Cholera Toxin
Cholera
Cholera Vaccines
G(M1) Ganglioside
Antitoxins
Enterotoxins
T-2 Toxin
Adenosine Diphosphate Ribose
Toxoids
Vibrio cholerae O1
Tetanus Toxin
Intestinal Secretions
Adenylate Cyclase
Adenylate Cyclase Toxin
Cyclic AMP
Toxins, Biological
Botulinum Toxins, Type A
Bacterial Toxins
Marine Toxins
Gangliosides
GTP-Binding Proteins
Shiga Toxins
Immunoglobulin A
Virulence Factors, Bordetella
Immunity, Mucosal
Pertussis Toxin
Immunization
Shiga Toxin 2
Colforsin
Vibrio cholerae O139
Amoebozoa
Intestinal Mucosa
Shiga Toxin 1
Adjuvants, Immunologic
Ileum
Haiti
Rabbits
Acetaldehyde
1-Methyl-3-isobutylxanthine
Jejunum
Immunoglobulin A, Secretory
Cell Membrane
Molecular Sequence Data
Diarrhea
Guanosine Triphosphate
ADP-Ribosylation Factors
Vibrio cholerae non-O1
Bacterial Vaccines
Receptors, Cell Surface
Immunoglobulin G
Escherichia coli
Ciliary Body
Vibrio
Amino Acid Sequence
Ricin
Adenosine Diphosphate Sugars
Intestine, Small
Guanylyl Imidodiphosphate
Hemolysin Proteins
Cells, Cultured
8-Bromo Cyclic Adenosine Monophosphate
Intestines
Cytotoxins
Guanosine 5'-O-(3-Thiotriphosphate)
Isoproterenol
Vaccines, Synthetic
GTP-Binding Protein alpha Subunits, Gs
Theophylline
Fimbriae Proteins
Role of DnaK in in vitro and in vivo expression of virulence factors of Vibrio cholerae. (1/2652)
The dnaK gene of Vibrio cholerae was cloned, sequenced, and used to construct a dnaK insertion mutant which was then used to examine the role of DnaK in expression of the major virulence factors of this important human pathogen. The central regulator of several virulence genes of V. cholerae is ToxR, a transmembrane DNA binding protein. The V. cholerae dnaK mutant grown in standard laboratory medium exhibited phenotypes characteristic of cells deficient in ToxR activity. Using Northern blot analysis and toxR transcriptional fusions, we demonstrated a reduction in expression of the toxR gene in the dnaK mutant strain together with a concomitant increase in expression of a htpG-like heat shock gene that is located immediately upstream and is divergently transcribed from toxR. This may be due to increased heat shock induction in the dnaK mutant. In vivo, however, although expression from heat shock promoters in the dnaK mutant was similar to that observed in vitro, expression of both toxR and htpG was comparable to that by the parental strain. In both strains, in vivo expression of toxR was significantly higher than that observed in vitro, but no reciprocal decrease in htpG expression was observed. These results suggest that the modulation of toxR expression in vivo may be different from that observed in vitro. (+info)Transcutaneous immunization with bacterial ADP-ribosylating exotoxins as antigens and adjuvants. (2/2652)
Transcutaneous immunization (TCI) is a new technique that uses the application of vaccine antigens in a solution on the skin to induce potent antibody responses without systemic or local toxicity. We have previously shown that cholera toxin (CT), a potent adjuvant for oral and nasal immunization, can induce both serum and mucosal immunoglobulin G (IgG) and IgA and protect against toxin-mediated mucosal disease when administered by the transcutaneous route. Additionally, CT acts as an adjuvant for coadministered antigens such as tetanus and diphtheria toxoids when applied to the skin. CT, a member of the bacterial ADP-ribosylating exotoxin (bARE) family, is most potent as an adjuvant when the A-B subunits are present and functional. We now show that TCI induces secondary antibody responses to coadministered antigens as well as to CT in response to boosting immunizations. IgG antibodies to coadministered antigens were also found in the stools and lung washes of immunized mice, suggesting that TCI may target mucosal pathogens. Mice immunized by the transcutaneous route with tetanus fragment C and CT developed anti-tetanus toxoid antibodies and were protected against systemic tetanus toxin challenge. We also show that bAREs, similarly organized as A-B subunits, as well as the B subunit of CT alone, induced antibody responses to themselves when given via TCI. Thus, TCI appears to induce potent, protective immune responses to both systemic and mucosal challenge and offers significant potential practical advantages for vaccine delivery. (+info)Zonula occludens toxin is a powerful mucosal adjuvant for intranasally delivered antigens. (3/2652)
