scholarly journals Vibrio cholerae Incursion in Africa, the Journey So Far

Author(s):  
Tarh, Jacqueline Ebob ◽  
C. I. Mboto ◽  
B. E. E. Asikong ◽  
Iroegbu Christian Ukwuoma

Indeed, a host of the plenty of reports about pathogenic Vibrios, have been from African researchers. And they assert that this severe diarrhea causing agent originated from Asia thousands of years ago and spread (first, via the sea route) affecting particularly the coastal towns and fishing villages, before moving to other parts of the world. Following the primary cholera outbreak of 1868, Vibrio cholera, appeared in the Atlantic coast of West Africa. The pathogen then invaded African countries chronologically beginning with Guinea, then Sierra Leone, Liberia, Cote d’ivoire, Mali, Togo, Dahomey, Upper Volt (Burki Na-faso) and finally Nigeria (Lagos) and Niger in December, 1970. Various serogroups (O139 and O1 with biotypes Classical and El Tor) and Serotypes of O1 (Ogawa, Inaba and Hikojima) and recently, the O395 strain have been reported; especially from outbreaks reported from hotspots that are close to riverine areas. This suggests that these emergent pathogenic species originate from around water environments probably from the non-pathogenic strains. This condition is likely harnessed by Lateral Gene Transfer (LGT), which is seen to occur usually between pandemic V. cholerae and environmental strains; a situation that may result in the creation of new pandemic strains. Therefore, in order to better understand and appreciate the evolution of the Vibrio cholerae strains that are involved in epidemics, and the relationship between the species causing particular epidemics in different regions of Africa, a study of the molecular picture of the environmental strains and the mechanisms by which the pathogenic Vibrio cholera strains appear and diffuse from these strains is necessary. This review seeks to trace the origin and spread route of Vibrio cholerae strains causing epidemics in different regions of the African continent (Nigeria in particular) with the aim of establishing relationships between the strains causing epidemics in these regions. This will help in the development of better intervention strategies to contain the disease.

2009 ◽  
Vol 77 (9) ◽  
pp. 3807-3816 ◽  
Author(s):  
Salvador Almagro-Moreno ◽  
E. Fidelma Boyd

ABSTRACT Sialic acids comprise a family of nine-carbon ketosugars that are ubiquitous on mammalian mucous membranes. However, sialic acids have a limited distribution among Bacteria and are confined mainly to pathogenic and commensal species. Vibrio pathogenicity island 2 (VPI-2), a 57-kb region found exclusively among pathogenic strains of Vibrio cholerae, contains a cluster of genes (nan-nag) putatively involved in the scavenging (nanH), transport (dctPQM), and catabolism (nanA, nanE, nanK, and nagA) of sialic acid. The capacity to utilize sialic acid as a carbon and energy source might confer an advantage to V. cholerae in the mucus-rich environment of the gut, where sialic acid availability is extensive. In this study, we show that V. cholerae can utilize sialic acid as a sole carbon source. We demonstrate that the genes involved in the utilization of sialic acid are located within the nan-nag region of VPI-2 by complementation of E scherichia coli mutants and gene knockouts in V. cholerae N16961. We show that nanH, dctP, nanA, and nanK are highly expressed in V. cholerae grown on sialic acid. By using the infant mouse model of infection, we show that V. cholerae ΔnanA strain SAM1776 is defective in early intestinal colonization stages. In addition, SAM1776 shows a decrease in the competitive index in colonization-competition assays comparing the mutant strain with both O1 El Tor and classical strains. Our data indicate an important relationship between the catabolism of sialic acid and bacterial pathogenesis, stressing the relevance of the utilization of the resources found in the host's environment.


