Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VIBRIO”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMed1995

The effect of incubation temperature and sodium chloride concentration on the growth kinetics of Vibrio anguillarum and Vibrio anguillarum-related organisms.

The effect of temperature and NaCl concentration on the growth kinetics of Vibrio anguillarum and V. anguillarum-related (VAR) strains was studied. For one wild VAR strain, NaCl concentration interfered with growth temperature parameters, in particular, with the maximum growth temperature but also with the optimum temperature (defined as the temperature at which mumax equals its maximal value muopt), and with muopt itself. For the same strain, optimal growth required the adding of NaCl to the medium to a final concentration of 1.5%. These results were not confirmed by tests on a V. anguillarum collection strain. When the NaCl concentration in the culture media was 1.5%, the optimum temperature for the nine strains studied ranged from 29.7 degrees C to 34 degrees C whereas the maximum temperature ranged between 35.3 degrees C and 38.5 degrees C. Hence, antibiotic susceptibility testing as well as biochemical identification might be carried out at 30 degrees C in the presence of 1.5% NaCl, which corresponded to a suboptimal growth.

Animals↗
PubMed2006

Changes to the phenotypic profile of Vibrio harveyi when infected with the Vibrio harveyi myovirus-like (VHML) bacteriophage.

AIMS: To determine if infection of Vibrio harveyi with the V. harveyi myovirus-like (VHML) bacteriophage causes a change to the phenotypic profile of this species. METHODS AND RESULTS: Using 46 biochemical and metabolic tests, phenotypic profiles for noninfected V. harveyi and VHML infected V. harveyi were developed. Comparison of the infected and bacteriophage-infected strains of V. harveyi 645, 20 and 45 were found to have different test results for d-gluconate utilization, gamma-glutamyl transpeptidase and sulfatase activity, respectively. Using probabilistic identification, VHML infected and noninfected strains were identified as V. harveyi and had similar Willcox probability scores though the modal likelihood scores were reduced for VHML infected strains. One VHML infected strain, 642b, was misidentified as V. campbellii by phenotyping but not by PCR. It would appear that the phenotype of V. harveyi strains infected with VHML, are sufficiently altered that they occur at the margins of the known range of strain variation for V. harveyi. CONCLUSION: Infection of V. harveyi with VHML causes the phenotypic profile of the bacterium to change. This change reduces the modal likelihood score resulting in a poorer level of assurance for an identification of V. harveyi, especially in the natural host, strain 642. The bacteriophage VHML integrates into different sites in different strains of V. harveyi. SIGNIFICANCE AND IMPACT OF THE STUDY: The identification of V. harveyi as the causative agent of mortality in aquatic organisms is predominantly achieved through phenotyping. Since bacteriophages alter virulence in V. harveyi, understanding the effect they have on phenotype is important.

Culture Media↗
PubMed2005

The impact of mutations in the quorum sensing systems of Aeromonas hydrophila, Vibrio anguillarum and Vibrio harveyi on their virulence towards gnotobiotically cultured Artemia franciscana.

Disruption of quorum sensing, bacterial cell-to-cell communication by means of small signal molecules, has been suggested as a new anti-infective strategy for aquaculture. However, data about the impact of quorum sensing on the virulence of aquatic pathogens are scarce. In this study, a model system using gnotobiotically cultured Artemia franciscana was developed in order to determine the impact of mutations in the quorum sensing systems of Aeromonas hydrophila, Vibrio anguillarum and V. harveyi on their virulence. Mutations in the autoinducer 2 (AI-2) synthase gene luxS, the AI-2 receptor gene luxP or the response regulator gene luxO of the dual channel quorum sensing system of V. harveyi abolished virulence of the strain towards Artemia. Moreover, the addition of an exogenous source of AI-2 could restore the virulence of an AI-2 non-producing mutant. In contrast, none of the mutations in either the acylated homoserine lactone (AHL)-mediated component of the V. harveyi system or the quorum sensing systems of Ae. hydrophila and V. anguillarum had an impact on virulence of these bacteria towards Artemia. Our results indicate that disruption of quorum sensing could be a good alternative strategy to combat infections caused by V. harveyi.

Aeromonas hydrophila↗
PubMed1992

Antibodies to outer membrane proteins of Vibrio cholerae induce protection by inhibition of intestinal colonization of vibrios.

