scholarly journals A novel antimicrobial peptide significantly enhances acid-induced killing of Shiga toxin-producing Escherichia coli O157 and non-O157 serotypes

Microbiology ◽  
2011 ◽  
Vol 157 (6) ◽  
pp. 1768-1775 ◽  
Author(s):  
M. Lino ◽  
J. V. Kus ◽  
S. L. Tran ◽  
Z. Naqvi ◽  
B. Binnington ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Dna Repair ◽  
Antimicrobial Peptide ◽  
Shiga Toxin ◽  
Antimicrobial Agents ◽  
Treatment Options ◽  
Survival Rates ◽  
Acid Stress ◽  
Toxin Production ◽  
Risk Of Progression

Shiga toxin-producing Escherichia coli (STEC) colonizes the human intestine, causing haemorrhagic colitis and haemolytic uraemic syndrome (HUS). Treatment options are limited to intravenous fluids in part because sublethal doses of some antibiotics have been shown to stimulate increased toxin release and enhance the risk of progression to HUS. Preventative antimicrobial agents, especially those that build on the natural antimicrobial action of the host defence, may provide a better option. In order to survive the acid stress of gastric passage, STEC is equipped with numerous acid resistance and DNA repair mechanisms. Inhibition of acid-induced DNA repair may offer a strategy to target survival of ingested STEC. We report here that brief pretreatment with a novel antimicrobial peptide, which was previously shown to inhibit bacterial DNA repair, significantly and profoundly reduces survival of acid-stressed O157 : H7 and non-O157 : H7 STEC seropathotypes that are highly associated with HUS. Reduction in survival rates of STEC range from 3 to 5 log. We also show that peptide/acid treatment results in little or no increase in toxin production, thereby reducing the risk of progression to HUS. This study identifies the peptide wrwycr as a potential new candidate for a preventative antimicrobial for STEC infection.

scholarly journals Role of Recent Therapeutic Applications and the Infection Strategies of Shiga Toxin-Producing Escherichia coli

2021 ◽  
Vol 11 ◽  
Author(s):  
Su-bin Hwang ◽  
Ramachandran Chelliah ◽  
Ji Eun Kang ◽  
Momna Rubab ◽  
Eric Banan-MwineDaliri ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Antimicrobial Agents ◽  
Bacterial Pathogen ◽  
Toxin Production ◽  
The Body ◽  
Cell Protein ◽  
Primary Role ◽  
Shiga Toxins

Shiga toxin-producing Escherichia coli (STEC) is a global foodborne bacterial pathogen that is often accountable for colon disorder or distress. STEC commonly induces severe diarrhea in hosts but can cause critical illnesses due to the Shiga toxin virulence factors. To date, there have been a significant number of STEC serotypes have been evolved. STECs vary from nausea and hemorrhoid (HC) to possible lethal hemolytic-based uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP). Inflammation-based STEC is usually a foodborne illness with Shiga toxins (Stx 1 and 2) thought to be pathogenesis. The STEC’s pathogenicity depends significantly on developing one or more Shiga toxins, which can constrain host cell protein synthesis leading to cytotoxicity. In managing STEC infections, antimicrobial agents are generally avoided, as bacterial damage and discharge of accumulated toxins are thought the body. It has also been documented that certain antibiotics improve toxin production and the development of these species. Many different groups have attempted various therapies, including toxin-focused antibodies, toxin-based polymers, synbiotic agents, and secondary metabolites remedies. Besides, in recent years, antibiotics’ efficacy in treating STEC infections has been reassessed with some encouraging methods. Nevertheless, the primary role of synbiotic effectiveness (probiotic and prebiotic) against pathogenic STEC and other enteropathogens is less recognized. Additional studies are required to understand the mechanisms of action of probiotic bacteria and yeast against STEC infection. Because of the consensus contraindication of antimicrobials for these bacterial pathogens, the examination was focused on alternative remedy strategies for STEC infections. The rise of novel STEC serotypes and approaches employed in its treatment are highlighted.

