Shigella: Virulence Factors and Pathogenicity

Bliven, Kimberly A.; Lampel, Keith A.

doi:10.1007/978-3-319-56836-2_7

Cited by 2 publications

(2 citation statements)

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“…As for these seven groups of virulence factors, T3SS shows most distinct differences between sensitive strains (158 VFs) and resistant strains (207 VFs) on average. As previously reported, T3SS is a group of specialized protein export systems utilized by bacteria to effectively exploit eukaryotic hosts and contributes to bacterial adherence, invasion, and manipulation of the host's intracellular trafficking and immune systems [10]. Thus, in the multi-resistant Shigella strains, high number of virulence factors in T3SS groups could be very likely to occur at the same time.…”

Section: Discussionmentioning

confidence: 89%

“…were evolved from non-pathogenic E. coli ancestors by acquisition of chromosomal pathogenicity islands and a large virulence plasmid while genes related with anti-virulence such as cadA and ompT , bacterial mobility like flagella and fimbriae, and catabolism were lost [9]. Pathogenicity of Shigella virulence mainly involves Type III secretion system (T3SS), adherence, invasion, intracellular mobility and spread, immune system manipulation and evasion, and toxin, etc [10]. Accepted paradigm indicated that increased antibiotic resistance is associated with fitness costs, resulting in reductions in in vivo virulence [11].…”

Section: Introductionmentioning

confidence: 99%

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Comparative genome analysis of 15 clinical <em>Shigella flexneri</em> strains regarding virulence and antibiotic resistance

et al. 2019

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Shigellosis is the major cause of dysentery globally. It is mainly attributed to two Shigella species, Shigella sonnei and Shigella flexneri, which leads to approximately 165 million infections and 1.1 million deaths each year. Rapid increase and widening of spectrum in antibiotics resistance make Shigella hard to be adequately controlled through existing prevention and treatment measures. It has also been observed that enhanced virulence and advent of antibiotic resistance (AR) could arise almost simultaneously. However, genetic linkages between the two factors are missing or largely ignored, which hinders experimental verification of the relationship. In this study, we sequenced 15 clinically isolated S. flexneri strains. Genome assembly, annotation and comparison were performed through routine pipelines. Differential resistant profiles of all 15 S. flexneri strains to nine antibiotics were experimentally verified. Virulence factors (VFs) belonging to 4 categories and 31 functional groups from the Virulence Factor Database (VFDB) were used to screen all Shigella translated CDSs. Distribution patterns of virulence factors were analysed by correlating with the profiles of bacterial antibiotics resistance. In addition, multi-resistant S. flexneri strains were compared with antibiotic-sensitive strains by focusing on the abundance or scarcity of specific groups of VFs. By doing these, a clear view of the relationships between virulence factors and antibiotics resistance in Shigella could be achieved, which not only provides a set of genetic evidence to support the interactions between VFs and AR but could also be used as a guidance for further verification of the relationships through manipulating specific groups of virulence factors.

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Section: Discussionmentioning

confidence: 89%