Zonula occludens toxin (Zot) is produced by toxigenic strains of Vibrio cholerae and has the ability to reversibly alter intestinal epithelial tight junctions, allowing the passage of macromolecules through the mucosal barrier. In the present study, we investigated whether Zot could be exploited to deliver soluble antigens through the nasal mucosa for the induction of antigen-specific systemic and mucosal immune responses. Intranasal immunization of mice with ovalbumin (Ova) and recombinant Zot, either fused to the maltose-binding protein (MBP-Zot) or with a hexahistidine tag (His-Zot), induced anti-Ova serum immunoglobulin G (IgG) titers that were approximately 40-fold higher than those induced by immunization with antigen alone. Interestingly, Zot also stimulated high anti-Ova IgA titers in serum, as well as in vaginal and intestinal secretions. A comparison with Escherichia coli heat-labile enterotoxin (LT) revealed that the adjuvant activity of Zot was only sevenfold lower than that of LT. Moreover, Zot and LT induced similar patterns of Ova-specific IgG subclasses. The subtypes IgG1, IgG2a, and IgG2b were all stimulated, with a predominance of IgG1 and IgG2b. In conclusion, our results highlight Zot as a novel potent mucosal adjuvant of microbial origin. (+info)Genetic characterization of a new type IV-A pilus gene cluster found in both classical and El Tor biotypes of Vibrio cholerae. (4/2652)
The Vibrio cholerae genome contains a 5.4-kb pil gene cluster that resembles the Aeromonas hydrophila tap gene cluster and other type IV-A pilus assembly operons. The region consists of five complete open reading frames designated pilABCD and yacE, based on the nomenclature of related genes from Pseudomonas aeruginosa and Escherichia coli K-12. This cluster is present in both classical and El Tor biotypes, and the pilA and pilD genes are 100% conserved. The pilA gene encodes a putative type IV pilus subunit. However, deletion of pilA had no effect on either colonization of infant mice or adherence to HEp-2 cells, demonstrating that pilA does not encode the primary subunit of a pilus essential for these processes. The pilD gene product is similar to other type IV prepilin peptidases, proteins that process type IV signal sequences. Mutational analysis of the pilD gene showed that pilD is essential for secretion of cholera toxin and hemagglutinin-protease, mannose-sensitive hemagglutination (MSHA), production of toxin-coregulated pili, and colonization of infant mice. Defects in these functions are likely due to the lack of processing of N termini of four Eps secretion proteins, four proteins of the MSHA cluster, and TcpB, all of which contain type IV-A leader sequences. Some pilD mutants also showed reduced adherence to HEp-2 cells, but this defect could not be complemented in trans, indicating that the defect may not be directly due to a loss of pilD. Taken together, these data demonstrate the effectiveness of the V. cholerae genome project for rapid identification and characterization of potential virulence factors. (+info)Ribotypes of clinical Vibrio cholerae non-O1 non-O139 strains in relation to O-serotypes. (5/2652)
The emergence of Vibrio cholerae O139 in 1992 and reports of an increasing number of other non-O1 serogroups being associated with diarrhoea, stimulated us to characterize V. cholerae non-O1 non-O139 strains received at the National Institute of Infectious Diseases, Japan for serotyping. Ribotyping with the restriction enzyme BglI of 103 epidemiological unrelated mainly clinical strains representing 10 O-serotypes yielded 67 different typing patterns. Ribotype similarity within each serotype was compared by using the Dice coefficient (Sd) and different levels of homogeneity were observed (serotypes O5, O41 and O17, Sd between 82 and 90%: serotypes O13 and O141 Sd of 72; and O2, O6, O7, O11, O24 Sd of 62-66%). By cluster analysis, the strains were divided into several clusters of low similarity suggesting a high level of genetic diversity. A low degree of similarity between serotypes and ribotypes was found as strains within a specific serotypes often did not cluster but clustered with strains from other serotypes. However, epidemiological unrelated O5 strains showed identical or closely related ribotypes suggesting that these strains have undergone few genetic changes and may correspond to a clonal line. Surprisingly, 10 of 16 O141 strains studied contained a cholera toxin (CT) gene, including 7 strains recovered from stool and water samples in the United States. This is to our knowledge the first report of CT-positive clinical O141 strains. The closely related ribotypes shown by eight CT-positive strains is disturbing and suggest that these strains may be of a clonal origin and have the potential to cause cholera-like disease. Despite the low degree of correlation found between ribotypes and serotypes, both methods appears to be valuable techniques in studying the epidemiology of emerging serotypes of V. cholerae. (+info)Environmental signals modulate ToxT-dependent virulence factor expression in Vibrio cholerae. (6/2652)
