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Pathogenicity and Virulence
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
“Pathogenicity islands.” discovered within recent years, are large segments of DNA carrying multiple virulence traits which have been found at specific locations on bacterial chromosomes. Analysis of the DNA revealed that these segments are “foreign” to the bacterial cell. It is suggested that these DNA segments are acquired either by transduction via phages or by conjugation. Pathogenicity islands have been identified on strains of E. coli, Salmonella, Shigella, V. cholerae, and Y. pestis. The significance of this discovery is awesome for it reveals that many virulence traits can be acquired in one step, thus converting a commensal bacterium into a pathogen.
Salmonella
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
S.I. Smith, A. Ajayi, A. Seriki
To be fully pathogenic, a number of Salmonella virulence mechanisms have been recognized to describe the disease presentation, including altered invasion gene regulation,47 expression of the typhoid toxin,48 altered flagellin gene regulation,49 and virulence-associated (Vi) capsular polysaccharide.50Salmonella pathogenicity islands (SPIs) play a major role in the virulence factors of the bacterium.41 Salmonella pathogenicity islands SPI-1 and SPI-2 are important virulence factors that encode a type III secretion system (T3SS) that injects bacterial proteins (effectors) through bacterial and host membranes into host cells. The SPI-1 secreted SipA induces the polymorphonuclear (PMN) recruitment across intestinal epithelia and SPI-1 translocated effector SipB activates caspase-1-mediated IL-1b/IL-18 and proinflammatory cell death. Survival within the phagosome is facilitated by SPI-2.51 SPI-7 is the most important pathogenicity island in Salmonella Typhi infection, because it codes for the Vi antigen that is expressed on the cell surface. The Vi antigen plays a major role in virulence and severity of symptoms.52 The Vi-positive strains of Salmonella Typhi are extremely virulent compared to Vi-negative strains.39
Bacteroides
Published in Dongyou Liu, Laboratory Models for Foodborne Infections, 2017
The B. fragilis enterotoxin (BFT) is a zinc metalloprotease that destroys the adherence tight junctions in intestinal epithelium by cleaving E-cadherin, resulting in rearrangements of the actin cytoskeleton of the epithelial cells, which causes diarrhea. Enterotoxigenic B. fragilis (ETBF) strains encode three isotypes of BFT on distinct bft loci, carried on a 6-kb genome segment that is unique and called the B. fragilis pathogenicity island, and the presence of the bft gene is generally detected by PCR techniques.6–9 This pathogenicity island is flanked by genes encoding mobilization proteins and may be transmissible to nontoxigenic strains (non-ETBF) (Figure 16.2). Recent studies have shown that the BFT has a possible role as a carcinogen in colorectal cancer.10
Atypical enteropathogenic E. coli are associated with disease activity in ulcerative colitis
Published in Gut Microbes, 2022
Maximilian Baumgartner, Rebecca Zirnbauer, Sabine Schlager, Daniel Mertens, Nikolaus Gasche, Barbara Sladek, Craig Herbold, Olga Bochkareva, Vera Emelianenko, Harald Vogelsang, Michaela Lang, Anton Klotz, Birgit Moik, Athanasios Makristathis, David Berry, Stefanie Dabsch, Vineeta Khare, Christoph Gasche
The microbiota of IBD patients is characterized by reduced diversity and temporal instability.7 During periods of disease flares, it shifts toward dysbiosis with a reduced abundance of short chain fatty acids producing obligate anaerobes such as F. prausnitzii and overgrowth of facultative anaerobes, particularly E. coli.8,9 However, the exact sequelae and mechanisms connecting dysbiosis with flares in IBD disease activity remain elusive. IBD patients harbor E. coli isolates that primarily belong to B2 and D phylogroups with virulence factors that have originally been described in extraintestinal pathogenic E. coli.10–12 Efficient horizontal gene transfer of pathogenicity islands (PAI) and high genetic plasticity in chromosomes and plasmids facilitate the rapid adaptation of E. coli to various ecological niches.13,14E. coli thrives in areas of ulcerations and its DNA has been detected in 80% of CD patient’s granulomas.15,16 Adherent-invasive E. coli in CD can replicate within macrophages and induce TNF-α secretion in vitro.17 UC-associated E. coli were shown to potentiate intestinal inflammation in vivo.18,19 Large-scale adoption of multiplex-PCR-based GI pathogen panels identified enteric pathogens, including attaching and effacing E. coli (AEEC), being connected to inflammatory flares in IBD.20,21
The ancestral stringent response potentiator, DksA has been adapted throughout Salmonella evolution to orchestrate the expression of metabolic, motility, and virulence pathways
Published in Gut Microbes, 2022
Helit Cohen, Boaz Adani, Emiliano Cohen, Bar Piscon, Shalhevet Azriel, Prerak Desai, Heike Bähre, Michael McClelland, Galia Rahav, Ohad Gal-Mor
Łyżeń and colleagues have previously demonstrated that in the presence of ppGpp, DksA strongly represses the transcription of the argX promoter, which controls the expression of the four tRNA genes argX, hisR, leuT, and proM. However, in the absence of ppGpp, under non-starved rapid cellular growth, DksA can activate transcription from the argX promoter.25 These results suggested that DksA might contribute to tRNA transcription regulation in E. coli either as a positive or negative regulator. Here, we showed that in S. Typhimurium, many of the genes organized in SPI-2, SPI-4, SPI-5, and in the fim cluster, which are all integrated into tDNA or tDNA-like sites are under the regulation of DksA. These results may suggest that the ancestral regulation of tRNA genes by DksA has evolved to control the expression of pathogenicity island genes, after their integration into tRNA loci.
Salmonella enterica subsp. II serovar 4,5,12:a:- may cause gastroenteritis infections in humans
Published in Gut Microbes, 2022
Meiying Yan, Yongming Zhou, Yang Cao, Zhenpeng Li, Xin Lu, Bo Pang, Shukun Wang, Biao Kan
The human-restricted serovars S. Typhi and S. Paratyphi cause an invasive, life-threatening systemic disease, typhoid or enteric fever,5 while nontyphoidal serovars (NTSs) usually cause self-limited gastroenteritis, associated with intestinal inflammation and diarrhea.6 The virulence genes responsible for invasion, survival, and extraintestinal spread are located in Salmonella pathogenicity islands (SPIs), which are considered to represent ‘quantum leaps’ in the evolution of Salmonella and play a fundamental role in pathogenesis and host specificity.7–9 A variety of fimbrial adhesins are involved in the initiation of contact with host cells, followed by the invasion of nonphagocytic cells, especially epithelial cells of the intestinal mucosa, which is predominantly mediated by effectors encoded by SPI-1 island at early stages of infection. S. enterica is a facultative intracellular pathogen that survives in macrophages and is able to proliferate in infected host cells within Salmonella-containing vacuoles, where SPI-2 promotes intracellular replication of bacteria, eventually leading to systemic infection.