2001 ◽  
Vol 69 (3) ◽  
pp. 1947-1952 ◽  
Author(s):  
David K. R. Karaolis ◽  
Ruiting Lan ◽  
James B. Kaper ◽  
Peter R. Reeves

ABSTRACT Epidemic Vibrio cholerae strains possess a large cluster of essential virulence genes on the chromosome called theVibrio pathogenicity island (VPI). The VPI contains thetcp gene cluster encoding the type IV pilus toxin-coregulated pilus colonization factor which can act as the cholera toxin bacteriophage (CTXΦ) receptor. The VPI also contains genes that regulate virulence factor expression. We have fully sequenced and compared the VPI of the seventh-pandemic (El Tor biotype) strain N16961 and the sixth-pandemic (classical biotype) strain 395 and found that the N16961 VPI is 41,272 bp and encodes 29 predicted proteins, whereas the 395 VPI is 41,290 bp. In addition to various nucleotide and amino acid polymorphisms, there were several proteins whose predicted size differed greatly between the strains as a result of frameshift mutations. We hypothesize that these VPI sequence differences provide preliminary evidence to help explain the differences in virulence factor expression between epidemic strains (i.e., the biotypes) of V. cholerae.


2009 ◽  
Vol 58 (1) ◽  
pp. 105-111 ◽  
Author(s):  
Ashrafus Safa ◽  
Nurul A. Bhuiyan ◽  
Denise Murphy ◽  
John Bates ◽  
Suraia Nusrin ◽  
...  

Episodes of cholera stemming from indigenous Vibrio cholerae strains in Australia are mainly associated with environmental sources. In the present study, 10 V. cholerae O1 strains of Australian origin were characterized. All of the strains were serogroup O1 and their conventional phenotypic traits categorized them as belonging to the El Tor biotype. Genetic screening of 12 genomic regions that are associated with virulence in V. cholerae showed variable results. Analysis of the ctxAB gene showed that the Australian environmental reservoir contains both toxigenic and non-toxigenic V. cholerae strains. DNA sequencing revealed that all of the toxigenic V. cholerae strains examined were of ctxB genotype 2. Whole genome PFGE analysis revealed that the environmental toxigenic V. cholerae O1 strains were more diverse than the non-toxigenic environmental O1 strains, and the absence of genes that make up the Vibrio seventh pandemic island-I and -II in all of the strains indicates their pre-seventh pandemic ancestry.


2008 ◽  
Vol 191 (1) ◽  
pp. 169-177 ◽  
Author(s):  
Brian K. Hammer ◽  
Bonnie L. Bassler

ABSTRACT Quorum sensing (QS), or cell-cell communication in bacteria, is achieved through the production and subsequent response to the accumulation of extracellular signal molecules called autoinducers (AIs). To identify AI-regulated target genes in Vibrio cholerae El Tor (V. cholerae El), the strain responsible for the current cholera pandemic, luciferase expression was assayed in an AI− strain carrying a random lux transcriptional reporter library in the presence and absence of exogenously added AIs. Twenty-three genes were identified and shown to require the QS transcription factor, HapR, for their regulation. Several of the QS-dependent target genes, annotated as encoding hypothetical proteins, in fact encode HD-GYP proteins, phosphodiesterases that degrade the intracellular second messenger cyclic dimeric GMP (c-di-GMP), which is important for controlling biofilm formation. Indeed, overexpression of a representative QS-activated HD-GYP protein in V. cholerae El reduced the intracellular concentration of c-di-GMP, which in turn decreased exopolysaccharide production and biofilm formation. The V. cholerae classical biotype (V. cholerae Cl), which caused previous cholera pandemics and is HapR−, controls c-di-GMP levels and biofilm formation by the VieA signaling pathway. We show that the VieA pathway is dispensable for biofilm formation in V. cholerae El but that restoring HapR in V. cholerae Cl reestablishes QS-dependent repression of exopolysaccharide production. Thus, different pandemic strains of V. cholerae modulate c-di-GMP levels and control biofilm formation in response to distinct sensory pathways.


2020 ◽  
Vol 9 (26) ◽  
Author(s):  
Leonid M. Irenge ◽  
Jean-François Durant ◽  
Jérôme Ambroise ◽  
Prudence N. Mitangala ◽  
Bertrand Bearzatto ◽  
...  

ABSTRACT We report here a complete genome sequence of a Vibrio cholerae O1 El Tor (Inaba; sequence type 515 [ST515]) strain isolated from a cholera patient in North Kivu Province, Democratic Republic of the Congo (DRC), which showed a complete deletion (∼80 kb) of the Vibrio pathogenicity island 1.