The regulatory protein ToxT directly activates the transcription of virulence factors in Vibrio cholerae, including cholera toxin (CT) and the toxin-coregulated pilus (TCP). Specific environmental signals stimulate virulence factor expression by inducing the transcription of toxT. We demonstrate that transcriptional activation by the ToxT protein is also modulated by environmental signals. ToxT expressed from an inducible promoter activated high-level expression of CT and TCP in V. cholerae at 30 degrees C, but expression of CT and TCP was significantly decreased or abolished by the addition of 0.4% bile to the medium and/or an increase of the temperature to 37 degrees C. Also, expression of six ToxT-dependent TnphoA fusions was modulated by temperature and bile. Measurement of ToxT-dependent transcription of genes encoding CT and TCP by ctxAp- and tcpAp-luciferase fusions confirmed that negative regulation by 37 degrees C or bile occurs at the transcriptional level in V. cholerae. Interestingly, ToxT-dependent transcription of these same promoters in Salmonella typhimurium was relatively insensitive to regulation by temperature or bile. These data are consistent with ToxT transcriptional activity being modulated by environmental signals in V. cholerae and demonstrate an additional level of complexity governing the expression of virulence factors in this pathogen. We propose that negative regulation of ToxT-dependent transcription by environmental signals prevents the incorrect temporal and spatial expression of virulence factors during cholera pathogenesis. (+info)G protein activation by human dopamine D3 receptors in high-expressing Chinese hamster ovary cells: A guanosine-5'-O-(3-[35S]thio)- triphosphate binding and antibody study. (7/2652)
Despite extensive study, the G protein coupling of dopamine D3 receptors is poorly understood. In this study, we used guanosine-5'-O-(3-[35S]thio)-triphosphate ([35S]-GTPgammaS) binding to investigate the activation of G proteins coupled to human (h) D3 receptors stably expressed in Chinese hamster ovary (CHO) cells. Although the receptor expression level was high (15 pmol/mg), dopamine only stimulated G protein activation by 1.6-fold. This was despite the presence of marked receptor reserve for dopamine, as revealed by Furchgott analysis after irreversible hD3 receptor inactivation with the alkylating agent, EEDQ (N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline). Thus, half-maximal stimulation of [35S]-GTPgammaS binding required only 11.8% receptor occupation of hD3 sites. In contrast, although the hD2(short) receptor expression level in another CHO cell line was 11-fold lower, stimulation by dopamine was higher (2.5-fold). G protein activation was increased at hD3 and, less potently, at hD2 receptors by the preferential D3 agonists, PD 128,907 [(+)-(4aR,10bR)-3,4,4a, 10b-tetrahydro-4-propyl-2H,5H- [1]benzopyrano[4,3-b]-1, 4-oxazin-9-ol] and (+)-7-OH-DPAT (7-hydroxy-2-(di-n-propylamino)tetralin). Furthermore, the selective D3 antagonists, S 14297 ((+)-[7-(N, N-dipropylamino)-5,6,7, 8-tetrahydro-naphtho(2,3b)dihydro-2,3-furane]) and GR 218,231 (2(R, S)-(dipropylamino)-6-(4-methoxyphenylsulfonylmethyl)-1,2,3,4- tetrahydronaphtalene), blocked dopamine-stimulated [35S]GTPgammaS binding more potently at hD3 than at hD2 sites. Antibodies against Galphai/alphao reduced dopamine-induced G protein activation at both CHO-hD3 and -hD2 membranes, whereas GalphaS antibodies had no effect at either site. In contrast, incubation with anti-Galphaq/alpha11 antibodies, which did not affect dopamine-induced G protein activation at hD2 receptors, attenuated hD3-induced G protein activation. These data suggest that hD3 receptors may couple to Galphaq/alpha11 and would be consistent with the observation that pertussis toxin pretreatment, which inactivates only Gi/o proteins, only submaximally (80%) blocked dopamine-stimulated [35S]GTPgammaS binding in CHO-hD3 cells. Taken together, the present data indicate that 1) hD3 receptors functionally couple to G protein activation in CHO cells, 2) hD3 receptors activate G proteins less effectively than hD2 receptors, and 3) hD3 receptors may couple to different G protein subtypes than hD2 receptors, including nonpertussis sensitive Gq/11 proteins. (+info)Dopamine receptor subtypes modulate olfactory bulb gamma-aminobutyric acid type A receptors. (8/2652)