Virulence properties and antimicrobial susceptibility of Shiga toxin-producing Escherichia coli strains isolated from healthy cattle from Paraná State, Brazil

2008 ◽  
Vol 54 (7) ◽  
pp. 588-593 ◽  
Author(s):  
Caroline P. Pigatto ◽  
Ruben P. Schocken-Iturrino ◽  
Emanuel M. Souza ◽  
Fábio O. Pedrosa ◽  
Larissa Comarella ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Antimicrobial Susceptibility ◽  
Shiga Toxin ◽  
Antimicrobial Agents ◽  
False Negative ◽  
Vero Cells ◽  
Toxin Production ◽  
Latex Agglutination ◽  
Negative Results ◽  
Virulence Markers

The presence of Shiga toxin-producing Escherichia coli (STEC) strains in feces samples of cattle was determined using the cytotoxicity assay on Vero cells and a screening PCR system to detect stx genes. The STEC isolates were serotyped, tested for antimicrobial susceptibility, and analyzed for virulence genes using multiplex PCR. The verocytotoxin-producing E. coli – reverse passive latex agglutination (VTEC–RPLA) assay was also used to detect Shiga toxin production. The frequency of cattle shedding STEC was 36%. The isolates belonged to 33 different serotypes, of which O10:H42, O98:H41, and O159:H21 had not previously been associated with STEC. The most frequent serotypes were ONT:H7 (10%), O22:H8 (7%), O22:H16 (7%), and ONT:H21 (7%). Most of the strains (96%) were susceptible to all antimicrobial agents tested. Shiga toxin was detected by the VTEC–RPLA assay in most (89%) of the STEC strains. The frequency of virulence markers was as follows: stx1, 10%; stx2, 43%; stx1 plus stx2, 47%; ehxA, 44%; eae, 1%; and saa, 38%. Several strains belong to serotypes associated with human disease, and most of them carried a stx2-type gene, suggesting that they represent a risk to human health. The screening PCR assay showed fewer false-negative results for STEC than the Vero-cell assay and is suitable for laboratory routine.

scholarly journals Comparative Genomics and Characterization of the Late Promoter pR’ from Shiga Toxin Prophages in Escherichia coli

Viruses ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 595 ◽  
Author(s):  
Ling Zhang ◽  
David Simpson ◽  
Lynn McMullen ◽  
Michael Gänzle
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Toxin Production ◽  
Late Promoter ◽  
Regulatory Systems ◽  
Human Illness ◽  
Late Transcription ◽  
Native Strains ◽  
Native Host

Shiga-toxin producing Escherichia coli (STEC) causes human illness ranging from mild diarrhea to death. The bacteriophage encoded stx genes are located in the late transcription region, downstream of the antiterminator Q. The transcription of the stx genes is directly under the control of the late promoter pR’, thus the sequence diversity of the region between Q and stx, here termed the pR’ region, may affect Stx toxin production. Here, we compared the gene structure of the pR’ region and the stx subtypes of nineteen STECs. The sequence alignment and phylogenetic analysis suggested that the pR’ region tends to be more heterogeneous than the promoter itself, even if the prophages harbor the same stx subtype. Furthermore, we established and validated transcriptional fusions of the pR’ region to the DsRed reporter gene using mitomycin C (MMC) induction. Finally, these constructs were transformed into native and non-native strains and examined with flow cytometry. The results showed that induction levels changed when pR’ regions were placed under different regulatory systems. Moreover, not every stx gene could be induced in its native host bacteria. In addition to the functional genes, the diversity of the pR’ region plays an important role in determining the level of toxin induction.

scholarly journals Application of Bacteriophages on Shiga Toxin-Producing Escherichia coli (STEC) Biofilm

Antibiotics ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1423
Author(s):  
Nicola Mangieri ◽  
Roberto Foschino ◽  
Claudia Picozzi
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Biofilm Formation ◽  
Pathogenic Bacteria ◽  
Antimicrobial Agents ◽  
Bacterial Cells ◽  
Abiotic Surfaces ◽  
Continuous Presence ◽  
Different Strains ◽  
Better Than