An antiserum was raised against the outer membrane (OM) preparation of a Vibrio cholerae 01 strain (Classical, Ogawa) and rendered specific for the outer membrane proteins (OMPs) by absorption with its lipopolysaccharide (LPS). The anti-OMP serum showed reactivity against OM preparations of other 01 and non-01 V. cholerae strains in enzyme-linked immunosorbent assay. The antiserum also induced significant protection against V. cholerae challenge in the suckling mouse model. This protection was found to be independent of biotype, serotype as well as serovar of the challenge organism and was demonstrable even at subagglutinating dilutions of antiserum. The Fab (IgG) fragment, prepared from the anti-OMP serum, also induced passive protection in similar experiments. Further studies demonstrated that the anti-OMP serum as well as its Fab (IgG) fragment markedly inhibited the intestinal colonization of a highly colonizing V. cholerae 01 strain A17 (El Tor, Ogawa). These results highlight the importance of V. cholerae OMPs in immunoprophylaxis against cholera.

Animals↗
PubMed1998

Vibrio cholerae O22 might be a putative source of exogenous DNA resulting in the emergence of the new strain of Vibrio cholerae O139.

The new epidemic strain O139 of Vibrio cholerae, the etiologic agent of cholera, has probably emerged from the pandemic strain O1 E1 Tor through a genetic rearrangement involving the horizontal transfer of exogenous O-antigen- and capsule-encoding genes of unknown origin. In V. cholerae O139, these genes are associated with an insertion sequence designated IS1358O139. In this work, we studied the distribution of seven genes flanking the IS1358O139 element in 13 serovars of V. cholerae strains. All these O139 genes and an IS1358 element designated IS1358O22-1 were only found in V. cholerae O22 with a similar genetic organization. Sequence analysis of a 4.5-kb fragment containing IS1358O22-1 and the adjacent genes revealed that these genes are highly homologous to those of V. cholerae O139. These results suggest that strains of V. cholerae O22 from the environment might have been the source of the exogenous DNA resulting in the emergence of the new epidemic strain O139.

Base Sequence↗
PubMed1999

Distribution of Vibrio cholerae O1 antigen biosynthesis genes among O139 and other non-O1 serogroups of Vibrio cholerae.

The organization and distribution of the genes responsible for O antigen biosynthesis in various serogroups of Vibrio cholerae were investigated using several DNA probes derived from various regions of the genes responsible for O1 antigen biosynthesis. Based on the reactivity pattern of the probes against the various serogroups, the cluster of genes responsible for the O1 antigen biosynthesis could be broadly divided into six groups, designated as class 1-6. The class 3 cluster of genes corresponding to gmd to wbeO, wbeT and a part of wbeU was specific for only the O1 serogroup. The other cluster of genes (class 1, 2, 4-6) reacted with other serogroups of V. cholerae. These data indicate that serotype conversion in V. cholerae does not depend on a simple mutational event but may involve horizontal gene transfer not only between V. cholerae strains but also between V. cholerae and species other than V. cholerae.

Base Sequence↗
PubMed1989

Survival of Vibrio anguillarum and Vibrio salmonicida at different salinities.

The fish pathogenic bacteria Vibrio anguillarum and V. salmonicida showed the capacity to survive for more than 50 and 14 months, respectively, in seawater microcosms. A salinity of 5% proved lethal to V. anguillarum harvested in the late-exponential growth phase, whereas a salinity of 9% was lethal to the bacterium after it had been starved at a salinity of 30% for 67 days. The lethal salinity for V. salmonicida harvested in the late-exponential growth phase was probably in the vicinity of 10%. V. anguillarum and V. salmonicida were very sensitive to nalidixic acid. Direct determination of viable cells after incubation with nalidixic acid was not possible, since the cells did not elongate. Samples of V. salmonicida were double stained with fluorescein isothiocyanate-labeled antibodies and 4',6-diamidino-2-phenylindole. After 3 or 4 days of starvation, there was a discrepancy between the total numbers of cells as determined by immunofluorescence versus by staining with 4',6-diamidino-2-phenylindole. The immunofluorescence counts remained high, which indicated the presence of intact cell envelopes but leakage of DNA and other cytoplasm components. After 2 weeks of starvation, for some of the cells, the region stained with 4',6-diamidino-2-phenylindole (i.e., DNA) was markedly smaller than the cell envelope. I attributed this to a shrinkage of the cytoplasm or a confined nucleoid or both. V. anguillarum lost its exoproteolytic activity before 11 days of starvation.