The gamma-aminobutyric acid type A (GABAA) receptor is the predominant Cl- channel protein mediating inhibition in the olfactory bulb and elsewhere in the mammalian brain. The olfactory bulb is rich in neurons containing both GABA and dopamine. Dopamine D1 and D2 receptors are also highly expressed in this brain region with a distinct and complementary distribution pattern. This distribution suggests that dopamine may control the GABAergic inhibitory processing of odor signals, possibly via different signal-transduction mechanisms. We have observed that GABAA receptors in the rat olfactory bulb are differentially modulated by dopamine in a cell-specific manner. Dopamine reduced the currents through GABA-gated Cl- channels in the interneurons, presumably granule cells. This action was mediated via D1 receptors and involved phosphorylation of GABAA receptors by protein kinase A. Enhancement of GABA responses via activation of D2 dopamine receptors and phosphorylation of GABAA receptors by protein kinase C was observed in mitral/tufted cells. Decreasing or increasing the binding affinity for GABA appears to underlie the modulatory effects of dopamine via distinct receptor subtypes. This dual action of dopamine on inhibitory GABAA receptor function in the rat olfactory bulb could be instrumental in odor detection and discrimination, olfactory learning, and ultimately odotopic memory formation. (+info)The symptoms of cholera include:
1. Diarrhea: Cholera causes profuse, watery diarrhea that can last for several days.
2. Dehydration: The loss of fluids and electrolytes due to diarrhea can lead to severe dehydration, which can be life-threatening if not treated promptly.
3. Nausea and vomiting: Cholera patients may experience nausea and vomiting, especially in the early stages of the disease.
4. Abdominal cramps: The abdomen may become tender and painful due to the inflammation caused by the bacteria.
5. Low-grade fever: Some patients with cholera may experience a mild fever, typically less than 102°F (39°C).
Cholera is spread through the fecal-oral route, which means that it is transmitted when someone ingests food or water contaminated with the bacteria. The disease can also be spread by direct contact with infected fecal matter, such as through poor hygiene practices or inadequate waste disposal.
There are several ways to diagnose cholera, including:
1. Stool test: A stool sample can be tested for the presence of Vibrio cholerae using a microscope or a rapid diagnostic test (RDT).
2. Blood test: A blood test can detect the presence of antibodies against Vibrio cholerae, which can indicate that the patient has been infected with the bacteria.
3. Physical examination: A healthcare provider may perform a physical examination to look for signs of dehydration and other symptoms of cholera.
Treatment of cholera typically involves replacing lost fluids and electrolytes through oral rehydration therapy (ORT) or intravenous fluids. Antibiotics may also be given to shorten the duration of diarrhea and reduce the risk of complications. In severe cases, hospitalization may be necessary to provide more intensive treatment.
Prevention of cholera involves maintaining good hygiene practices, such as washing hands with soap and water, and avoiding consumption of contaminated food and water. Vaccines are also available to protect against cholera, particularly for people living in areas where the disease is common.
In conclusion, cholera is a highly infectious disease that can cause severe dehydration and even death if left untreated. Early diagnosis and treatment are critical to preventing complications and reducing the risk of transmission. Prevention measures such as vaccination and good hygiene practices can also help control the spread of the disease.
There are several types of diarrhea, including:
1. Acute diarrhea: This type of diarrhea is short-term and usually resolves on its own within a few days. It can be caused by a viral or bacterial infection, food poisoning, or medication side effects.
2. Chronic diarrhea: This type of diarrhea persists for more than 4 weeks and can be caused by a variety of conditions, such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), or celiac disease.
3. Diarrhea-predominant IBS: This type of diarrhea is characterized by frequent, loose stools and abdominal pain or discomfort. It can be caused by a variety of factors, including stress, hormonal changes, and certain foods.
4. Infectious diarrhea: This type of diarrhea is caused by a bacterial, viral, or parasitic infection and can be spread through contaminated food and water, close contact with an infected person, or by consuming contaminated food.
