scholarly journals Genotypic and Phenotypic Characterization of Incompatibility Group FIB Positive Salmonella enterica Serovar Typhimurium Isolates from Food Animal Sources

Genes ◽  
2020 ◽  
Vol 11 (11) ◽  
pp. 1307
Author(s):  
Nesreen H. Aljahdali ◽  
Bijay K. Khajanchi ◽  
Kennedi Weston ◽  
Joanna Deck ◽  
Justin Cox ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Salmonella Enterica ◽  
Virulence Genes ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Incompatibility Group ◽  
Cell Counts ◽  
Food Animal ◽  
Animal Populations ◽  
Plasmid Replicon ◽  
Serovar Typhimurium

Salmonella enterica is one of the most common bacterial foodborne pathogens in the United States, causing illnesses that range from self-limiting gastroenteritis to more severe, life threatening invasive disease. Many Salmonella strains contain plasmids that carry virulence, antimicrobial resistance, and/or transfer genes which allow them to adapt to diverse environments, and these can include incompatibility group (Inc) FIB plasmids. This study was undertaken to evaluate the genomic and phenotypic characteristics of IncFIB-positive Salmonella enterica serovar Typhimurium isolates from food animal sources, to identify their plasmid content, assess antimicrobial resistance and virulence properties, and compare their genotypic isolates with more recently isolated S. Typhimurium isolates from food animal sources. Methods: We identified 71 S. Typhimurium isolates that carried IncFIB plasmids. These isolates were subjected to whole genome sequencing and evaluated for bacteriocin production, antimicrobial susceptibility, the ability to transfer resistance plasmids, and a subset was evaluated for their ability to invade and persist in intestinal human epithelial cells. Results: Approximately 30% of isolates (n = 21) displayed bacteriocin inhibition of Escherichia coli strain J53. Bioinformatic analyses using PlasmidFinder software confirmed that all isolates contained IncFIB plasmids along with multiple other plasmid replicon types. Comparative analyses showed that all strains carried multiple antimicrobial resistance genes and virulence factors including iron acquisition genes, such as iucABCD (75%), iutA (94%), sitABCD (76%) and sitAB (100%). In 17 cases (71%), IncFIB plasmids, along with other plasmid replicon types, were able to conjugally transfer antimicrobial resistance and virulence genes to the susceptible recipient strain. For ten strains, persistence cell counts (27%) were noted to be significantly higher than invasion bacterial cell counts. When the genome sequences of the study isolates collected from 1998–2003 were compared to those published from subsequent years (2005–2018), overlapping genotypes were found, indicating the perseverance of IncFIB positive strains in food animal populations. This study confirms that IncFIB plasmids can play a potential role in disseminating antimicrobial resistance and virulence genes amongst bacteria from several food animal species.

scholarly journals Whole-Genome Sequences of 66 Incompatibility Group FIB Plasmid-Carrying Salmonella enterica Serovar Typhimurium Isolates from Food Animal Sources

2020 ◽  
Vol 9 (5) ◽  
Author(s):  
Nesreen H. Aljahdali ◽  
Steven L. Foley ◽  
Jing Han ◽  
Yasser M. Sanad ◽  
Rajesh Nayak ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Resistance Genes ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Incompatibility Group ◽  
Content Type ◽  
Factors Associated ◽  
Food Animal ◽  
Antimicrobial Resistance Genes ◽  
Serovar Typhimurium

Sixty-six Salmonella enterica serovar Typhimurium isolates carrying incompatibility group FIB (IncFIB) plasmids were sequenced to further characterize the IncFIB plasmid-encoded factors associated with virulence and antimicrobial resistance genes. In addition to the IncFIB plasmid, many of these isolates harbored additional plasmids encoding virulence and antimicrobial resistance genes.

scholarly journals Salmonella enterica Serovars Typhi and Paratyphi A are avirulent in newborn and infant mice even when expressing virulence plasmid genes of Salmonella Typhimurium