Animals↗
PubMed1996

Phenotypic characterization of Vibrio vulnificus biotype 2, a lipopolysaccharide-based homogeneous O serogroup within Vibrio vulnificus.

In this study, we have reevaluated the taxonomic position of biotype 2 of Vibrio vulnificus. For this purpose, we have biochemically and serologically characterized 83 biotype 2 strains from diseased eels, comparing them with 17 biotype 1 strains from different sources. Selected strains were also molecularly analyzed and tested for eel and mouse pathogenicity. Results have shown that biotype 2 (i) is biochemically homogeneous, indole production being the main trait that distinguishes it from biotype 1, (ii) presents small variations in DNA restriction profiles and outer membrane protein patterns, some proteins being immunologically related to outer membrane proteins from biotype 1, (iii) expresses a common lipopolysaccharide (LPS) profile, which is immunologically identical among strains and distinct from that of LPS of tested biotype 1 strains, and (iv) contains at least two high-Mr plasmids. Regarding host range, we have confirmed that both biotypes are pathogenic for mice but only biotype 2 is pathogenic for eels. On the basis of these data, we propose that biotype 2 of V. vulnificus constitutes an LPS-based O serogroup which is phenotypically homogeneous and pathogenic for eels. In this article, the serogroup is designated serogroup E (for eels).

Animals↗
PubMed2001

Antacid increases survival of Vibrio vulnificus and Vibrio vulnificus phage in a gastrointestinal model.

Viable counts of three strains of Vibrio vulnificus and its phage were determined during exposure to a mechanical gastrointestinal model with or without antacid for 9 h at 37 degrees C. V. vulnificus was eliminated (>4-log reduction) within 30 min in the gastric compartment (pH decline from 5.0 to 3.5). Viable V. vulnificus cells delivered from the gastric compartment during the first 30 min of exposure reached 10(6) to 10(8) CFU/ml in the intestinal compartment after 9 h (pH 7.0). Phages were eliminated within 45 min in the gastric compartment (pH decline from 5.1 to 2.5). Less than a 2-log reduction of phage was observed in the intestinal compartment after 9 h (pH 7.0). When the gastric compartment contained antacid V. vulnificus counts decreased slightly (<2 log) during 2 h of exposure (pH decline from 7.7 to 6.0), while counts in the intestinal compartment (pH 7.5) reached 10(7) to 10(9) CFU/ml. Phage numbers decreased 1 log after 2 h in the gastric compartment (pH decline from 7.7 to 5.7) containing antacid and decreased 1 log in the intestinal compartment (pH 7.6) after 9 h. Presence of antacid in the gastric compartment of the model greatly increased the ability of both V. vulnificus and its phage to survive simulated gastrointestinal transit and may be a factor involved with oyster-associated illness.

Animals↗
PubMed1995

Comparison of the vibriocidal antibody response in cholera due to Vibrio cholerae O139 Bengal with the response in cholera due to Vibrio cholerae O1.

Vibrio cholerae serogroup O139, now considered to be the second organism capable of causing epidemic severe dehydrating cholera, contains a capsular polysaccharide which makes it difficult for it to be used in the conventional vibriocidal antibody assay optimized for V. cholerae O1. After modification of the procedure, which involved the use of specific bacterial strains, a lower bacterial inoculum, and increased amounts of complement, the vibriocidal antibody responses to V. cholerae O139 were measured in acute- and convalescent-phase sera from 33 V. cholerae O139-infected and 18 V. cholerae O1-infected patients and in single serum samples from 20 healthy control subjects. The responses in these individuals to V. cholerae O1 strains were also determined. Significant elevations in the homologous antibody response were found only in the convalescent-phase sera from both groups of patients with cholera. These findings may explain the basis for the lack of heterologous protection between the two serogroups of V. cholerae. Healthy controls had higher background levels of vibriocidal antibody to V. cholerae O1 than to V. cholerae O139.

Adult↗
PubMed1987

Comparative study of Vibrio cholerae non-O1 protease and soluble hemagglutinin with those of Vibrio cholerae O1.

