scholarly journals Ecology of Vibrio cholerae serogroup 01 in aquatic environments

Author(s):  
René J. Borroto
2020 ◽  
Vol 10 (3) ◽  
pp. 186-191
Author(s):  
Sara M. Van Bonn ◽  
Sebastian P. Schraven ◽  
Tobias Schuldt ◽  
Markus M. Heimesaat ◽  
Robert Mlynski ◽  
...  

AbstractWe report a case of a chronic mesotympanic otitis media with a smelly purulent secretion from both ears and recurrent otalgia over the last five years in a six-year-old girl after swimming in the German Baltic Sea. Besides Staphylococcus aureus a non-O1/non-O139 Vibrio cholerae strain could be isolated from patient samples. An antibiotic therapy with ciprofloxacin and ceftriaxone was administered followed by atticotomy combined with tympanoplasty. We conclude that V. cholerae should not be overlooked as a differential diagnosis to otitis infections, especially when patients present with extra-intestinal infections after contact with brackish- or saltwater aquatic environments.


1992 ◽  
Vol 7 (1) ◽  
pp. 43-46 ◽  
Author(s):  
MASAHIKO NISHIMURA ◽  
KUMIKO KITA-TSUKAMOTO ◽  
KAZUHIRO KOGURE ◽  
KOUICHI OHWADA

2019 ◽  
Vol 116 (5) ◽  
pp. 1627-1632 ◽  
Author(s):  
Cecilia A. Silva-Valenzuela ◽  
Andrew Camilli

Vibrio cholerae, the causative agent of cholera, has reservoirs in fresh and brackish water where it interacts with virulent bacteriophages. Phages are the most abundant biological entity on earth and coevolve with bacteria. It was reported that concentrations of phage and V. cholerae inversely correlate in aquatic reservoirs and in the human small intestine, and therefore that phages may quench cholera outbreaks. Although there is strong evidence for phage predation in cholera patients, evidence is lacking for phage predation of V. cholerae in aquatic environments. Here, we used three virulent phages, ICP1, ICP2, and ICP3, commonly shed by cholera patients in Bangladesh, as models to understand the predation dynamics in microcosms simulating aquatic environments. None of the phages were capable of predation in fresh water, and only ICP1 was able to prey on V. cholerae in estuarine water due to a requirement for salt. We conclude that ICP2 and ICP3 are better adapted for predation in a nutrient rich environment. Our results point to the evolution of niche-specific predation by V. cholerae-specific virulent phages, which complicates their use in predicting or monitoring cholera outbreaks as well as their potential use in reducing aquatic reservoirs of V. cholerae in endemic areas.


2006 ◽  
Vol 74 (12) ◽  
pp. 6547-6556 ◽  
Author(s):  
Sang Sun Yoon ◽  
John J. Mekalanos

ABSTRACT Vibrio cholerae is an aquatic bacterium that causes the severe diarrheal disease cholera. V. cholerae strains of the O1 serogroup exist as two biotypes, classical and El Tor. Toxigenic strains of the El Tor biotype emerged to cause the seventh pandemic of cholera in 1961 and subsequently displaced strains of the classical biotype both in the environment and as a cause of cholera within a decade. The factors that drove emergence of the El Tor biotype and the displacement of the classical biotype are unknown. Here, we show a unique difference in carbohydrate metabolism between these two biotypes. When grown with added carbohydrates, classical biotype strains generated a sharp decrease in medium pH, resulting in loss of viability. However, growth of El Tor biotype strain N16961 was enhanced due to its ability to produce 2,3-butanediol, a neutral fermentation end product, and suppress the accumulation of organic acids. An N16961 mutant (SSY01) defective in 2,3-butanediol synthesis showed the same defect in growth that classical biotype strains show in media rich in carbohydrates. Importantly, the SSY01 mutant was attenuated in its ability to colonize the intestines of infant mice, suggesting that host carbohydrates may be available to V. cholerae within the intestinal environment. Similarly, the SSY01 mutant failed to develop biofilms when utilizing N-acetyl-d-glucosamine as a carbon source. Because growth on N-acetyl-d-glucosamine likely reflects the ability of a strain to grow on chitin in certain aquatic environments, we conclude that the strains of classical biotype are likely defective compared to those of El Tor in growth in any environmental niche that is rich in chitin and/or other metabolizable carbohydrates. We propose that the ability to metabolize sugars without production of acid by-products might account for the improved evolutionary fitness of the V. cholerae El Tor biotype compared to that of the classical biotype both as a global cause of cholera and as an environmental organism.


2021 ◽  
Author(s):  
Sean Giacomucci ◽  
Antony T Vincent ◽  
Marylise Duperthuy

Vibrio cholerae is the bacteria responsible for the cholera disease and a natural inhabitant of aquatic environments. Biofilm formation is important for human colonization and environmental survival. Motility is essential for adhesion and biofilm formation by V. cholerae. In a previous study, we showed that motility and biofilm formation are altered in the presence of sub-inhibitory concentrations of polymyxin B in V. cholerae. In this study, we performed an experimental evolution to identify genes rescuing the motility in the presence of polymyxin B. Mutations in 5 genes have been identified: ihfA, vacJ (mlaA), mlaF, dacB and ccmH. The details of these mutations, their potential impact on the function of the proteins they encode and on the motility in presence of polymyxin B are discussed.


