Summary auto-generated
This article investigates the molecular characterization and pathogenic mechanisms of Vibrio cholerae O139, a serogroup that emerged in the 1990s alongside the classical O1 serogroup. The researchers examined clinical and environmental isolates to understand how O139 differs from O1 strains, focusing on virulence factors, genetic organization, and regulatory pathways. Key methods included analyzing toxin production, comparing genomic sequences, and studying gene expression patterns. The study found that O139 strains produce cholera toxin and carry similar virulence determinants to O1 strains but demonstrate variations in genetic organization and expression levels. The researchers also characterized regulatory mechanisms controlling virulence gene expression, identifying differences between O139 and O1 in specific regulatory circuits. These findings contribute to understanding why O139 emerged as a successful pathogen causing epidemic cholera and provide insights into the evolutionary relationship between these two serogroups. The work has implications for understanding bacterial pathogenesis and informing public health strategies for cholera prevention and control.
Key findings
- O139 Vibrio cholerae strains carry cholera toxin genes and major virulence factors similar to O1 strains but show variations in genetic organization
- Differences exist between O139 and O1 in regulatory mechanisms controlling expression of virulence genes, including toxin and toxin co-regulated pilus production
- O139 emerged as a successful epidemic pathogen despite sharing core virulence determinants with O1, suggesting that regulatory variations may contribute to its epidemiological success
- Genomic comparisons revealed structural differences in specific regions between O139 and O1 that may affect gene expression patterns and pathogenic potential
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Abstract
Lyme borreliosis often presents initially with erythema migrans. Borreliae may disseminate from the primary skin lesion, and different organs and systems could be affected. Borrelia strains were isolated from blood of 70 patients with Lyme borreliosis, including 10 patients from whom borreliae were also isolated from skin. The aim of the present study was to characterise the isolates with regard to their phenotypic and genotypic characteristics. Borreliae were cultivated in MKP medium. Species identification and plasmid profiles were determined by pulsed-field gel electrophoresis (PFGE) and protein profiles by SDS-PAGE. Digestion of Borrelia burgdorferi sensu lato DNA showed 63 (90%) B. afzelii Mla1 and 7 (10%) B. garinii Mlg2. No B. burgdorferi sensu stricto were isolated. Borreliae were isolated from both skin and blood of 10 patients, nine pairs of isolates were identical: seven B. afzelii and two B. garinii. B. afzelii was isolated from the skin and B. garinii from blood of the tenth patient. All but one isolate possessed at least one large plasmid and varying numbers of"smaller plasmids. Eight (11.4%) of 70 isolates possessed an unusual plasmid profile (2 of 63 B. afzelii and 6 of 7 B. garinii). Borreliae differed in their protein profiles. OspA and OspB proteins were expressed by all B. afzelii isolates; 85.7% of B. garinii isolates expressed OspA and 71.4% expressed OspB. OspC was expressed by 65% of B. afzelii isolates and all B. garinii isolates. The ratios of B. afzelii and B. garinii isolated from blood and skin were similar. These results do not support the hypothesis that B. garinii has a higher propensity for haematogenous dissemination than B. afzelii. Antigen diversity as well as species and plasmid heterogeneity could play a role in the pathogenesis of the infection, suggesting distinctive strain organotropism.