Protease and soluble hemagglutinating activities produced by a non-O1 Vibrio cholerae strain isolated from a patient with diarrhea were compared with similar activities produced by V. cholerae O1. The soluble protease activities were indistinguishable in heat stability, immunodiffusion, inhibition by antiserum, and electrophoretic analysis. On the other hand, the soluble hemagglutinating activities of both strains were not completely identical. The hemagglutinating activity of the non-O1 V. cholerae strain was not inhibited by Zincov; it was more sensitive to inhibition by normal serum, and it had an unusual pattern of heat stability. Heating at 100 degrees C resulted in some recovery of activity of a sample previously inactivated by heating at 60 degrees C.

Hemagglutination↗
PubMed1994

Vibrio cholerae O139 synonym bengal is closely related to Vibrio cholerae El Tor but has important differences.

Although Vibrio cholerae O139 synonym Bengal strains, from the current epidemics in India and Bangladesh, are closely related to seventh-pandemic strains, as shown by multilocus enzyme electrophoresis, Bengal strains are encapsulated and portions of the O1 antigen biosynthetic complex genes found in O1 strains are altered or lacking. Encapsulated Bengal strains showed resistance to killing by normal human serum. The presence of the capsule suggests the potential for bloodstream invasion in susceptible hosts and has profound implications for vaccine development.

Animals↗
PubMed2003

Examination of diverse toxin-coregulated pilus-positive Vibrio cholerae strains fails to demonstrate evidence for Vibrio pathogenicity island phage.

The major virulence factors of toxigenic Vibrio cholerae are cholera toxin, which is encoded by a lysogenic filamentous bacteriophage (CTXPhi), and toxin-coregulated pilus (TCP), an essential colonization factor that is also the receptor for CTXPhi. The genes involved in the biosynthesis of TCP reside in a pathogenicity island, which has been reported to correspond to the genome of another filamentous phage (designated VPIPhi) and to encode functions necessary for the production of infectious VPIPhi particles. We examined 46 V. cholerae strains having diverse origins and carrying different genetic variants of the TCP island for the production of the VPIPhi and CTXPhi in different culture conditions, including induction of prophages with mitomycin C and UV irradiation. Although 9 of 10 V. cholerae O139 strains and 12 of 15 toxigenic El Tor strains tested produced extracellular CTXPhi, none of the 46 TCP-positive strains produced detectable VPIPhi in repeated assays, which detected as few as 10 particles of a control CTX phage per ml. These results contradict the previous report regarding VPIPhi-mediated horizontal transfer of the TCP genes and suggest that the TCP island is unable to support the production of phage particles. Further studies are necessary to understand the mechanism of horizontal transfer of the TCP island.

Bacteriophages↗
PubMed2006

Regulation of Vibrio polysaccharide synthesis and virulence factor production by CdgC, a GGDEF-EAL domain protein, in Vibrio cholerae.

In Vibrio cholerae, the second messenger 3',5'-cyclic diguanylic acid (c-di-GMP) regulates several cellular processes, such as formation of corrugated colony morphology, biofilm formation, motility, and virulence factor production. Both synthesis and degradation of c-di-GMP in the cell are modulated by proteins containing GGDEF and/or EAL domains, which function as a diguanylate cyclase and a phosphodiesterase, respectively. The expression of two genes, cdgC and mbaA, which encode proteins harboring both GGDEF and EAL domains is higher in the rugose phase variant of V. cholerae than in the smooth variant. In this study, we carried out gene expression analysis to determine the genes regulated by CdgC in the rugose and smooth phase variants of V. cholerae. We determined that CdgC regulates expression of genes required for V. cholerae polysaccharide synthesis and of the transcriptional regulator genes vpsR, vpsT, and hapR. CdgC also regulates expression of genes involved in extracellular protein secretion, flagellar biosynthesis, and virulence factor production. We then compared the genes regulated by CdgC and by MbaA, during both exponential and stationary phases of growth, to elucidate processes regulated by them. Identification of the regulons of CdgC and MbaA revealed that the regulons overlap, but the timing of regulation exerted by CdgC and MbaA is different, suggesting the interplay and complexity of the c-di-GMP signal transduction pathways operating in V. cholerae.

Amino Acid Sequence↗
PubMed1986

Cloning of the Vibrio cholerae recA gene and construction of a Vibrio cholerae recA mutant.