Shiga toxin-producing Escherichia coli are pathogenic bacteria able to form biofilms both on abiotic surfaces and on food, thus increasing risks for food consumers. Moreover, biofilms are difficult to remove and more resistant to antimicrobial agents compared to planktonic cells. Bacteriophages, natural predators of bacteria, can be used as an alternative to prevent biofilm formation or to remove pre-formed biofilm. In this work, four STEC able to produce biofilm were selected among 31 different strains and tested against single bacteriophages and two-phage cocktails. Results showed that our phages were able to reduce biofilm formation by 43.46% both when used as single phage preparation and as a cocktail formulation. Since one of the two cocktails had a slightly better performance, it was used to remove pre-existing biofilms. In this case, the phages were unable to destroy the biofilms and reduce the number of bacterial cells. Our data confirm that preventing biofilm formation in a food plant is better than trying to remove a preformed biofilm and the continuous presence of bacteriophages in the process environment could reduce the number of bacteria able to form biofilms and therefore improve the food safety.

scholarly journals Replication of plasmids derived from Shiga toxin-converting bacteriophages in starved Escherichia coli

Microbiology ◽  
2011 ◽  
Vol 157 (1) ◽  
pp. 220-233 ◽  
Author(s):  
Bożena Nejman ◽  
Beata Nadratowska-Wesołowska ◽  
Agnieszka Szalewska-Pałasz ◽  
Alicja Węgrzyn ◽  
Grzegorz Węgrzyn
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Transcriptional Activation ◽  
Stringent Response ◽  
Toxin Production ◽  
Replication Initiation ◽  
Host Cells ◽  
Regulation Of Transcription ◽  
E Coli ◽  
Dna Replication Initiation

The pathogenicity of Shiga toxin-producing Escherichia coli (STEC) depends on the expression of stx genes that are located on lambdoid prophages. Effective toxin production occurs only after prophage induction, and one may presume that replication of the phage genome is important for an increase in the dosage of stx genes, positively influencing their expression. We investigated the replication of plasmids derived from Shiga toxin (Stx)-converting bacteriophages in starved E. coli cells, as starvation conditions may be common in the intestine of infected humans. We found that, unlike plasmids derived from bacteriophage λ, the Shiga toxin phage-derived replicons did not replicate in amino acid-starved relA + and relA − cells (showing the stringent and relaxed responses to starvation, respectively). The presence of the stable fraction of the replication initiator O protein was detected in all tested replicons. However, while ppGpp, the stringent response effector, inhibited the activities of the λ P R promoter and its homologues from Shiga toxin-converting bacteriophages, these promoters, except for λ P R, were only weakly stimulated by the DksA protein. We suggest that this less efficient (relative to λ) positive regulation of transcription responsible for transcriptional activation of the origin contributes to the inhibition of DNA replication initiation of Shiga toxin-converting bacteriophages in starved host cells, even in the absence of ppGpp (as in starved relA − hosts). Possible clinical implications of these results are discussed.

Disinfectant and Antimicrobial Susceptibility Profiles of the Big Six Non-O157 Shiga Toxin–Producing Escherichia coli Strains from Food Animals and Humans

2016 ◽  
Vol 79 (8) ◽  
pp. 1355-1370 ◽  
Author(s):  
ROSS C. BEIER ◽  
EELCO FRANZ ◽  
JAMES L. BONO ◽  
ROBERT E. MANDRELL ◽  
PINA M. FRATAMICO ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Antimicrobial Susceptibility ◽  
Shiga Toxin ◽  
Human Exposure ◽  
Antimicrobial Agents ◽  
Active Components ◽  
Food Animals ◽  
Low Prevalence ◽  
Susceptibility Profiles ◽  
Animal Strains