Symptoms of diarrhea may include:
* Frequent, loose, and watery stools
* Abdominal cramps and pain
* Bloating and gas
* Nausea and vomiting
* Fever and chills
* Headache
* Fatigue and weakness
Diagnosis of diarrhea is typically made through a physical examination, medical history, and laboratory tests to rule out other potential causes of the symptoms. Treatment for diarrhea depends on the underlying cause and may include antibiotics, anti-diarrheal medications, fluid replacement, and dietary changes. In severe cases, hospitalization may be necessary to monitor and treat any complications.
Prevention of diarrhea includes:
* Practicing good hygiene, such as washing hands frequently and thoroughly, especially after using the bathroom or before preparing food
* Avoiding close contact with people who are sick
* Properly storing and cooking food to prevent contamination
* Drinking safe water and avoiding contaminated water sources
* Avoiding raw or undercooked meat, poultry, and seafood
* Getting vaccinated against infections that can cause diarrhea
Complications of diarrhea can include:
* Dehydration: Diarrhea can lead to a loss of fluids and electrolytes, which can cause dehydration. Severe dehydration can be life-threatening and requires immediate medical attention.
* Electrolyte imbalance: Diarrhea can also cause an imbalance of electrolytes in the body, which can lead to serious complications.
* Inflammation of the intestines: Prolonged diarrhea can cause inflammation of the intestines, which can lead to abdominal pain and other complications.
* Infections: Diarrhea can be a symptom of an infection, such as a bacterial or viral infection. If left untreated, these infections can lead to serious complications.
* Malnutrition: Prolonged diarrhea can lead to malnutrition and weight loss, which can have long-term effects on health and development.
Treatment of diarrhea will depend on the underlying cause, but may include:
* Fluid replacement: Drinking plenty of fluids to prevent dehydration and replace lost electrolytes.
* Anti-diarrheal medications: Over-the-counter or prescription medications to slow down bowel movements and reduce diarrhea.
* Antibiotics: If the diarrhea is caused by a bacterial infection, antibiotics may be prescribed to treat the infection.
* Rest: Getting plenty of rest to allow the body to recover from the illness.
* Dietary changes: Avoiding certain foods or making dietary changes to help manage symptoms and prevent future episodes of diarrhea.
It is important to seek medical attention if you experience any of the following:
* Severe diarrhea that lasts for more than 3 days
* Diarrhea that is accompanied by fever, blood in the stool, or abdominal pain
* Diarrhea that is severe enough to cause dehydration or electrolyte imbalances
* Diarrhea that is not responding to treatment
Prevention of diarrhea includes:
* Good hand hygiene: Washing your hands frequently, especially after using the bathroom or before preparing food.
* Safe food handling: Cooking and storing food properly to prevent contamination.
* Avoiding close contact with people who are sick.
* Getting vaccinated against infections that can cause diarrhea, such as rotavirus.
Overall, while diarrhea can be uncomfortable and disruptive, it is usually a minor illness that can be treated at home with over-the-counter medications and plenty of fluids. However, if you experience severe or persistent diarrhea, it is important to seek medical attention to rule out any underlying conditions that may require more formal treatment.
Cholera toxin
Keratinocyte
Hes3 signaling axis
Enterocyte
AB5 toxin
Nirmal Kumar Dutta
Cyclic adenosine monophosphate
TA-CD
Heat-labile enterotoxin family
Cocaine
NPLOC4
Vibrio
Cocaine dependence
John Woollam (physicist)
Substance dependence
UFD1L
Virginia L. Miller
Shiga toxin
AB toxin
Cholera
GM1
Robert Koch
John Mekalanos
Cystic fibrosis
CTXφ bacteriophage
Symporter
Vibrio mimicus
Differentiation therapy
Alfred G. Gilman
Affinity chromatography
Diseases of poverty
Anterograde tracing
Rhodesia and weapons of mass destruction
Rihab Taha
Cholera vaccine
Adenia
List of unsolved deaths
Amanita sphaerobulbosa
Vaccine hesitancy
Unit 731
Cystic fibrosis transmembrane conductance regulator
Kaimingjie germ weapon attack
Olivocochlear system
Toxoid
Vibriocin
Samuel Thomson
Spiroligomer
James Scarth Combe
Salton Sea
ARF6
Giuseppe Sanarelli
Japan and weapons of mass destruction
Saccharomyces boulardii
Vibrio vulnificus
Seawater
Émile Roux
Paul W. Ewald
"Expression of Cholera Toxin B-Proinsulin Fusion Protein in Lettuce and" by Tracey Ruhlman, Ruhlman Ahangari et al.
