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J Delmas

Publications and source records attributed to J Delmas.

13 recordsLinked to original sources

Prediction of the evolution of ceftazidime resistance in extended-spectrum beta-lactamase CTX-M-9.

A random mutagenesis technique was used to predict the evolutionary potential of beta-lactamase CTX-M-9 toward the acquisition of improved catalytic activity against ceftazidime. Thirty CTX-M mutants were obtained during three rounds of mutagenesis. These mutants conferred 1- to 128-fold-higher MICs of ceftazidime than the parental enzyme CTX-M-9. The CTX-M mutants contained one to six amino acid substitutions. Mutants harbored the substitutions Asp240Gly and Pro167Ser, which were previously observed in clinical CTX-M enzymes. Additional substitutions, notably Arg164His, Asp179Gly, and Arg276Ser, were observed near the active site. The kinetic constants of the three most active mutants revealed two distinct ways of improving catalytic efficiency against ceftazidime. One enzyme had a 17-fold-higher k(cat) value than CTX-M-9 against ceftazidime. The other two had 75- to 300-fold-lower Km values than CTX-M-9 against ceftazidime. The current emergence of CTX-M beta-lactamases with improved activity against ceftazidime may therefore be the beginning of an evolutionary process which might subsequently generate a great diversity of CTX-M-type ceftazidimases.

Ceftazidime↗

[VCA agar (bioMérieux) for selective isolation of vancomycin-resistant Enterococci (VRE) from fecal specimens].

Screening for Vancomycin Resistant Enterococci (VRE) is recommended for preventing nosocomial infections with VRE. The aim of this study was to assess the performance of VCA3 agar (bioMérieux) in VRE isolation from fecal specimens. 220 specimens were cultured on VCA3 agar, which contains vancomycin and in parallel, on CAP agar (Oxoid), which is vancomycin-free. 36 vancomycin resistant enterococci were isolated: 24 isolates of Enterococcus faecium expressed a high-level resistance to vancomycin and 12 isolates of E. gallinarum/casseliflavus exhibited resistance at low-level. The sensitivity of VCA3 appeared greater than that of CAP for VRE isolation: 92% (22/24) vs 79% (19/24) for E. faecium (NS, P>0.05) ; 83% (10/12) vs 50% (6/12) for E. gallinarum/casselliflavus (NS, P>0.05). As expected, initial cultures of multiple gram positive organisms were far more frequent on CAP agar than on VCA3 agar. The isolation rate of vancomycin susceptible gram positive strains was impressively lower on VCA3 medium than on CAP medium. VCA3 agar avoided therefore additional subcultures, useless identification and susceptibility tests. In conclusion, VCA3 medium could be useful for the direct, rapid and selective isolation of VRE from fecal specimens.

Cross Infection↗

[Necrotizing bacterial skin and software tissue infection with muscular involvement revealing of cancer of the colon].

We report the case of a 38-year-old woman with a necrotizing bacterial skin and soft tissue infection with muscular involvement. The clinical picture was similar to a gaseous gangrene of the right lower limb with a septic shock and multiple organ failure, without predisposing factor such as trauma, and necessitating a hip amputation. The primary site of the disease was a perforated colic adenocarcinoma with peritoneal and retroperitoneal infection. The association of necrotizing skin and soft tissue infection with muscular involvement due to Clostridium septicum to a neoplasma is classical and in front of such an infection a neoplasma should be researched.

Adenocarcinoma↗

Unexpected enzyme TEM-126: role of mutation Asp179Glu.

The clinical isolate Escherichia coli CF884 exhibited low-level resistance to ceftazidime (4 mug/ml) by a positive double-disk synergy test and apparent susceptibility to cefuroxime, cefotaxime, cefepime, cefpirome, and aztreonam. The enzyme implicated in this phenotype was a novel 180-kb plasmid-encoded TEM-type extended-spectrum beta-lactamase designated TEM-126 which harbors the mutations Asp179Glu and Met182Thr. TEM-126 exhibited significant hydrolytic activity (k(cat), 2 s(-1)) and a K(m) value of 82 muM against ceftazidime. Molecular dynamics simulations suggested that the substitution Asp179Glu induces subtle conformational changes to the omega loop which may favor the insertion of ceftazidime in the binding site and the correct positioning of the crucial residue Glu166. Overall, these results highlight the remarkable plasticity of TEM enzymes, which can expand their activity against ceftazidime by the addition of one carbon atom in the side chain of residue 179.

Amino Acid Sequence↗

TEM-109 (CMT-5), a natural complex mutant of TEM-1 beta-lactamase combining the amino acid substitutions of TEM-6 and TEM-33 (IRT-5).

Escherichia coli CF349 exhibited a complex beta-lactam resistance phenotype, including resistance to amoxicillin and ticarcillin alone and in combination with clavulanate and to some extended-spectrum cephalosporins. The double-disk synergy test was positive. CF349 harbored an 85-kb conjugative plasmid which encoded a beta-lactamase of pI 5.9. The corresponding bla gene was identified by PCR and sequencing as a bla(TEM) gene. The deduced protein sequence revealed a new complex mutant of TEM-1 beta-lactamase designated TEM-109 (CMT-5). TEM-109 contained both the substitutions Glu104Lys and Arg164His of the expanded-spectrum beta-lactamase (ESBL) TEM-6 and Met69Leu of the inhibitor-resistant TEM-33 (IRT-5). TEM-109 exhibited hydrolytic activity against ceftazidime similar to that of TEM-6 (k(cat), 56 s(-1) and 105 s(-1), respectively; K(m) values, 226 and 247 microM, respectively). The 50% inhibitory concentrations of clavulanate and tazobactam (0.13 microM and 0.27 microM, respectively) were 5- to 10-fold higher for TEM-109 than for TEM-6 (0.01 and 0.06 microM, respectively) but were almost 10-fold lower than those for TEM-33. The characterization of this novel CMT, which exhibits a low level of resistance to inhibitors, highlights the emergence of this new ESBL type.

Amino Acid Substitution↗

[Splenic rupture and anticoagulant therapy].

Splenic rupture associated with anticoagulant therapy is a rare entity. We report a case of spontaneous splenic rupture in a 62-year-old man who was treated by acenocoumarol orally after an aortic-valve replacement. Unrecognised, minor trauma may lead to splenic haemorrhage in patients receiving anticoagulant therapy. The symptoms and signs may mimic those of acute myocardial infarction and cardiogenic shock. Early diagnosis is essential. Reversal of the anticoagulant and emergent splenectomy are the treatments of choice.

Acenocoumarol↗

[Angiography of hepatic angiomatosis in Rendu-Osler disease. Apropos of 3 cases].

The hepatic changes in hereditary hemorrhagic telangiectasia (Rendu Osler's disease) involve the extra- and intrahepatic vessels (enlarged hepatic artery, arteriovenous fistulas and inhomogeneous perfusion) and the hepatic parenchyma (fibrosis, telangiectasic cirrhosis). From three observations with liver involvement and imaged with angiography and dynamic CT, the authors emphasize on the role of the latter for detection of these changes, mostly arteriovenous fistulas.

Adult↗

[Not Available].

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Child Welfare↗