Antimicrobial resistance and virulence factor gene profiles of Enterococcus spp. isolates from wild Arctocephalus australis (South American fur seal) and Arctocephalus tropicalis (Subantarctic fur seal)

2015 ◽  
Vol 31 (12) ◽  
pp. 1935-1946 ◽  
Author(s):  
Naiara Aguiar Santestevan ◽  
Dejoara de Angelis Zvoboda ◽  
Janira Prichula ◽  
Rebeca Inhoque Pereira ◽  
Guilherme Raffo Wachholz ◽  
...  
2006 ◽  
Vol 72 (10) ◽  
pp. 6680-6686 ◽  
Author(s):  
Peter Schierack ◽  
Hartmut Steinrück ◽  
Sylvia Kleta ◽  
Wilfried Vahjen

ABSTRACT Nonpathogenic, intestinal Escherichia coli (commensal E. coli) supports the physiological intestinal balance of the host, whereas pathogenic E. coli with typical virulence factor gene profiles can cause severe outbreaks of diarrhea. In many reports, E. coli isolates from diarrheic animals were classified as putative pathogens. Here we describe a broad variety of virulence gene-positive E. coli isolates from swine with no clinical signs of intestinal disease. The isolation of E. coli from 34 pigs from the same population and the testing of 331 isolates for genes encoding heat-stable enterotoxins I and II, heat-labile enterotoxin I, Shiga toxin 2e, and F4, F5, F6, F18, and F41 fimbriae revealed that 68.6% of the isolates were positive for at least one virulence gene, with a total of 24 different virulence factor gene profiles, implying high rates of horizontal gene transfer in this E. coli population. Additionally, we traced the occurrence of hemolytic E. coli over a period of 1 year in this same pig population. Hemolytic isolates were differentiated into seven clones; only three were found to harbor virulence genes. Hemolytic E. coli isolates without virulence genes or with only the fedA gene were found to be nontypeable by slide agglutination tests with OK antisera intended for screening live cultures against common pathogenic E. coli serogroups. The results appear to indicate that virulence gene-carrying E. coli strains are a normal part of intestinal bacterial populations and that high numbers of E. coli cells harboring virulence genes and/or with hemolytic activity do not necessarily correlate with disease.


Odontology ◽  
2020 ◽  
Vol 109 (1) ◽  
pp. 18-28
Author(s):  
Vijay M. Kumbar ◽  
Malleswara Rao Peram ◽  
Manohar S. Kugaji ◽  
Tejas Shah ◽  
Sanjivani P. Patil ◽  
...  

2016 ◽  
Vol 6 (2) ◽  
pp. e00420 ◽  
Author(s):  
Nhan Tu ◽  
Ronan K. Carroll ◽  
Andy Weiss ◽  
Lindsey N. Shaw ◽  
Gael Nicolas ◽  
...  

2007 ◽  
Vol 67 (4) ◽  
pp. 729-746 ◽  
Author(s):  
Smirla Ramos-Montañez ◽  
Ho-Ching Tiffany Tsui ◽  
Kyle J. Wayne ◽  
Jordan L. Morris ◽  
Lindsey E. Peters ◽  
...  

2019 ◽  
Vol 87 (5) ◽  
Author(s):  
Chance J. Cosgriff ◽  
Chelsea R. White ◽  
Wei Ping Teoh ◽  
James P. Grayczyk ◽  
Francis Alonzo

ABSTRACTGram-positive bacteria process and release small peptides, or pheromones, that act as signals for the induction of adaptive traits, including those involved in pathogenesis. One class of small signaling pheromones is the cyclic autoinducing peptides (AIPs), which regulate expression of genes that orchestrate virulence and persistence in a range of microbes, including staphylococci, listeriae, clostridia, and enterococci. In a genetic screen forStaphylococcus aureussecreted virulence factors, we identified anS. aureusmutant containing an insertion in the geneSAUSA300_1984(mroQ), which encodes a putative membrane-embedded metalloprotease. A ΔmroQmutant exhibited impaired induction of Toll-like receptor 2-dependent inflammatory responses from macrophages but elicited greater production of the inflammatory cytokine interleukin-1β and was attenuated in a murine skin and soft tissue infection model. The ΔmroQmutant phenocopies anS. aureusmutant containing a deletion of the accessory gene regulatory system (Agr), wherein both strains have significantly reduced production of secreted toxins and virulence factors but increased surface protein A abundance. The Agr system controls virulence factor gene expression inS. aureusby sensing the accumulation of AIP via the histidine kinase AgrC and the response regulator AgrA. We provide evidence to suggest that MroQ acts within the Agr pathway to facilitate the optimal processing or export of AIP for signal amplification through AgrC/A and induction of virulence factor gene expression. Mutation of MroQ active-site residues significantly reduces AIP signaling and attenuates virulence. Altogether, this work identifies a new component of the Agr quorum-sensing circuit that is critical for the production ofS. aureusvirulence factors.


1999 ◽  
Vol 32 (5) ◽  
pp. 1043-1053 ◽  
Author(s):  
Herve Agaisse ◽  
Myriam Gominet ◽  
Ole Andreas Okstad ◽  
Anne-Brit Kolsto ◽  
Didier Lereclus

2019 ◽  
Author(s):  
Chance J. Cosgriff ◽  
Chelsea R. White ◽  
Wei Ping Teoh ◽  
James P. Grayczyk ◽  
Francis Alonzo

AbstractGram-positive bacteria process and release small peptides or “pheromones” that act as signals for the induction of adaptive traits including those involved in pathogenesis. One class of small signaling pheromones is the cyclic auto-inducing peptides (AIPs), which regulate expression of genes that orchestrate virulence and persistence in a range of microbes including Staphylococci, Listeria, Clostridia, and Enterococci. In a genetic screen for Staphylococcus aureus secreted virulence factors, we identified a S. aureus mutant containing an insertion in gene SAUSA300_1984 (mroQ), which encodes a putative membrane-embedded metalloprotease. A ΔmroQ mutant exhibits impaired induction of TLR2-dependent inflammatory responses from macrophages, but elicits greater production of the inflammatory cytokine IL-1β and is attenuated in a murine skin and soft tissue infection model. The ΔmroQ mutant phenocopies a S. aureus mutant containing a deletion of the accessory gene regulatory system (Agr), wherein both strains have significantly reduced production of secreted toxins and virulence factors, but increased surface Protein A abundance. The Agr system controls virulence factor gene expression in S. aureus through sensing accumulation of AIP via the histidine kinase AgrC and response regulator AgrA. We provide evidence to suggest that MroQ acts within the Agr pathway to facilitate optimal processing or export of AIP for signal amplification through AgrC/A and induction of virulence factor gene expression. Mutation of MroQ active site residues significantly reduces AIP signaling and attenuates virulence. Altogether, this work identifies a new component of the Agr quorum sensing circuit that is critical for the production of S. aureus virulence factors.


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