High-level resistance to mecillinam produced by inactivation of soluble lytic transglycosylase in Salmonella enterica serovar Typhimurium

2006 ◽  
Vol 256 (2) ◽  
pp. 311-317 ◽  
Author(s):  
Cristina S. Costa ◽  
Dora N. Antón
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Lytic Transglycosylase ◽  
Serovar Typhimurium ◽  
High Level ◽  
Level Resistance

scholarly journals Multiple Outbreaks of Nosocomial Salmonellosis in Russia and Belarus Caused by a Single Clone of Salmonella enterica Serovar Typhimurium Producing an Extended-Spectrum β-Lactamase

2004 ◽  
Vol 48 (8) ◽  
pp. 2808-2815 ◽  
Author(s):  
M. Edelstein ◽  
M. Pimkin ◽  
T. Dmitrachenko ◽  
V. Semenov ◽  
N. Kozlova ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Extended Spectrum ◽  
Serovar Typhimurium ◽  
Single Clone ◽  
Clonal Origin ◽  
Resistance To Penicillin ◽  
Arbitrarily Primed Pcr ◽  
High Level ◽  
Level Resistance

ABSTRACT Thirty-four cefotaxime-resistant Salmonella enterica serovar Typhimurium isolates representative of the isolates that caused outbreaks of gastroenteritis in 10 hospitals in seven regions of Russia and Belarus from 1994 to 2003 were analyzed. All isolates produced the CTX-M-5-like extended-spectrum β-lactamase, which confers high-level resistance to cefotaxime and ceftriaxone and decreased susceptibility to ceftazidime. The bla CTX-M genes were located on small (7.4- to 12-kb) non-self-transferable plasmids approximately 20 bp downstream of the ISEcp1 insertion sequences. Some isolates carried additional conjugative plasmids mediating resistance to penicillin-inhibitor combinations and various non-β-lactam agents, including tetracycline, chloramphenicol, gentamicin, tobramycin, and co-trimoxazole. Despite the minor differences in susceptibility patterns, all isolates were considered clonally related on the basis of arbitrarily primed PCR and pulsed-field gel electrophoresis analysis. The similarities of the restriction profiles of the CTX-M-coding plasmids further supported the clonal origin of these isolates.

scholarly journals Characterization of a Laboratory-Derived, High-Level Ampicillin-Resistant Salmonella enterica Serovar Typhimurium Strain That Caused Meningitis in an Infant

2002 ◽  
Vol 46 (5) ◽  
pp. 1604-1606 ◽  
Author(s):  
Cheng-Hsun Chiu ◽  
Chishih Chu ◽  
Lin-Hui Su ◽  
Wan-Yu Wu ◽  
Tsu-Lan Wu
Keyword(s):  
Cerebrospinal Fluid ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Cloning Vector ◽  
Typhimurium Strain ◽  
Serovar Typhimurium ◽  
High Level ◽  
Lactamase Gene

ABSTRACT A Salmonella enterica serovar Typhimurium strain that harbored a plasmid carrying a TEM-1-type β-lactamase gene was isolated from the blood and cerebrospinal fluid of an infant with meningitis. This 3.2-kb plasmid was further characterized to be a nonconjugative pGEM series cloning vector containing a foreign insert. The strain was likely laboratory derived and contaminated the environment before it caused the infection.

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 Roles of hilC and hilD in Regulation of hilA Expression in Salmonella enterica Serovar Typhimurium

2001 ◽  
Vol 183 (9) ◽  
pp. 2733-2745 ◽  
Author(s):  
Robin L. Lucas ◽  
Catherine A. Lee
Keyword(s):  
Environmental Conditions ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Pathogenicity Island ◽  
Transcriptional Regulators ◽  
Regulatory Factors ◽  
Serovar Typhimurium ◽  
High Level

ABSTRACT Sequences between −332 and −39 upstream of the hilApromoter are required for repression of hilA. An unidentified repressor is thought to bind these upstream repressing sequences (URS) to inhibit hilA expression. Two AraC-like transcriptional regulators encoded on Salmonellapathogenicity island 1 (SPI1), HilC and HilD, bind to the URS to counteract the repression of hilA. The URS is required for regulation of hilA by osmolarity, oxygen, PhoP/PhoQ, and SirA/BarA. Here, we show that FadD, FliZ, PhoB, and EnvZ/OmpR also require the URS to regulate hilA. These environmental and regulatory factors may affect hilA expression by altering the expression or activity of HilC, HilD, or the unknown repressor. To begin investigating these possibilities, we tested the effects of environmental and regulatory factors on hilC andhilD expression. We also examined hilAregulation when hilC or hilD was disrupted or expressed to a high level. Although hilC is regulated by all environmental conditions and regulatory factors that modulatehilA expression, hilC is not required for the regulation of hilA by any conditions or factors except EnvZ/OmpR. In contrast, hilD is absolutely required forhilA expression, but environmental conditions and regulatory factors have little or no effect on hilDexpression. We speculate that EnvZ/OmpR regulates hilA by altering the expression and/or activity of hilC, while all other regulatory conditions and mutations regulate hilA by modulating hilD posttranscriptionally. We also discuss models in which the regulation of hilA expression is mediated by modulation of the expression or activity of one or more repressors.

scholarly journals RamA, a Member of the AraC/XylS Family, Influences Both Virulence and Efflux in Salmonella enterica Serovar Typhimurium

2010 ◽  
Vol 192 (6) ◽  
pp. 1607-1616 ◽  
Author(s):  
Andrew M. Bailey ◽  
Al Ivens ◽  
Rob Kingsley ◽  
Jennifer L. Cottell ◽  
John Wain ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Target Genes ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Consensus Sequence ◽  
Altered Expression ◽  
Expression Of Genes ◽  
Mouse Macrophages ◽  
Serovar Typhimurium ◽  
Genes Encoding ◽  
High Level

ABSTRACT The transcriptomes of Salmonella enterica serovar Typhimurium SL1344 lacking a functional ramA or ramR or with plasmid-mediated high-level overexpression of ramA were compared to those of the wild-type parental strain. Inactivation of ramA led to increased expression of 14 SPI-1 genes and decreased expression of three SPI-2 genes, and it altered expression of ribosomal biosynthetic genes and several amino acid biosynthetic pathways. Furthermore, disruption of ramA led to decreased survival within RAW 264.7 mouse macrophages and attenuation within the BALB/c ByJ mouse model. Highly overexpressed ramA led to increased expression of genes encoding multidrug resistance (MDR) efflux pumps, including acrAB, acrEF, and tolC. Decreased expression of 34 Salmonella pathogenicity island (SPI) 1 and 2 genes, decreased SipC production, decreased adhesion to and survival within macrophages, and decreased colonization of Caenorhabditis elegans were also seen. Disruption of ramR led to the increased expression of ramA, acrAB, and tolC, but not to the same level as when ramA was overexpressed on a plasmid. Inactivation of ramR had a more limited effect on pathogenicity gene expression. In silico analysis of a suggested RamA-binding consensus sequence identified target genes, including ramR, acrA, tolC, sipABC, and ssrA. This study demonstrates that the regulation of a mechanism of MDR and expression of virulence genes show considerable overlap, and we postulate that such a mechanism is dependent on transcriptional activator concentration and promoter sensitivity. However, we have no evidence to support the hypothesis that increased MDR via RamA regulation of AcrAB-TolC gives rise to a hypervirulent strain.

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