A recombinant plasmid carrying the recA gene of Vibrio cholerae was isolated from a V. cholerae genomic library, using complementation in Escherichia coli. The plasmid complements a recA mutation in E. coli for both resistance to the DNA-damaging agent methyl methanesulfonate and recombinational activity in bacteriophage P1 transductions. After determining the approximate location of the recA gene on the cloned DNA fragment, we constructed a defined recA mutation by filling in an XbaI site located within the gene. The 4-base pair insertion resulted in a truncated RecA protein as determined by minicell analysis. The mutation was spontaneously recombined onto the chromosome of a derivative of V. cholerae strain P27459 by screening for methyl methanesulfonate-sensitive variants. Southern blot analysis confirmed the presence of the inactivated XbaI site in the chromosome of DNA isolated from one of these methyl methanesulfonate-sensitive colonies. The recA V. cholerae strain was considerably more sensitive to UV light than its parent, was impaired in homologous recombination, and was deficient in induction of a temperate vibriophage upon exposure to UV light. We conclude that the V. cholerae RecA protein has activities which are analogous to those described for the RecA protein of E. coli.

Cloning, Molecular↗
PubMed1996

Serogroup conversion of Vibrio cholerae non-O1 to Vibrio cholerae O1: effect of growth state of cells, temperature, and salinity.

Recently, we reported the occurrence of seroconversion from Vibrio cholerae non-O1 to V. cholerae O1, but little is known about the environmental and physiological factors influencing seroconversion. We investigated effects of temperature (4, 25, and 35 degrees C) and salinity ( < 0.05 and 10%0.), as well as the stage of growth of cells, on serogroup conversion. Seroconversion of V. cholerae occurred under various environmental conditions. However, the rate of seroconversion in natural water ( < 0.5% salinity) and synthetic seawater microcosms (10%0 salinity), employing cells harvested from stationary phase culture, was approximately 2 logs higher than cells harvested from cultures in the logarithmic phase (i.e., 10(5) versus 10(3) per 10(10) cells. Thus, the physiological state of the cells, and to a lesser degree, temperature and salinity, is an important factor in the conversion of V. cholerae from non-O1 to O1 serogroup.

Antigens, Bacterial↗
PubMed2002

The Zymovars of Vibrio cholerae: multilocus enzyme electrophoresis of Vibrio cholerae.

Zymovars analysis also known as multilocus enzyme electrophoresis is applied here to investigate the genetic variation of Vibrio cholerae strains and characterise strains or group of strains of medical and epidemiological interest. Fourteen loci were analyzed in 171 strains of non-O1 non-O139, 32 classical and 61 El Tor from America, Africa, Europe and Asia. The mean genetic diversity was 0.339. It is shown that the same O antigen (both O1 and non-O1) may be present in several genetically diverse (different zymovars) strains. Conversely the same zymovar may contain more than one serogroup. It is confirmed that the South American epidemic strain differs from the 7th pandemic El Tor strain in locus LAP (leucyl leucyl aminopeptidase). Here it is shown that this rare allele is present in 1 V. mimicus and 4 non-O1 V. cholerae. Non toxigenic O1 strains from South India epidemic share zymovar 14A with the epidemic El Tor from the 7th pandemic, while another group have diverse zymovars. The sucrose negative epidemic strains isolated in French Guiana and Brazil have the same zymovar of the current American epidemic V. cholerae.

Animals↗
PubMed2000

Effect of simulated gastric fluid and bile on survival of Vibrio vulnificus and Vibrio vulnificus phage.

Bacteria and phages may be exposed to acid conditions in the stomach and to bile in the intestine. Survival of three strains of Vibrio vulnificus and three strains of its phages was examined at 37 degrees C after exposure to simulated gastric fluid at pH 3 to 4 or to 0, 1, and 2% bile in broth or buffer. Mean D-values (decimal reduction times) at pH 4 and 3 were 3.3 and 1.3 min for V. vulnificus and 97.8 and 0.7 min for its phages. No V. vulnificus survivors were found at pH 2.0. There were few survival differences among strains of V. vulnificus or its phages. Numbers of V. vulnificus increased 1 log in tryptic soy broth containing 1 or 2% bile after 3 h. Numbers of V. vulnificus and its phages remained constant in phosphate-buffered saline regardless of bile concentrations up to 3 h. Those V. vulnificus bacteria and phages that survive stomach acidity may proliferate in the small intestine, since they are resistant to bile.

Bacteriophages↗