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Cholera causes substantial illness and death in Africa. We analyzed 24 toxigenic Vibrio cholerae O1 strains isolated in 2015-2017 from patients in the Great Lakes region of the Democratic Republic of the Congo. Strains originating in southern Asia appeared to be part of the T10 introduction event in eastern Africa. We identified 2 main strain lineages, most recently a lineage corresponding to sequence type 515, a V. cholerae cluster previously reported in the Lake Kivu region. In 41% of fecal samples from cholera patients, we also identified a novel ICP1 (Bangladesh cholera phage 1) bacteriophage, genetically distinct from ICP1 isolates previously detected in Asia. Bacteriophage resistance occurred in distinct clades along both internal and external branches of the cholera phylogeny. This bacteriophage appears to have served as a major driver for cholera evolution and spread, and its appearance highlights the complex evolutionary dynamic that occurs between predatory phage and bacterial host. [ABSTRACT FROM AUTHOR]

The article presents information related to cholera, caused by the bacterium Vibrio cholera. Topics discussed include its transmission by water and food, specially cooked rice, the impact of cholera toxin on glucose transport across the intestine, studied by researcher Robert Phillips in the 1960s, and the most severe form of cholera, characterized by diarrheal stool.

Toxigenic Vibrio cholerae strains, including strains in serogroups O1 and O139 associated with the clinical disease cholera, are ubiquitous in aquatic reservoirs, including fresh, estuarine, and marine environments. Humans acquire cholera by consuming water and/or food contaminated with the microorganism. The genome of toxigenic V. cholerae harbors a cholera-toxin producing prophage (CT-prophage) encoding genes that promote expression of cholera toxin. The CT-prophage in V. cholerae is flanked by two satellite prophages, RS1 and TLC. Using cell surface appendages (TCP and/or MSHA pili), V. cholerae can sequentially acquire TLC, RS1, and CTX phages by transduction; the genome of each of these phages ultimately integrates into V. cholerae's genome in a site-specific manner. Here, we showed that a non-toxigenic V. cholerae O1 biotype El Tor strain, lacking the entire RS1-CTX-TLC prophage complex (designated as RCT: R for RS1, C for CTX and T for TLC prophage, respectively), was able to acquire RCT from donor genomic DNA (gDNA) of a wild-type V. cholerae strain (E7946) via chitin-induced transformation. Moreover, we demonstrated that a chitin-induced transformant (designated as AAS111) harboring RCT was capable of producing cholera toxin. We also showed that recA , rather than xerC and xerD recombinases, promoted the acquisition of RCT from donor gDNA by the recipient non-toxigenic V. cholerae strain. Our data document the existence of an alternative pathway by which a non-toxigenic V. cholerae O1 strain can transform to a toxigenic strain by using chitin induction. As chitin is an abundant natural carbon source in aquatic reservoirs where V. cholerae is present, chitin-induced transformation may be an important driver in the emergence of new toxigenic V. cholerae strains. [ABSTRACT FROM AUTHOR]

Vibrio cholerae causes cholera, a severe diarrheal disease. Understanding the local genetic diversity and transmission of V. cholerae will improve our ability to control cholera. Vibrio cholerae isolates clustered in genetically related groups (clonal complexes, CC) by multilocus variable tandem-repeat analysis (MLVA) were compared by whole genome sequencing (WGS). Isolates in CCI had been isolated from two geographical locations. Isolates in a second genetically distinct group, CC2, were isolated only at one location. Using WGS, CCI isolates from both locations revealed, on average, 43.8 nucleotide differences, while those strains comprising CC2 averaged 19.7 differences. Strains from both MLVA-CCs had an average difference of 106.6. Thus, isolates comprising CCI were more closely related (P < 10-6) to each other than to isolates in CC2. Within a MLVA-CC, after removing all paralogs, alternative alleles were found in all possible combinations on separate chromosomes indicative of recombination within the core genome. Including recombination did not affect the distinctiveness of the MLVA-CCs when measured by WGS. We found that WGS generally reflected the same genetic relatedness of isolates as MLVA, indicating that isolates from the same MLVA-CC shared a more recent common ancestor than isolates from the same location that clustered in a distinct MLVA-CC. [ABSTRACT FROM AUTHOR]

A cholera outbreak began in Haiti during October, 2010. Spatiotemporal patterns of household-level cholera in Ouest Department showed that the initial clusters tended to follow major roadways; subsequent clusters occurred further inland. Our data highlight transmission pathway complexities and the need for case and household-level analysis to understand disease spread and optimize interventions. [ABSTRACT FROM AUTHOR]