PCR - Cholera toxin
Results of search for 'su:{Cholera toxin.}'
›
WHO HQ Library catalog
Immunological effects of recombinant Lactobacillus casei expressing pilin MshB fused with cholera toxin B subunit adjuvant as...
Neurobiology of Tourette Syndrome: Current Status and Need for Further Investigation | Journal of Neuroscience
Vibrio cholera toxin secretion channel<...
Lipid Sorting by Ceramide Structure from Plasma Membrane to ER for the Cholera Toxin Receptor Ganglioside GM1 • MatTek Life...
Figure 1 - Population-Based Serologic Survey of Vibrio cholerae Antibody Titers before Cholera Outbreak, Haiti, 2022 - Volume...
Sunlight-induced propagation of the lysogenic phage encoding cholera toxin<...
1md2.1 | SWISS-MODEL Template Library
Neutralization of Salmonella toxin induced elongation of Chinese hamster ovary cells by cholera antitoxin<...
Age-related immunogenicity and reactogenicity of live oral cholera vaccine CVD 103-HgR in a randomized, controlled clinical...
Shamima Islam, M.B.B.S., Ph.D. | About NIAMS | NIAMS
Cholera toxin binds to LewisX and fucosylated glycoproteins play a functional role in human intestinal cell intoxication -...
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Vaccines | Free Full-Text | Anti-Flavivirus Vaccines: Review of the Present Situation and Perspectives of Subunit Vaccines...
Toxins: MedlinePlus Medical Encyclopedia
Neuroscience - Biotium
Advanced Search Results - Public Health Image Library(PHIL)
Update: Cholera -- Western Hemisphere
Vaccine adjuvants that induce an immune response
Publication Detail
Pittman, Margaret 1988 - Office of NIH History and Stetten Museum
Biomarkers Search
Translational Research | NHLBI, NIH
Explore More Research | National Institute of Biomedical Imaging and Bioengineering
Berberine: MedlinePlus Supplements
Carl-Fredrik Flach | Göteborgs universitet
Subunit4
- Lettuce and tobacco chloroplast transgenic lines expressing the cholera toxin B subunit-human proinsulin (CTB-Pins) fusion protein were generated. (upenn.edu)
- Immunological effects of recombinant Lactobacillus casei expressing pilin MshB fused with cholera toxin B subunit adjuvant as an oral vaccine against Aeromonas veronii infection in crucian carp. (bvsalud.org)
- Herein, we developed vaccine candidates by inserting MSH type VI pili B (MshB) from A. veronii as an antigen and cholera toxin B subunit (CTB) as a molecular adjuvant into Lactobacillus casei and evaluated their immunological effect as vaccines in a crucian carp ( Carassius auratus ) model. (bvsalud.org)
- The catalytic subunit of cholera toxin. (nih.gov)
Vaccine6
- Attenuated recombinant Vibrio cholerae O1 vaccine strain CVD 103-HgR elicits a rapid serum vibriocidal antibody (SVA) response and protects against cholera diarrhea in volunteer challenge studies but has not been studied in older adults. (nih.gov)
- NIAID efforts to develop a preventive cholera vaccine have targeted two distinct but overlapping approaches: live and "killed" vaccines. (nih.gov)
- An important re-analysis of a large study involving a vaccine containing inactivated cholera found that the incidence of cholera among the placebo recipients varied inversely with the level of vaccination in the community. (nih.gov)
- In the case of cholera, one epidemiological model in Bangladesh showed that because of community immunity, a vaccine containing inactivated cholera conferring relatively short-lived immunity could eliminate cholera entirely if 70 percent of the population was vaccinated. (nih.gov)
- The development of a vaccine containing live cholera involves reducing the bacteria's virulence and ability to cause diarrhea while preserving its ability to induce an immune response. (nih.gov)
- The technology used to create Dukoral was later transferred to Vietnam and India, where a modified killed cholera vaccine is being produced as OCV-Vax in Vietnam and as Shanchol in India. (nih.gov)
Bacterial toxin2
- Early in his career, Dr. Moss and collaborators discovered that the bacterial toxin, cholera toxin, exerted its effects on mammalian cells by ADP-ribosylation, the transfer of an ADP-ribose group from NAD to an acceptor molecule. (nih.gov)
- They also showed that these synthetic mucins could effectively neutralize the bacterial toxin that causes cholera. (nih.gov)
Bacteria7
