinophilic leucocytes were counted. Both peroral and intravenous immunizations induced high levels of serum antibodies, while antibodies in bile appeared only after peroral immunization. The number of eosinophilic leucocytes in the intestinal mucosa increased in response to peroral immunization. CT-induced stimulation of intestinal adenylate cyclase was significantly suppressed, i.e., desensitized, after peroral immunization, but was equally stimulated in intravenous immunized and in control animals. A constant and long-lasting protection against CT-induced secretion was obtained after peroral immunization. This protection correlated neither to the concentrations of antitoxic antibodies in serum, nor to those in bile, nor to the number of ACC, but did correlate to the desensitization of adenylate cyclase.

Adenylyl Cyclases↗
PubMed1986

Protection of rats against cholera toxin and cholera-like enterotoxins by immunization with enteric-coated cholera toxin.

Pure cholera toxin (CT) given as a booster in enteric-coated tablets to rats produced a humoral and intestinal immune response similar to the result of instilling the boosting dose of CT directly into the duodenum. This method protects the antigen against gastric acid and allows delivery of the immunogen to intestinal mucosa, an essential step in producing intestinal secretory IgA. Immunization gave protection against pure CT during intestinal perfusion but also significantly protected against the secretory effects of E. coli LT and CT-like toxin of A. sobria. The use of enteric-coated vaccines offers advantages for mass immunization programmes and our results suggest that immunization with preparations containing CT holotoxin may protect against heterologous toxins which cross-react with CT.

Aeromonas↗
PubMed1996

Changing epidemiology of cholera due to Vibrio cholerae O1 and O139 Bengal in Dhaka, Bangladesh.

At the International Centre for Diarrhoeal Disease Research, Bangladesh (ICDDR, B) Dhaka we studied the trends in cholera for the period January 1992 to May 1995. Vibrio cholerae O139 Bengal emerged as a second aetiologic agent of cholera in Dhaka in January 1993. In 1993, the majority of cholera cases was due to V. cholerae O139, with V. cholerae O1 accounting for a small proportion of cases. During the latter part of the study period (Jan 1994-May 1995), V. cholerae O1 re-emerged as the predominant cholera strain. The predominant age group affected in endemic cholera due to V. cholerae O1 was children 2-9 years old, and the organism was isolated from more females than from males at all ages. In contrast, cholera due to V. cholerae O139 caused disease mostly in adults 15 years and older, which indicated that this organism was new in this population. As with V. cholerae O1, V. cholerae O139 was isolated from more females than males. The initial rapid emergence and predominance of V. cholerae O139 was considered possibly to herald the start of the eighth pandemic of cholera. However, just after a year, the prevalence of V. cholerae O139 decreased dramatically with V. cholerae O1 resuming the role of the dominant cholera strain. The factor(s) contributing to the dramatic decline in prevalence of V. cholerae O139 is not well understood.

Adolescent↗
PubMed1986

Epidemiological differences between cholera due to multiple antibiotic resistant and multiple antibiotic sensitive Vibrio cholerae infection.

The appearance of cholera caused by multiply antibiotic resistant Vibrio cholerae in Bangladesh provided an opportunity to compare epidemiological features of infection caused by resistant and by sensitive V. cholerae. A prospective study was carried out using 46 families of hospital in-patient cholera cases due to resistant V. cholerae and 11 families of hospital cases due to sensitive V. cholerae and nine cases of cholera due to resistant and six cases due to sensitive V. cholerae detected in the neighbourhoods of hospital patients. All families were visited daily during ten days for cultures of rectal swabs, samples of domestic water and for history of diarrhoea. The results showed no significant difference in secondary infection and case rates in contacts of hospital cholera cases due to resistant and sensitive V. cholerae. However, the secondary infection rate (57%) in contacts of cases due to resistant V. cholerae detected from the neighbourhoods of hospital cases was significantly higher (p less than 0.05), than in the neighbourhood case-contacts (29%) of cases due to sensitive V. cholerae. The mean duration of diarrhoea in untreated resistant V. cholerae cases who were contacts of hospital cases (3.3 days) was significantly longer (p less than 0.05) than that of untreated sensitive V. cholerae (2.2 days). Higher isolation rates of V. cholerae were obtained from water sources used by cholera cases due to resistant V. cholerae, than from sources used by cases due to sensitive V. cholerae, but the differences were not statistically significant (p greater than 0.05). The study suggests that resistant V. cholerae poses an additional threat through a higher secondary infection rate and by causing illnesses of longer duration.

Anti-Bacterial Agents↗
PubMed1996

Randomised controlled comparison of single-dose ciprofloxacin and doxycycline for cholera caused by Vibrio cholerae 01 or 0139.