2010 ◽  
Vol 4 (11) ◽  
pp. 723-731 ◽  
Author(s):  
Javier Santander ◽  
Roy Curtiss III
Keyword(s):  
Salmonella Enterica ◽  
Virulence Genes ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Systemic Infection ◽  
Virulence Plasmid ◽  
Susceptible Animal ◽  
Human Host ◽  
Adult Mice ◽  
Serovar Typhimurium ◽  
Plasmid Genes

Background: Salmonella enterica serovars Typhi and Paratyphi A are human host-restricted pathogens. Therefore, there is no small susceptible animal host that can be used to assess the virulence and safety of vaccine strains derived from these Salmonella serovars.  However, infant mice have been used to evaluate virulence and colonization by another human host-restricted pathogen, Vibrio cholerae.  Methodology: The possibility that infant mice host could be adapted for Salmonella led us to investigate the susceptibility of newborn and infant mice to oral infection with S. Typhi and S. Paratyphi A. Salmonella enterica serovar Typhimurium causes enteric fever in adult mice and this system has been used as a model for human typhoid. The pSTV virulence plasmid, not present in S. Typhi and S. Paratyphi A, plays an essential role in S. Typhimurium colonization and systemic infection of mice. We also conjugated pSTV into S. Typhi and S. Paratyphi A serovars and evaluated these transconjugants in newborn and infant mice.  Results: We determined that the spv virulence genes from the S. Typhimurium virulence plasmid are expressed in S. Typhi and S. Paratyphi A in a RpoS dependent fashion. Also, we determined that S. Typhi and S. Paratyphi A with and without pSTV transiently colonize newborn and infant mice tissues. Conclusion: Newborn and infant mice infected with S. Typhi and S. Paratyphi A do not succumb to the infection and that carriage of the S. Typhimurium virulence plasmid, pSTV, did not influence these results.

scholarly journals Whole-Genome Sequences of 35 Incompatibility Group I1 Plasmid-Carrying Salmonella enterica Isolates from Food Animal and Clinical Sources

2019 ◽  
Vol 8 (35) ◽  
Author(s):  
Nesreen H. Aljahdali ◽  
Pravin R. Kaldhone ◽  
Steven L. Foley ◽  
Bijay K. Khajanchi
Keyword(s):  
Antimicrobial Resistance ◽  
Resistance Genes ◽  
Salmonella Enterica ◽  
Whole Genome ◽  
Genome Sequences ◽  
Incompatibility Group ◽  
Content Type ◽  
Food Animal ◽  
Antimicrobial Resistance Genes ◽  
Genotypic Characteristics

We sequenced 35 Salmonella enterica isolates carrying incompatibility group I1 (IncI1) plasmids from different serotypes to study their genotypic characteristics. The isolates originated from food animals (n = 32) and human patients (n = 3). All isolates carried IncI1 plasmids, and many had additional plasmids detected along with virulence and antimicrobial resistance genes.

scholarly journals Identification of GtgE, a Novel Virulence Factor Encoded on the Gifsy-2 Bacteriophage of Salmonella enterica Serovar Typhimurium

2002 ◽  
Vol 184 (19) ◽  
pp. 5234-5239 ◽  
Author(s):  
Theresa D. Ho ◽  
Nara Figueroa-Bossi ◽  
Minhua Wang ◽  
Sergio Uzzau ◽  
Lionello Bossi ◽  
...  
Keyword(s):  
Virulence Factor ◽  
Salmonella Enterica ◽  
Virulence Genes ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Systemic Infection ◽  
Open Reading Frames ◽  
Effector Protein ◽  
Protein Sequence Analysis ◽  
Serovar Typhimurium ◽  
Reading Frames