Toxigenic Vibrio cholerae, ubiquitous in aquatic environments, is responsible for cholera; humans can become infected after consuming food and/or water contaminated with the bacterium. The underlying basis of persistence of V. cholerae in the aquatic environment remains poorly understood despite decades of research. We recently described a “persister” phenotype of V. cholerae that survived in nutrient-poor “filter sterilized” lake water (FSLW) in excess of 700-days. Previous reports suggest that microorganisms can assume a growth advantage in stationary phase (GASP) phenotype in response to long-term survival during stationary phase of growth. Here we report a V. cholerae GASP phenotype (GASP-700D) that appeared to result from 700 day-old persister cells stored in glycerol broth at −80°C. The GASP-700D, compared to its wild-type N16961, was defective in motility, produced increased biofilm that was independent of vps (p<0.005) and resistant to oxidative stress when grown specifically in FSLW (p<0.005). We propose that V. cholerae GASP-700D represents cell populations that may better fit and adapt to stressful survival conditions while serving as a critical link in the cycle of cholera transmission. [ABSTRACT FROM AUTHOR]

An epidemic of cholera infections was documented in Haiti for the first time in more than 100 years during October 2010. Cases have continued to occur, raising the question of whether the microorganism has established environmental reservoirs in Haiti. We monitored 14 environmental sites near the towns of Gressier and Leogane during April 2012-March 2013. Toxigenic Vibrio cholerae O1 El Tor biotype strains were isolated from 3 (1.7%) of 179 water samples; nontoxigenic O1 V. cholerae was isolated from an additional 3 samples. All samples containing V. cholerae O1 also contained non-O1 V. cholerae. V. cholerae O1 was isolated only when water temperatures were ≥31°C. Our data substantiate the presence of toxigenic V. cholerae O1 in the aquatic environment in Haiti. These isolations may reflect establishment of long-term environmental reservoirs in Haiti, which may complicate eradication of cholera from this coastal country. [ABSTRACT FROM AUTHOR]

Cholera remains a major public health problem. To compare the relative contribution of strains from the environment with strains isolated from patients during outbreaks, we performed multilocus variable tandem repeat analyses on samples collected during the 2010 and 2011 outbreak seasons in 2 geographically distinct areas of Bangladesh. A total of 222 environmental and clinical isolates of V. cholerae O1 were systematically collected from Chhatak and Mathbaria. In Chhatak, 75 of 79 isolates were from the same clonal complex, in which extensive differentiation was found in a temporally consistent pattern of successive mutations at single loci. A total of 59 isolates were collected from 6 persons; most isolates from 1 person differed by sequential single-locus mutations. In Mathbaria, 60 of 84 isolates represented 2 separate clonal complexes. The small number of genetic lineages in isolates from patients, compared with those from the environment, is consistent with accelerated transmission of some strains among humans during an outbreak. [ABSTRACT FROM AUTHOR]

Background: Fine-scale and longitudinal geospatial analysis of health risks in challenging urban areas is often limited by the lack of other spatial layers even if case data are available. Underlying population counts, residential context, and associated causative factors such as standing water or trash locations are often missing unless collected through logistically difficult, and often expensive, surveys. The lack of spatial context also hinders the interpretation of results and designing intervention strategies structured around analytical insights. This paper offers a ubiquitous spatial data collection approach using a spatial video that can be used to improve analysis and involve participatory collaborations. A case study will be used to illustrate this approach with three health risks mapped at the street scale for a coastal community in Haiti. Methods: Spatial video was used to collect street and building scale information, including standing water, trash accumulation, presence of dogs, cohort specific population characteristics, and other cultural phenomena. These data were digitized into Google Earth and then coded and analyzed in a GIS using kernel density and spatial filtering approaches. The concentrations of these risks around area schools which are sometimes sources of diarrheal disease infection because of the high concentration of children and variable sanitary practices will show the utility of the method. In addition schools offer potential locations for cholera education interventions. Results: Previously unavailable fine scale health risk data vary in concentration across the town, with some schools being proximate to greater concentrations of the mapped risks. The spatial video is also used to validate coded data and location specific risks within these "hotspots". Conclusions: Spatial video is a tool that can be used in any environment to improve local area health analysis and intervention. The process is rapid and can be repeated in study sites through time to track spatio-temporal dynamics of the communities. Its simplicity should also be used to encourage local participatory collaborations. [ABSTRACT FROM AUTHOR]