BACKGROUND: Effective antimicrobial therapy can reduce the duration and volume of cholera diarrhoea by half. However, such treatment is currently limited by Vibrio cholerae resistance to the drugs commonly prescribed for cholera, and by the difficulties involved in the administration of multi-drug doses under field conditions. Because of its favourable pharmacokinetics we thought it likely that single-dose ciprofloxacin would be effective in the treatment of cholera. METHODS: In this double-blind study treatment was either a single 1 g oral dose of ciprofloxacin plus doxycycline placebo, or a single 300 mg oral dose of doxycycline plus ciprofloxacine placebo. 130 moderately or severely dehydrated men infected with V cholerae 01 and 130 infected with V cholerae 0139 were randomly assigned treatment. Patients stayed in hospital for 5 days. We measured fluid intake and stool volume every 6 h, and a sample of stool for culture was obtained daily. The primary outcome measures were clinical success--the cessation of watery stool within 48 h; and bacteriological success--absence of V cholerae from cultures of stool after study day 2. FINDINGS: Among patients infected with V cholerae 01, treatment was clinically successful in 62 (94%) of 66 patients who received ciprofloxacin and in 47 (73%) of 64 who receive doxycycline (difference 21% [95% Cl 8-33]); the corresponding proportions with bacteriological success were 63 (95%) and 44 (69%) (27% [14-39]). Among patients infected with V cholerae 0139, treatment was clinically successful in 54 (92%) of 59 patients who received ciprofloxacin and in 65 (92%) of 71 who received doxycycline (< 1% [-9 to 9]), and bacteriologically successful in 58 (98%) and 56 (79%), respectively (19% [9-30]). Total volume of watery stool did not differ significantly between ciprofloxacin-group and doxycycline-group patients infected with either V cholerae 01 or 0139. All but one of the V cholerae 01 and all of the 0139 isolates were susceptible in vitro to doxycycline, whereas 48 (37%) of the V cholerae 01 isolates and none of the 0139 isolates were resistant to tetracycline. Treatment clinically failed in 14 (52%) of 27 doxycycline-treated patients infected with a tetracycline-resistant V cholerae 01 strain, compared with three (8%) of 37 patients infected with a tetracycline-susceptible strain (44% [23-65]). INTERPRETATION: Single-dose ciprofloxacin is effective in the treatment of cholera caused by V cholerae 01 or 0139 and is better than single-dose doxycycline in the eradication of V cholerae from stool. Single-dose ciprofloxacin may also be the preferred treatment in areas where tetracycline-resistant V cholerae are common. In V cholerae, in-vitro doxycycline susceptibilities are not a useful indicator of the in-vivo efficacy of the drug.

Administration, Oral↗
PubMed2000

Vaccines for preventing cholera.

BACKGROUND: Oral cholera vaccines (either killed whole cell or live recombinant vaccines) are newer alternatives to the parenteral vaccines which have been thought to confer only moderate and short-term immunity. OBJECTIVES: The objective of this review was to assess the effect of cholera vaccines in preventing cases of cholera and preventing deaths. SEARCH STRATEGY: We searched the Cochrane Infectious Diseases Group trials register, Medline, Embase and reference lists of articles. We handsearched the journal Vaccine, contacted researchers in the field and manufacturers. SELECTION CRITERIA: Randomised and quasi-randomised studies comparing cholera vaccines (killed or live) with placebo, control vaccines or no intervention, or comparing types, doses or schedules of cholera vaccine. We included adults and children irrespective of immune status or special risk category. DATA COLLECTION AND ANALYSIS: Data extraction and assessment of trial quality was done independently by two reviewers. MAIN RESULTS: Thirty-two trials were included. Seventeen efficacy trials of relatively good quality, testing parenteral and oral killed whole cell vaccines and involving over 2. 6 million adults, children and infants were included. Nineteen safety trials have been conducted for both types of killed whole cell vaccines and for live vaccines and have involved 11,459 people. For all types of vaccines compared to placebo, the relative risk of contracting cholera at 12 months was 0.49, 95% confidence interval 0. 41 to 0.59 (random effects model). This translates to an efficacy of 51%, 95% confidence interval 41% to 59%. Both parenteral and oral administration were relatively efficacious, but significant protection extended into the third year for oral killed whole cell vaccines. Children under 5 were only protected for up to a year, while older children or adults were protected for up to three years. Parenteral killed whole cell vaccines were associated with increased systemic and local adverse effects compared to placebo. Oral killed whole cell vaccines or oral live vaccines were not. REVIEWER'S CONCLUSIONS: Cholera killed whole cell vaccines appear to be relatively effective and safe. Live oral recombinant vaccines appear to be safe, but efficacy data are not available. Protection against cholera appears to persist for up to two years following a single dose of vaccine, and for three to four years with an annual booster.