ABSTRACT The disinfectant and antimicrobial susceptibility profiles of 138 non-O157 Shiga toxin–producing Escherichia coli strains (STECs) from food animals and humans were determined. Antimicrobial resistance (AMR) was moderate (39.1% of strains) in response to 15 antimicrobial agents. Animal strains had a lower AMR prevalence (35.6%) than did human strains (43.9%) but a higher prevalence of the resistance profile GEN-KAN-TET. A decreasing prevalence of AMR was found among animal strains from serogroups O45 > O145 > O121 > O111 > O26 > O103 and among human strains from serogroups O145 > O103 > O26 > O111 > O121 > O45. One animal strain from serogroups O121 and O145 and one human strain from serogroup O26 had extensive drug resistance. A high prevalence of AMR in animal O45 and O121 strains and no resistance or a low prevalence of resistance in human strains from these serogroups suggests a source other than food animals for human exposure to these strains. Among the 24 disinfectants evaluated, all strains were susceptible to triclosan. Animal strains had a higher prevalence of resistance to chlorhexidine than did human strains. Both animal and human strains had a similar low prevalence of low-level benzalkonium chloride resistance, and animal and human strains had similar susceptibility profiles for most other disinfectants. Benzyldimethylammonium chlorides and C10AC were the primary active components in disinfectants DC&R and P-128, respectively, against non-O157 STECs. A disinfectant FS512 MIC ≥ 8 μg/ml was more prevalent among animal O121 strains (61.5%) than among human O121 strains (25%), which may also suggest a source of human exposure to STEC O121 other than food animals. Bacterial inhibition was not dependent solely on pH but was correlated with the presence of dissociated organic acid species and some undissociated acids.

scholarly journals A putative microcin amplifies Shiga toxin 2a production ofEscherichia coliO157:H7

2019 ◽  
Author(s):  
Hillary M. Figler ◽  
Lingzi Xiaoli ◽  
Kakolie Banerjee ◽  
Maria Hoffmann ◽  
Kuan Yao ◽  
...  
Keyword(s):  
Shiga Toxin ◽  
Bacterial Infections ◽  
Bacterial Species ◽  
Treatment Options ◽  
Gene Clusters ◽  
Toxin Production ◽  
Additional Treatment ◽  
Proteinase K ◽  
Gut Microflora ◽  
E Coli

AbstractEscherichia coliO157:H7 is a foodborne pathogen, implicated in various multi-state outbreaks. It encodes Shiga toxin on a prophage, and Shiga toxin production is linked to phage induction. AnE. colistrain, designated 0.1229, was identified that amplified Stx2a production when co-cultured withE. coliO157:H7 strain PA2. Growth of PA2 in 0.1229 cell-free supernatants had a similar effect, even when supernatants were heated to 100°C for 10 min, but not after treatment with Proteinase K. The secreted molecule was shown to use TolC for export and the TonB system for import. The genes sufficient for production of this molecule were localized to a 5.2 kb region of a 12.8 kb plasmid. This region was annotated, identifying hypothetical proteins, a predicted ABC transporter, and a cupin superfamily protein. These genes were identified and shown to be functional in two otherE. colistrains, and bioinformatic analyses identified related gene clusters in similar and distinct bacterial species. These data collectively suggestE. coli0.1229 and otherE. coliproduce a microcin that induces the SOS response in target bacteria. Besides adding to the limited number of microcins known to be produced byE. coli, this study provides an additional mechanism by whichstx2aexpression is increased in response to the gut microflora.ImportanceHow the gut microflora influences the progression of bacterial infections is only beginning to be understood. Antibiotics are counter-indicated forE. coliO157:H7 infections, and therefore treatment options are limited. An increased understanding of how the gut microflora directs O157:H7 virulence gene expression may lead to additional treatment options. This work identifiedE. colithat enhance the production of Shiga toxin by O157:H7, through the secretion of a proposed microcin. This work demonstrates another mechanism by which non-O157E. colistrains may increase Shiga toxin production, and adds to our understanding of microcins, a group of antimicrobials that are less well understood than colicins.

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