2021 ◽  
Author(s):  
Fatema-Tuz Johura ◽  
Sahitya Ranjan Biswas ◽  
Shah M Rashed ◽  
Mohammad Tarequl Islam ◽  
Saiful Islam ◽  
...  

Vibrio cholerae O1 El Tor, causative agent of the ongoing seventh cholera pandemic, is native to the aquatic environment of the Ganges Delta, Bay of Bengal (GDBB). Recent studies traced pandemic strains to the GDBB and proposed global spread of cholera had occurred via intercontinental transmission. In the research presented here, Not I-digested genomic DNA extracted from V. cholerae O1 clinical and environmental strains isolated in Bangladesh during 2004 – 2014 was analyzed by pulsed-field gel electrophoresis (PFGE). Results of cluster analysis showed 94.67% of the V. cholerae isolates belonged to clade A and included the majority of clinical isolates of spatio-temporal origin and representing different cholera endemic foci. The rest of the strains were estuarine, all environmental isolates from Mathbaria, Bangladesh, and occurred as singletons, clustered in clades B and C, or in the small clades D and E. Cluster analysis of the Bangladeshi strains and including 157 El Tor strains from thirteen countries in Asia, Africa, and the Americas revealed 85% of the total set of isolates belonged to clade A, indicating all were related, yet did not form an homogeneous cluster. Overall, 15% of the global strains comprised multiple small clades or segregated as singletons. Three sub-clades could be discerned within the major clade A, reflecting distinct lineages of V. cholerae El Tor associated with cholera in Asia, Africa, and the Americas. The presence in Asia and the Americas of non-pandemic V. cholerae El Tor populations differing by PFGE and from strains associated with cholera globally suggests different ecotypes are resident in distant geographies.


2012 ◽  
Vol 17 (1) ◽  
pp. 39-45
Author(s):  
Yu. M. Lomov ◽  
N. R. Telesmanich ◽  
I. T. Andrusenko ◽  
E. A. Moskvitina ◽  
O. A. Areshina

The review deals with the properties of Vibrio cholerae (classical, El Tor, 0139, non-01/non-0139 strains) circulating worldwide during the seventh cholera pandemic. Particular attention is given to the variability in the cholera pathogen: the replacement of classical Vibrio cholerae by the El Tor biotype and subsequently the emergence of serogroup Vibrio cholerae 0139 and genetically altered El Tor Vibrio cholerae; the causes giving rise to these changes and spread of Vibrio cholera in the countries of the Asian continent. A large genetic variability found in Asian strains suggests that there is a real possibility of the emergence of new clones with new properties, including those with an epidemic potential. The Vibrio cholerae strains, that periodically appear in Asia and have an epidemic potential and new properties, spread over all continents, by causing cholera infection. The cholera pathogen adapts to new existence conditions in some cases, by altering some properties and, by having been rooted in a certain area, causes mainly sporadic cases of the disease. These Vibrio cholerae strains, unlike the Asian strains (the pathogens of the seventh pandemic), may be virulent, by preserving the virulence genes in the genome; however, they are, in most cases, non-endemic and unable to spread widely.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Benjamin Kostiuk ◽  
Francis J. Santoriello ◽  
Laura Diaz-Satizabal ◽  
Fabiana Bisaro ◽  
Kyung-Jo Lee ◽  
...  

AbstractThe gram-negative bacterium Vibrio cholerae is the causative agent of the diarrhoeal disease cholera and is responsible for seven recorded pandemics. Several factors are postulated to have led to the decline of 6th pandemic classical strains and the rise of El Tor biotype V. cholerae, establishing the current 7th pandemic. We investigated the ability of classical V. cholerae of the 2nd and 6th pandemics to engage their type six secretion system (T6SS) in microbial competition against non-pandemic and 7th pandemic strains. We report that classical V. cholerae underwent sequential mutations in T6SS genetic determinants that initially exposed 2nd pandemic strains to microbial attack by non-pandemic strains and subsequently caused 6th pandemic strains to become vulnerable to El Tor biotype V. cholerae intraspecific competition. The chronology of these T6SS-debilitating mutations agrees with the decline of 6th pandemic classical strains and the emergence of 7th pandemic El Tor V. cholerae.


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