Drug-resistance mechanisms in Vibrio cholerae O1 outbreak strain, Haiti, 2010

To increase understanding of drug-resistant Vibrio cholerae, we studied selected molecular mechanisms of antimicrobial drug resistance in the 2010 Haiti V. cholerae outbreak strain. Most resistance resulted from acquired genes located on an integrating conjugative element showing high homology to an integrating conjugative element identified in a V. cholerae isolate from India.     

Monitoring Water Sources for Environmental Reservoirs of Toxigenic Vibrio cholerae O1, Haiti

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.     

Outbreak of Imported Seventh Pandemic Vibrio cholerae O1 El Tor,Algeria, 2018

After a lull of >20 years, Algeria experienced a cholera outbreak in 2018 that included 291 suspected cases. We found that outbreak isolates were Vibrio cholerae O1 serotype Ogawa from seventh pandemic El Tor sublineage AFR14, which corresponds to a new introduction of cholera into Africa from South Asia.     

Consecutive outbreaks of Vibrio cholerae O139 and V. cholerae O1 cholera in a fishing village near Karachi, Pakistan

In July 2002 and June 2003, cholera outbreaks were detected by a diarrhoea surveillance system in a village outside Karachi, Pakistan. Specimens were culture confirmed. The first outbreak was caused by Vibrio cholerae O139 (n = 30) and the second outbreak by V. cholerae O1 (n = 39). Demographic and clinical features of patients were recorded and case-control studies were conducted following each outbreak. Clinical information was obtained for 29 of the 30 patients in the first outbreak, and 2 of the patients in the second outbreak were either out of the area or lost to follow-up, leaving 29 and 37 cases in the analysis for the first and second outbreak, respectively. Eighteen (49%) of the 37 V. cholerae O1 patients were under 2 years of age compared with 6 (21%) of the 29 V. cholerae O139 patients (P = 0.02). Vibrio cholerae O139-infected patients were more likely to be febrile (16/29) than those infected with V. cholerae O1 (2/37; P<0.001). A household contact with cholera was a risk factor in both outbreaks; water source was a risk factor in the first outbreak only. Geographically, cases were clustered during the first outbreak but not during the second. Person-to-person contact and water reservoirs appear to be the main transmission routes for cholera in this setting.     

Fluoroquinolone-resistant Vibrio cholerae isolated during a cholera outbreak in India

During the cholera epidemic of 2002 in and around Hubli, south India, Vibrio cholerae strains resistant to fluoroquinolones were isolated. Among the isolates of V. cholerae non-O1, non-O139 serogroups, 55.9% and 47.1% were resistant to norfloxacin and ciprofloxacin, respectively. However, only 12.5% of the O1 serogroup strains were resistant to both norfloxacin and ciprofloxacin. Though the O139 serogroup strains were susceptible to these antibiotics, they exhibited multidrug resistance. Emergence of fluoroquinolone-resistant V. cholerae that also exhibited multidrug resistance is of great significance in the epidemiology and control of cholera.     

Comparison of Escherichia coli ST131 pulsotypes, by epidemiologic traits, 1967-2009

Escherichia coli sequence type 131 (ST131), an emerging disseminated public health threat, causes multidrug-resistant extraintestinal infections. Among 579 diverse E. coli ST131 isolates from 1967-2009, we compared pulsotypes (>94% similar XbaI pulsed-field gel electrophoresis profiles) by collection year, geographic origin, source, and antimicrobial drug-resistance traits. Of 170 pulsotypes, 65 had >2 isolates and accounted for 85% of isolates. Although extensively dispersed geographically, pulsotypes were significantly source specific (e.g., had little commonality between humans vs. foods and food animals). The most prevalent pulsotypes were associated with recent isolation, humans, and antimicrobial drug resistance. Predominant pulsotype 968 was associated specifically with fluoroquinolone resistance but not with extended-spectrum β-lactamase production or bla(CTX-M-15). Thus, several highly successful antimicrobial drug-resistant lineages within E. coli ST131 have recently emerged and diffused extensively among locales while maintaining a comparatively restricted host/source range. Identification of factors contributing to this behavior of ST131 could help protect public health.     