- Other serogroups of V. cholerae, and nontoxigenic V. cholerae O1, may be isolated from stools of patients with diarrhea, but these bacteria are not associated with epidemic cholera. (cdc.gov)
- Most toxins that cause problems in humans come from germs such as bacteria. (nih.gov)
- For example, the symptoms of cholera are caused by a toxin made by cholera bacteria. (nih.gov)
- Killed" or inactivated vaccines are those that contain cholera bacteria that have been made harmless so as not to infect the vaccinated recipient. (nih.gov)
- Some bacteria, such as those that cause cholera, use a special system to inject toxins into the cells of host organisms and other bacteria. (nih.gov)
- So far, researchers have found that there are at least 6 different ways that bacteria can transport proteins (like toxins) through the 2 membranes and into neighboring cells. (nih.gov)
- Type VI secretion, the most recent type of transport to be discovered, is common to many types of bacteria, including Vibrio cholerae , a waterborne pathogen that infects millions worldwide and causes cholera. (nih.gov)
Epidemic cholera3
- Epidemic cholera appeared in Peru in January 1991 and subsequently spread to Ecuador, Colombia, Chile, Brazil, Mexico, and Guatemala (Table 1) (1-3). (cdc.gov)
- Clinical suspicion should be increased for persons returning from areas known to have epidemic cholera or for persons with a recent history of ingestion of raw or undercooked shellfish. (cdc.gov)
- It is also antigenically distinct from the V. cholerae O1 and O139 strains, which cause epidemic cholera in many countries. (who.int)
Binds1
- The B protomer binds cholera toxin to intestinal epithelial cells and facilitates the uptake of the A1 fragment. (nih.gov)
Vibrio5
- In collaboration with Wim Hol (UW) we studied the structure of the vibrio cholera toxin secretion channel. (ucla.edu)
- The T2SS is responsible for the secretion of virulence factors such as cholera toxin (CT) and heat-labile enterotoxin (LT) from Vibrio cholerae and enterotoxigenic Escherichia coli, respectively. (ucla.edu)
- Vibrio cholerae -specific and functional antibodies among participants in a serologic study conducted before a cholera outbreak in Haiti, 2022. (cdc.gov)
- In toxigenic Vibrio cholerae, the cholera enterotoxin (CT) is encoded by CTXΦ, a lysogenic bacteriophage. (johnshopkins.edu)
- Vibrio cholerae species can be divided into 2 major groups: cholera-causing strains of the serogroups O1 and O139, and non-O1 V. cholerae (NOVC) [1]. (who.int)
Enterotoxin2
Electrolytes2
- At present, World Health Organization ORS packets (WHO-ORS,* Jianas Brothers, St. Louis), RicelyteTM (Mead Johnson), and RehydralyteR (Ross Laboratories) are the only oral solutions available in the United States that contain the proper balance of electrolytes for treating cholera. (cdc.gov)
- Oral rehydration therapy (ORT), or the administration of an oral solution containing glucose and electrolytes, is currently the predominant treatment for cholera worldwide. (nih.gov)
Adjuvant1
- Mucosal adjuvant activity of cholera toxin requires Th17 cells and protects against inhalation anthrax. (nih.gov)
Strains2
19781
- Cholera and related diarrheas : molecular aspects of a global health problem, 43rd Nobel Symposium, Stockholm, August 6-11, 1978 / editors, Oerjan Ouchterlony and Jan Holmgren. (who.int)
Proteins2
- We report here the presence of G-proteins in Y-organs and control (neural) tissue as determined by (1) ADP-ribosylation catalyzed by bacterial toxins and (2) western blot analysis using antibodies raised against mammalian G-proteins. (sicb.org)
- As many as 20 different proteins make up the type VI transport machinery, but how these proteins work together to send proteins and toxins out of the bacterial cell has, until now, remained a mystery. (nih.gov)
Mammalian1
- He later discovered that mammalian cells contain endogenous enzymes with activities that mimic the ADP-ribosyltransferase (ART) activity of cholera toxin. (nih.gov)
Cholerae2
NIAID1
- NIAID supports university-based and pharmaceutical and biotechnology researchers who are working to develop new cholera treatments and vaccines to prevent infection. (nih.gov)
Intestinal1
- In cholera, the toxin-generated level of intestinal cyclic AMP system activation is significantly greater than normally observed. (nih.gov)