ABSTRACT The Gifsy-2 temperate bacteriophage of Salmonella enterica serovar Typhimurium contributes significantly to the pathogenicity of strains that carry it as a prophage. Previous studies have shown that Gifsy-2 encodes SodCI, a periplasmic Cu/Zn superoxide dismutase, and at least one additional virulence factor. Gifsy-2 encodes a Salmonella pathogenicity island 2 type III secreted effector protein. Sequence analysis of the Gifsy-2 genome also identifies several open reading frames with homology to those of known virulence genes. However, we found that null mutations in these genes did not individually have a significant effect on the ability of S. enterica serovar Typhimurium to establish a systemic infection in mice. Using deletion analysis, we have identified a gene, gtgE, which is necessary for the full virulence of S. enterica serovar Typhimurium Gifsy-2 lysogens. Together, GtgE and SodCI account for the contribution of Gifsy-2 to S. enterica serovar Typhimurium virulence in the murine model.

scholarly journals Comparison of Subtyping Methods for Differentiating Salmonella enterica Serovar Typhimurium Isolates Obtained from Food Animal Sources

2006 ◽  
Vol 44 (10) ◽  
pp. 3569-3577 ◽  
Author(s):  
S. L. Foley ◽  
D. G. White ◽  
P. F. McDermott ◽  
R. D. Walker ◽  
B. Rhodes ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Food Animal ◽  
Serovar Typhimurium

scholarly journals Salmonella enterica Serovar Typhimurium Periplasmic Superoxide Dismutase SodCI Is a Member of the PhoPQ Regulon and Is Induced in Macrophages

2006 ◽  
Vol 188 (22) ◽  
pp. 7853-7861 ◽  
Author(s):  
Yekaterina A. Golubeva ◽  
James M. Slauch
Keyword(s):  
Salmonella Enterica ◽  
Virulence Genes ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Regulatory System ◽  
Differential Regulation ◽  
Superoxide Dismutases ◽  
High Level Expression ◽  
Fusion Strain ◽  
Serovar Typhimurium ◽  
High Level

ABSTRACT Salmonella enterica serovar Typhimurium replicates within host macrophages during the systemic stage of infection. In the macrophage, the bacteria must survive the respiratory burst that produces superoxide. Serovar Typhimurium strain 14028 produces two periplasmic superoxide dismutases, SodCI and SodCII, but only SodCI contributes to virulence. Although we have shown that this is primarily due to differences in the two proteins, evidence suggests differential regulation of the two genes. Using transcriptional sodCI- and sodCII-lac fusions, we show that sodCII is under the control of the RpoS sigma factor, as was known for the Escherichia coli ortholog, sodC. In contrast, we show that sodCI is transcriptionally controlled by the PhoPQ two-component regulatory system, which regulates an array of virulence genes required for macrophage survival. Introduction of a phoP-null mutation into the sodCI fusion strain resulted in a decrease in transcription and loss of regulation. The sodCI-lac fusion showed high-level expression in a background containing a phoQ constitutive allele. The sodCI gene is induced 15-fold in bacteria recovered from either the tissue culture macrophages or the spleens of infected mice. Induction in macrophages is dependent on PhoP. The sodCII fusion was induced three- to fourfold in macrophages and animals; this induction was unaffected by loss of PhoP. Thus, sodCI, which is horizontally transferred by the Gifsy-2 phage, is regulated by PhoPQ such that it is induced at the appropriate time and place to combat phagocytic superoxide.

scholarly journals Secretion of the orgC Gene Product by Salmonella enterica Serovar Typhimurium

2003 ◽  
Vol 71 (11) ◽  
pp. 6680-6685 ◽  
Author(s):  
James B. Day ◽  
Catherine A. Lee
Keyword(s):  
Gene Product ◽  
Type Iii Secretion ◽  
Salmonella Enterica ◽  
Virulence Genes ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Type Iii Secretion System ◽  
Pathogenicity Island ◽  
Secretion System ◽  
Serovar Typhimurium ◽  
Transposon Insertions

ABSTRACT HilA activates the transcription of genes on Salmonella pathogenicity island 1 (SPI1), which encodes a type III secretion system (TTSS). Previous studies showed that transposon insertions in orgC, a gene located on SPI1, increase hilA expression. We characterize the orgC gene product and show that it is secreted via the SPI1 TTSS. We propose a model whereby OrgC functions as a secreted repressor of the SPI1 virulence genes.

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