2000 ◽  
Vol 182 (10) ◽  
pp. 2937-2944 ◽  
Author(s):  
Sophie Vimont ◽  
Patrick Berche

ABSTRACT Vibrio cholerae, the agent of cholera, is a normal inhabitant of aquatic environments, in which it survives under a wide range of conditions of pH and salinity. In this work, we identified thenhaA gene in a wild-type epidemic strain of V. cholerae O1. nhaA encodes a protein of 382 amino acids that is very similar to the proteins NhaA of Vibrio parahaemolyticus, Vibrio alginolyticus (∼87% identity), and Escherichia coli (56% identity). V. cholerae NhaA complements an E. coli nhaA mutant, enabling it to grow in 700 mM NaCl, pH 7.5, indicating functional homology to E. coli NhaA. However, unlike E. coli, the growth of a nhaA-inactivated mutant ofV. cholerae was not restricted at various pH and NaCl concentrations, although it was inhibited in the presence of 120 mM LiCl at pH 8.5. Nevertheless, using a nhaA′-lacZtranscriptional fusion, we observed induction of nhaAtranscription by Na+, Li+, and K+. These results strongly suggest that NhaA is an Na+/H+ antiporter contributing to the Na+/H+ homeostasis of V. cholerae. nhaA-related sequences were detected in all strains ofV. cholerae from the various serogroups. This gene is presumably involved in the survival and persistence of free-living bacteria in their natural habitat.


2010 ◽  
Vol 79 (3) ◽  
pp. 716-728 ◽  
Author(s):  
David K. Giles ◽  
Jessica V. Hankins ◽  
Ziqiang Guan ◽  
M. Stephen Trent

2000 ◽  
Vol 68 (4) ◽  
pp. 1967-1974 ◽  
Author(s):  
Afsar Ali ◽  
Judith A. Johnson ◽  
Augusto A. Franco ◽  
Daniel J. Metzger ◽  
Terry D. Connell ◽  
...  

ABSTRACT Vibrio cholerae is the causal organism of the diarrheal disease cholera. The rugose variant of V. cholerae is associated with the secretion of an exopolysaccharide. The rugose polysaccharide has been shown to confer increased resistance to a variety of agents, such as chlorine, bioacids, and oxidative and osmotic stresses. It also promotes biofilm formation, thereby increasing the survival of the bacteria in the aquatic environments. Here we show that the extracellular protein secretion system (gene designated eps) is involved directly or indirectly in the production of rugose polysaccharide. A TnphoA insertion inepsD gene of the eps operon abolished the production of rugose polysaccharide, reduced the secretion of cholera toxin and hemolysin, and resulted in a nonmotile phenotype. We have constructed defined mutations of the epsD andepsE genes that affected these phenotypes and complemented these defects by plasmid clones of the respective wild-type genes. These results suggest a major role for the eps system in pathogenesis and environmental survival of V. cholerae.


2018 ◽  
Author(s):  
Cecilia A. Silva-Valenzuela ◽  
Andrew Camilli

AbstractVibrio cholerae, the causative agent of cholera, has reservoirs in fresh and brackish water where it interacts with virulent bacteriophages. Phages are the most abundant biological entity on earth and co-evolve with bacteria. It was reported that concentrations of phage and V. cholerae inversely correlate in aquatic reservoirs and in the human small intestine, and therefore that phages may quench cholera outbreaks. Although there is strong evidence for phage predation in cholera patients, evidence is lacking for phage predation of V. cholerae in aquatic environments. Here, we used three virulent phages, ICP1, ICP2, and ICP3, commonly shed by cholera patients in Bangladesh, as models to understand the predation dynamics in microcosms simulating aquatic environments. None of the phages were capable of predation in fresh water, and only ICP1 was able to prey on V. cholerae in estuarine water due to a requirement for salt. We conclude that ICP2 and ICP3 are better adapted for predation in a nutrient rich environment. Our results point to the evolution of niche-specific predation by V. cholerae-specific virulent phages, which complicates their use in predicting or monitoring cholera outbreaks as well as their potential use in reducing aquatic reservoirs of V. cholerae in endemic areas.Significance statementVirulent phages can reduce populations of bacteria and help shape bacterial evolution. Here, we used three virulent phages to understand their equilibrium with V. cholerae in nutrient-limiting aquatic microcosms. It has been proposed that phages quench cholera outbreaks, but no direct evidence of phage predation in aquatic environments had been established. Here we show that different phages possess varied abilities to infect in certain niches or stages of the host bacterial life cycle. Unveiling the phage/bacterial interactions in their natural setting is important to the understanding of cholera outbreaks and could be ultimately used to help develop a method for outbreak prediction and/or control.


2010 ◽  
Vol 15 (3) ◽  
pp. 117-121 ◽  
Author(s):  
SUMIO SHINODA ◽  
MAYUMI IWASAKI ◽  
TETSUYA SONODA ◽  
YUKI FURUMAI ◽  
CHIZUKO MIYAKE-NAKAYAMA ◽  
...  

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