Placebo1
- Vaccines are usually evaluated in field studies by comparing the incidence of disease (in this case, cholera) in a vaccinated population to an unvaccinated placebo control population. (nih.gov)
Symptoms1
- With clinical awareness of signs and symptoms of cholera, and knowledge of appropriate treatment, cholera should not pose a major risk to health in the United States. (cdc.gov)
Search1
- Results of search for 'su:{Cholera toxin. (who.int)
Vaccines2
- Currently, two of these types of cholera vaccines are available and both are administered orally as opposed to injection. (nih.gov)
- If used on a broader scale, the vaccines could reduce global cholera rates, especially if antimicrobial and oral rehydration therapies are also available, and sanitation programs are supported by community education. (nih.gov)
Diarrhea1
- Cholera should be suspected in a patient with severe watery diarrhea, vomiting, and dehydration. (cdc.gov)
Infection2
- Dunn Sandefur, P & Peterson, JW 1977, ' Neutralization of Salmonella toxin induced elongation of Chinese hamster ovary cells by cholera antitoxin ', Infection and immunity , vol. 15, no. 3, pp. 988-992. (utmb.edu)
- The conclusion drawn was that vaccination reduced the amount of cholera in the environment, and therefore, the risk of infection to everyone in the community. (nih.gov)
Cells1
- Immunogenicity endpoints included SVA and anti-cholera toxin (CT) antibody levels on days 1, 11, 29, 91 and 181 and lipopolysaccharide (LPS) and CT-specific IgA and IgG memory B cells on days 1, 91 and 181. (nih.gov)
Clinical2
- This report provides an update on cholera in the Western Hemisphere and provides recommendations on the clinical diagnosis and treatment of cholera in the United States. (cdc.gov)
- However, cholera may still have limited niches of low endemicity, especially in Northern Lebanon, where sub-clinical cases may occur. (who.int)
Mice1
- Dr. Moss and his colleagues showed that in mice lacking the opposing ARH, ARH1, the effects of cholera toxin were demonstrably amplified. (nih.gov)
Patients1
- Patients suspected of having cholera should be treated aggressively while awaiting culture results. (cdc.gov)
Activity1
- The elongation effect and the skin test activity were blocked by monospecific rabbit antisera against cholera toxin and against the B fragment of cholera toxin. (utmb.edu)
Levels1
- Simple benchtop polishing procedures render a smooth surface that supports propagation of surface plasmon polaritons with a deposited gold layer, which exhibit high bulk refractive index sensitivities and are capable of discriminating trace levels of cholera toxin on a supported lipid membrane interface. (nih.gov)
Effects1
- Effects of combined cholera toxin and cyclosporine therapy on renal allograft survival in the rat. (nih.gov)
Large1
- Toxins may also include some medicines that are helpful in small doses, but poisonous in large amounts. (nih.gov)
Cell1
- The cell membrane binding component of cholera toxin. (nih.gov)
Transmission1
- Proper treatment of sewage and drinking water in the United States should prevent transmission of cholera by these routes within the United States. (cdc.gov)
Structure1
- article{pmid20852644, title = {Structure of the cholera toxin secretion channel in its closed state}, author = {Steve L Reichow and Konstantin V Korotkov and Wim G J Hol and Tamir Gonen}, url = {https://cryoem.ucla.edu/wp-content/uploads/reichow_2010.pdf, Main text}, doi = {10.1038/nsmb.1910}, year = {2010}, date = {2010-09-19}, journal = {Nat. (ucla.edu)
Report1
- We report here 3D printing of high-quality, custom prisms by stereolithography that enable Kretschmann-configured plasmonic sensing of bacterial toxins. (nih.gov)
Treatment1
- Detoxified aggregate of cholera toxin formed by heat treatment of purified cholera toxin. (nih.gov)
Studies2
- Here we extend these studies by characterizing the binding of the cholera toxin B-pentamer to VcGspD using electron microscopy of negatively stained preparations. (ucla.edu)
- Solution and crystallographic studies of branched multivalent ligands that inhibit the receptor-binding of cholera toxin. (expasy.org)
Production1
- A second candidate, CVD-103HgR, was licensed in Europe, but is not currently in production or slated for use in cholera-endemic regions. (nih.gov)