Adult↗
PubMed2006

Seasonal cholera caused by Vibrio cholerae serogroups O1 and O139 in the coastal aquatic environment of Bangladesh.

Since Vibrio cholerae O139 first appeared in 1992, both O1 El Tor and O139 have been recognized as the epidemic serogroups, although their geographic distribution, endemicity, and reservoir are not fully understood. To address this lack of information, a study of the epidemiology and ecology of V. cholerae O1 and O139 was carried out in two coastal areas, Bakerganj and Mathbaria, Bangladesh, where cholera occurs seasonally. The results of a biweekly clinical study (January 2004 to May 2005), employing culture methods, and of an ecological study (monthly in Bakerganj and biweekly in Mathbaria from March 2004 to May 2005), employing direct and enrichment culture, colony blot hybridization, and direct fluorescent-antibody methods, showed that cholera is endemic in both Bakerganj and Mathbaria and that V. cholerae O1, O139, and non-O1/non-O139 are autochthonous to the aquatic environment. Although V. cholerae O1 and O139 were isolated from both areas, most noteworthy was the isolation of V. cholerae O139 in March, July, and September 2004 in Mathbaria, where seasonal cholera was clinically linked only to V. cholerae O1. In Mathbaria, V. cholerae O139 emerged as the sole cause of a significant outbreak of cholera in March 2005. V. cholerae O1 reemerged clinically in April 2005 and established dominance over V. cholerae O139, continuing to cause cholera in Mathbaria. In conclusion, the epidemic potential and coastal aquatic reservoir for V. cholerae O139 have been demonstrated. Based on the results of this study, the coastal ecosystem of the Bay of Bengal is concluded to be a significant reservoir for the epidemic serogroups of V. cholerae.

Bangladesh↗
PubMed2005

Vibrio cholerae infection of Drosophila melanogaster mimics the human disease cholera.

Cholera, the pandemic diarrheal disease caused by the gram-negative bacterium Vibrio cholerae, continues to be a major public health challenge in the developing world. Cholera toxin, which is responsible for the voluminous stools of cholera, causes constitutive activation of adenylyl cyclase, resulting in the export of ions into the intestinal lumen. Environmental studies have demonstrated a close association between V. cholerae and many species of arthropods including insects. Here we report the susceptibility of the fruit fly, Drosophila melanogaster, to oral V. cholerae infection through a process that exhibits many of the hallmarks of human disease: (i) death of the fly is dependent on the presence of cholera toxin and is preceded by rapid weight loss; (ii) flies harboring mutant alleles of either adenylyl cyclase, Gsalpha, or the Gardos K channel homolog SK are resistant to V. cholerae infection; and (iii) ingestion of a K channel blocker along with V. cholerae protects wild-type flies against death. In mammals, ingestion of as little as 25 mug of cholera toxin results in massive diarrhea. In contrast, we found that ingestion of cholera toxin was not lethal to the fly. However, when cholera toxin was co-administered with a pathogenic strain of V. cholerae carrying a chromosomal deletion of the genes encoding cholera toxin, death of the fly ensued. These findings suggest that additional virulence factors are required for intoxication of the fly that may not be essential for intoxication of mammals. Furthermore, we demonstrate for the first time the mechanism of action of cholera toxin in a whole organism and the utility of D. melanogaster as an accurate, inexpensive model for elucidation of host susceptibility to cholera.

Journal Article↗
PubMed1990

[The capacity to produce cholera exotoxin in natural strains of Vibrio cholerae].

The study of 27 V. cholerae strains, isolated from cholera patients and found to be hemolytically inactive, with a view to establish their capacity for the production of cholera toxin has revealed that 4 strains (V. cholerae cholerae Dacca 35, V. cholerae cholerae Dacca 3, V. cholerae cholerae B1307, V. cholerae cholerae J89) produce this protein. The quantitative determination of enterotoxin has been made with the use of GM1 ELISA technique. Strain Dacca 35 has been found to be highly toxigenic and, as regards the amount of exotoxin it produces, no different from V. cholerae cholerae strain 569B, a well-known producer of cholera toxin. In strain Dacca 35 correlation between the capacity of the cells for toxin production and the morphology of colonies has been established. The study has revealed that the chromosome of strain Dacca 35 contains two copies of gene vctAB responsible for the synthesis of cholera toxin.

Animals↗