In response to antibiotic and/or environmental stress, some species of bacteria shift to a "persister" phenotype. Although toxigenic Vibrio cholerae, responsible for the disease cholera, can be found in nutrient-poor aquatic environments in endemic areas, the underlying mechanism(s) by which culturable cells persist in these environmental reservoirs is largely unknown. Here we report that introduction of V. cholerae into a nutrient-poor filter sterilized lake water (FSLW) microcosm promoted a shift to what we have defined as a "persister" phenotype (PP) which was culturable for >700 days. Direct transfer of PP of V. cholerae from original microcosms to freshly prepared FSLW resulted in the same pattern of persistence seen in the original microcosms. Scanning electron microscopy of cells persisting for over 700 days demonstrated cell morphologies that were very small in size, with a high degree of aggregation associated with flagella emanating from all aspects of the cell. V. cholerae PP cells reverted to a typical V. cholerae morphology when transferred to nutrient-rich L-broth. Cell-free supernatants obtained from microcosms at 24 hours, 180 days, and 700 days all showed >2-fold increase in CAI-1 signaling molecules, consistent with quorum sensing activity, as has been described for Pseudomonas aeruginosa persister cells. Chitin and phosphate promoted cell growth. Our data suggest that nutrient stress can select a V. cholerae persister phenotype in environmental reservoirs, with these strains then seeding subsequent cholera epidemics in response to chitin and phosphate availability. [ABSTRACT FROM AUTHOR]

Cholera has affected humans for at least a millennium and persists as a major cause of illness and death worldwide, with recent epidemics in Zimbabwe (2008-2009) and Haiti (2010). Clinically, evidence exists of increasing severity of disease linked with emergence of atypical Vibrio cholerae organisms that have incorporated genetic material from classical biotype strains into an El Tor biotype background. A key element in transmission may be a recently recognized hyperinfectious phase, which persists for hours after passage in diarrheal feces. We propose a model of transmission in which environmental triggers (such as temperature) lead to increases in V. cholerae in environmental reservoirs, with spillover into human populations. However, once the microorganism is introduced into a human population, transmission occurs primary by "fast" transmission from person to person (taking advantage of the hyperinfectious state), without returning to the aquatic environment. [ABSTRACT FROM AUTHOR]

Cholera remains an important global cause of morbidity and mortality, capable of causing periodic epidemic disease. Beginning in August 2008, a major cholera epidemic occurred in Zimbabwe, with 98,585 reported cases and 4,287 deaths. The dynamics of such outbreaks, particularly in nonestuarine regions, are not well understood. We explored the utility of mathematical models in understanding transmission dynamics of cholera and in assessing the magnitude of interventions necessary to control epidemic disease. Weekly data on reported cholera cases were obtained from the Zimbabwe Ministry of Health and Child Welfare (MoHCW) for the period from November 13, 2008 to July 31, 2009. A mathematical model was formulated and fitted to cumulative cholera cases to estimate the basic reproductive numbers R0 and the partial reproductive numbers from all 10 provinces for the 2008-2009 Zimbabwe cholera epidemic. Estimated basic reproductive numbers were highly heterogeneous, ranging from a low value of just above unity to 2.72. Partial reproductive numbers were also highly heterogeneous, suggesting that the transmission routes varied by province; human-to-human transmission accounted for 41-95% of all transmission. Our models suggest that the underlying patterns of cholera transmission varied widely from province to province, with a corresponding variation in the amenability of outbreaks in different provinces to control measures such as immunization. These data underscore the heterogeneity of cholera transmission dynamics, potentially linked to differences in environment, socio-economic conditions, and cultural practices. The lack of traditional estuarine reservoirs combined with these estimates of R0 suggest that mass vaccination against cholera deployed strategically in Zimbabwe and surrounding regions could prevent future cholera epidemics and eventually eliminate cholera from the region. [ABSTRACT FROM AUTHOR]

Studies the disease pandemic cholera caused on consumption of shellfish and other seafood due to presence of the bacteria vibrio. Production of cholera toxin by the strain Vibrio cholerae; Diseases caused by different strains of vibrio.