霍乱弧菌产毒株的形成

在细菌进化过程中,非致病菌向致病菌进化的一个主要策略是由携带毒力基因的噬菌体进入宿主菌,并在宿主细菌中进行基因交流,改变宿主菌的表型或增加宿主菌的毒力,使无致病力的菌株转变为致病菌。本文就致病性霍乱弧菌的分子进化、CTXФ霍乱弧菌|产毒株|毒力相关基因和VPI基因家族的结构、功能和基因组的多样性,以及CTXФ基因组整合的分子生物学机制进行综述。     

Clonal origins of Vibrio cholerae O1 El Tor strains, Papua New Guinea, 2009-2011

We used multilocus sequence typing and variable number tandem repeat analysis to determine the clonal origins of Vibrio cholerae O1 El Tor strains from an outbreak of cholera that began in 2009 in Papua New Guinea. The epidemic is ongoing, and transmission risk is elevated within the Pacific region.     

Molecular epidemiology of geographically dispersed Vibrio cholerae, Kenya, January 2009-May 2010

Numerous outbreaks of cholera have occurred in Kenya since 1971. To more fully understand the epidemiology of cholera in Kenya, we analyzed the genetic relationships among 170 Vibrio cholerae O1 isolates at 5 loci containing variable tandem repeats. The isolates were collected during January 2009-May 2010 from various geographic areas throughout the country. The isolates grouped genetically into 5 clonal complexes, each comprising a series of genotypes that differed by an allelic change at a single locus. No obvious correlation between the geographic locations of the isolates and their genotypes was observed. Nevertheless, geographic differentiation of the clonal complexes occurred. Our analyses showed that multiple genetic lineages of V. cholerae were simultaneously infecting persons in Kenya. This finding is consistent with the simultaneous emergence of multiple distinct genetic lineages of V. cholerae from endemic environmental reservoirs rather than recent introduction and spread by travelers.     

Emergence and Evolutionary Response of Vibrio cholerae to Novel Bacteriophage,Democratic Republic of the Congo

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.     

Genotypic Characterization of Vibrio vulnificus Clinical Isolates in Korea

Objectives

Vibrio vunificus is known to cause septicemia and severe wound infections in patients with chronic liver diseases or an immuno-compromised condition. We carried out the molecular characterization of V. vulnificus isolates from human Vibrio septicemia cases based on pulsed-field gel electrophoresis (PFGE) using NotI and SfiI.

Methods and Results

PFGE was used to characterize a total of 78 strains from clinical cases after NotI or SfiI digestion. The geographical distribution of PFGE patterns for the strains from the southern part of Korea, a high-risk region for Vibrio septicemia, indicated that the isolates from southeastern Korea showed a comparatively higher degree of homology than those from southwestern Korea.

Conclusions

We report the genetic distribution of V. vulnficus isolated from Vibrio septicemia cases during 2000–2004 in Korea. This method has potential use as a subspecies-typing tool for V. vulnificus strains isolated from distant geographic regions.     

Construction of novel vaccine strains of Vibrio cholerae co-expressing the Inaba and Ogawa serotype antigens

The approach of inducing protective immunity against cholera by oral vaccination with killed whole Vibrio cholerae cells is effective, but the complexity of current cholera vaccines makes them difficult and relatively expensive to manufacture, especially if recombinant cholera toxin B subunit is included in the formulation. In an effort to simplify the composition of a new generation of oral cholera vaccines we have generated a novel non-toxigenic candidate vaccine strain of V. cholerae O1 that stably expresses both the Ogawa and Inaba serotype antigens on its surface. This was done by introducing a functional wbeT gene without a functional promoter into the chromosome of an O1 Inaba strain. The resulting low levels of expression of the wbeT gene product allowed for the desired partial serotype switching. This strain (MS1342) can potentially replace the three virulent strains used in currently manufactured cholera vaccines. Oral immunization of mice with formalin-killed MS1342 bacteria gave rise to Ogawa-specific, Inaba-specific and cross-reactive serum antibodies that were detectable both by lipopolysaccharide (LPS)-specific ELISAs and as vibriocidal antibodies that are considered to predict protective efficacy. These responses as well as intestinal mucosal IgA anti-LPS antibody responses were fully comparable with those obtained by immunization with the internationally licensed oral cholera vaccine Dukoral^®. We propose that such a strain may form the basis of a single strain killed whole cell cholera vaccine protecting against cholera caused by either the Inaba or Ogawa serotype of V. cholerae O1.