Vibrio cholerae in O-group 139 was first isolated in 1992 and by 1993 had been found throughout the Indian subcontinent. This epidemic expansion probably resulted from a single source after a lateral gene transfer (LGT) event that changed the serotype of an epidemic V. cholerae O1 El Tor strain to O139. However, some studies found substantial genetic diversity, perhaps caused by multiple origins. To further explore the relatedness of O139 strains, we analyzed nine sequenced loci from 96 isolates from patients at the Infectious Diseases Hospital, Calcutta, from 1992 to 2000. We found 64 novel alleles distributed among 51 sequence types. LGT events produced three times the number of nucleotide changes compared to mutation. In contrast to the traditional concept of epidemic spread of a homogeneous clone, the establishment of variant alleles generated by LGT during the rapid expansion of a clonal bacterial population may be a paradigm in infections and epidemics. [ABSTRACT FROM AUTHOR]

Vibrio cholerae serogroup O139 Bengal is the first documented serogroup other than O1 to cause epidemic cholera. The O139 Bengal strains are very similar to V. cholerae serogroup O1 biotype El Tor strains. The major differences between the two serogroups are that O139 Bengal contains a distinct O antigen and produces a polysaccharide capsule. We previously described three TnphoA mutants of O139 strain Al1837 which abolish both O antigen and capsule production. These TnphoA insertions were mapped to a 21.5 kb EcoRI fragment of the O139 chromosome. We describe here the cloning and mapping of this 21.5 kb EcoRI fragment and it was shown to complement each of the mutants in trans to produce O antigen and capsule. The EcoRI fragment contains 13 kb of DNA that is specific to O139 and 8.5 kb of DNA that is common to O1 and O139. Sequence analysis of the 13 kb of O139-specific DNA revealed that it contains 11 open reading frames all of which are transcribed in the same direction. Eight of the 11 open reading frames are homologous to sugar biosynthesis genes from other organisms. Using extended polymerase chain reactions, we show that the extent of the DNA region in O139 that is not present in O1 is approximately 35kb. The site of insertion of this O139-specific DNA in the O1 chromosome was mapped to the rfbO1 region. We also demonstrate that O139 Bengal strain Al1837 contains a deletion of 22 kb that in serogroup O1 strains contains the rfb region. Therefore, O139 Bengal probably arose from an O1 strain that had undergone genetic rearrangements including deletion of the O1 rfb region and acquisition of a 35 kb region of DNA which encodes O139 surface polysaccharide. [ABSTRACT FROM AUTHOR]

Altered El Tor Vibrio cholerae O1, with classical cholera toxin B gene, was isolated from 16 patients with severe diarrhea at St. Mark's Hospital, Arbonite, Haiti, <3 weeks after onset of the current cholera epidemic. Variable-number tandem-repeat typing of 187 isolates showed minimal diversity, consistent with a point source for the epidemic. [ABSTRACT FROM AUTHOR]

Cholera causes substantial illness and death in Africa. We analyzed 24 toxigenic Vibrio cholerae O1 strains isolated in 2015-2017 from patients in the Great Lakes region of the Democratic Republic of the Congo. Strains originating in southern Asia appeared to be part of the T10 introduction event in eastern Africa. We identified 2 main strain lineages, most recently a lineage corresponding to sequence type 515, a V. cholerae cluster previously reported in the Lake Kivu region. In 41% of fecal samples from cholera patients, we also identified a novel ICP1 (Bangladesh cholera phage 1) bacteriophage, genetically distinct from ICP1 isolates previously detected in Asia. Bacteriophage resistance occurred in distinct clades along both internal and external branches of the cholera phylogeny. This bacteriophage appears to have served as a major driver for cholera evolution and spread, and its appearance highlights the complex evolutionary dynamic that occurs between predatory phage and bacterial host. [ABSTRACT FROM AUTHOR]

The occurrence of outbreaks of cholera in Africa in 1970 and in Latin America in 1991, mainly in coastal communities, and the appearance of the new serotype Vibrio cholerae 0139 in India and subsequently in Bangladesh have stimulated efforts to understand environmental factors influencing the growth and geographic distribution of epidemic Vibrio cholerae serotypes. Because of the severity of recent epidemics, cholera is now being considered by some infectious disease investigators as a "reemerging" disease, prompting new work on the ecology of vibrios. Epidemiological and ecological surveillance for cholera has been under way in four rural, geographically separated locations in Bangladesh for the past 4 years, during which both clinical and environmental samples were collected at biweekly intervals. The clinical epidemiology portion of the research has been published (Sack et al., J. Infect. Dis. 187:96-101, 2003). The results of environmental sampling and analysis of the environmental and clinical data have revealed significant correlations of water temperature, water depth, rainfall, conductivity, and copepod counts with the occurrence of cholera toxin- producing bacteria (presumably V. cholerae). The lag periods between increases or decreases in units of factors, such as temperature and salinity, and occurrence of cholera correlate with biological parameters, e.g., plankton population blooms. The new information on the ecology of V. cholerae is proving useful in developing environmental models for the prediction of cholera epidemics. [ABSTRACT FROM AUTHOR]