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Biomedical subjects

C Roudier

Publications and source records attributed to C Roudier.

15 recordsLinked to original sources
PubMed1999

HLA-DR polymorphism influences T-cell precursor frequencies to Epstein-Barr virus (EBV) gp110: implications for the association of HLA-DR antigens with rheumatoid arthritis.

To study whether HLA-DR haplotypes associated with susceptibility to develop rheumatoid arthritis (RA) may influence T-cell responses to the Epstein-Barr virus (EBV) gp110 (a protein of the late replicative cycle of EBV), we evaluated the frequency in peripheral blood of T cells capable to proliferate to EBV gp110 by direct limiting dilution analysis in 50 HLA-DR-typed healthy subjects. NVe found that HLA-DRB1*07, an allele associated with reduced risk to develop RA, is associated with the highest frequencies of T cells specific for gp110 in peripheral blood. In contrast, HLA-DRB1*0404, one of the susceptibility alleles is associated with the lowest frequencies of gp110 specific T cells. Finally, people expressing both HLA-DRB1*07 and HLA-DRB1*0404 display low precursor frequencies to EBV gp110.

Animals↗
PubMed1994

Effect of corticosteroids on the incidence of adverse cutaneous reactions to trimethoprim-sulfamethoxazole during treatment of AIDS-associated Pneumocystis carinii pneumonia.

We retrospectively studied all courses of treatment with trimethoprim-sulfamethoxazole (TMP-SMZ) alone and with adjuvant corticosteroids for AIDS-associated Pneumocystis carinii pneumonia. The corticosteroids were administered for 8-21 days (mean, 14 days) because of hypoxemia. We evaluated the influence of corticosteroids on the incidence of cutaneous adverse reactions to TMP-SMZ and on the course of AIDS during 3 months of follow-up. Of 38 patients treated with TMP-SMZ alone, 18 (47%) developed cutaneous side effects, whereas three (13%) of the 23 patients who received adjuvant corticosteroid therapy experienced such effects (P = .014). Of the 21 reactive patients, 14 were treated throughout the duration of hypersensitivity. Therapy was interrupted for seven patients (18%) treated with TMP-SMZ alone and for none of those who were given adjuvant corticosteroid therapy (P = .23). During follow-up, the incidence of mucocutaneous herpes simplex virus infection was higher among patients who received adjuvant corticosteroids than among those treated with TMP-SMZ alone (P = .005). Adjuvant corticosteroids thus reduce the incidence of adverse cutaneous reactions to TMP-SMZ in patients with AIDS who are treated for hypoxemic P. carinii pneumonia.

AIDS-Related Opportunistic Infections↗
PubMed1994

Adverse cutaneous reactions to trimethoprim-sulfamethoxazole in patients with the acquired immunodeficiency syndrome and Pneumocystis carinii pneumonia.

BACKGROUND AND DESIGN: Patients with the acquired immunodeficiency syndrome are predisposed to cutaneous drug reactions. The reasons are poorly understood and the circumstances in which such patients can be treated through hypersensitivity are a matter of discussion. We assessed the value of clinical and laboratory parameters for predicting trimethoprim-sulfamethoxazole-induced skin reactions and the effects of continued trimethoprim-sulfamethoxazole therapy in such patients. We retrospectively studied all episodes of nonhypoxemic Pneumocystis carinii pneumonia in patients with the acquired immunodeficiency syndrome who were treated with trimethoprim-sulfamethoxazole. RESULTS: No clinical or laboratory parameters were found to be predictive of trimethoprim-sulfamethoxazole-induced cutaneous reactions. Of 38 patients treated with trimethoprim-sulfamethoxazole, 18 (47%) developed cutaneous reactions; these occurred within a median of 11 days (range, 7 to 20 days). Of these 18 patients, 12 (67%) continued to be treated with trimethoprim-sulfamethoxazole through hypersensitivity. Trimethoprim-sulfamethoxazole treatment was continued in 19 (95%) of the 20 patients who did not develop cutaneous reactions (P = .067). The mean duration of trimethoprim-sulfamethoxazole therapy was shorter (18 days) in patients who developed skin reactions than in those who did not (20 days) (P = .016). Noncutaneous side effects accounted for all but one interruption of therapy. CONCLUSION: No clinical or laboratory parameters were found to be predictive of cutaneous reactions. By treating through hypersensitivity, 67% of our patients, who otherwise might have had to stop taking trimethoprim-sulfamethoxazole, were able to continue this essential drug therapy.

AIDS-Related Opportunistic Infections↗
PubMed1994

[Cutaneous metastasis disclosing adrenal cortical carcinoma].

Metastases to the skin from internal malignant neoplasms are uncommon and often preterminal event. Cutaneous metastases from an adrenal cortical carcinoma have rarely been reported even in the advanced stages of the disease. A patient was initially seen with a small cutaneous lesion on the cheek and was found to have a large adrenal cortical tumor. Histologic comparison proved that the cutaneous lesion was a metastase from an adrenal cortical carcinoma.

Adrenal Cortex Neoplasms↗
PubMed1992

Characterization of translation termination mutations in the spv operon of the Salmonella virulence plasmid pSDL2.

The spv region of the Salmonella virulence plasmids consists of five genes located on an 8-kb fragment previously shown to be essential for virulence in mice. Four structural genes, spvABCD, form an operon that is transcriptionally activated by the spvR gene product in the stationary phase of growth. The role of the individual spv genes in the virulence phenotype was tested by isolating translation termination linker insertions in each gene. Analysis of proteins synthesized in minicells identified each of the spvABCD gene products and confirmed the dependence of spv structural gene expression on the SpvR regulatory protein. The oligonucleotide insertions in spvA, -B, and -C were shown to be nonpolar. Virulence testing indicated that the SpvB protein, regulated by SpvR, is essential for Salmonella dublin to cause lethal disease in mice. Inserts in spvC and spvD were unstable in vivo for unknown reasons, but these mutants still killed mice at slightly higher inocula. Abolition of spvA had no effect on virulence in this system.

Bacterial Proteins↗
PubMed1992

Mechanism of resistance to complement-mediated killing of bacteria encoded by the Salmonella typhimurium virulence plasmid gene rck.

We find that pADEO16, a recombinant cosmid carrying the rck gene of the Salmonella typhimurium virulence plasmid, when cloned into either rough or smooth Escherichia coli and Salmonella strains, confers high level resistance to the bactericidal activity of pooled normal human serum. The rck gene encodes a 17-kD outer membrane protein that is homologous to a family of virulence-associated outer membrane proteins, including pagC and Ail. Complement depletion, C3 and C5 binding, and membrane-bound C3 cleavage products are similar in strains with and without rck. Although a large difference in C9 binding was not seen, trypsin cleaved 55.7% of bound 125I-C9 counts from rough S. typhimurium with pADEO16, whereas only 26.4% were released from S. typhimurium with K2011, containing a mutation in rck. The majority of C9 extracted from rck strain membranes sediments at a lower molecular weight than in strains without rck, suggesting less C9 polymerization. Furthermore, SDS-PAGE analysis of gradient peak fractions indicated that the slower sedimenting C9-containing complexes in rck strains did not contain polymerized C9 typical of the tubular membrane attack complex. These results indicate that complement resistance mediated by Rck is associated with a failure to form fully polymerized tubular membrane attack complexes.

Antibodies, Monoclonal↗
PubMed1991

Molecular analysis of the virulence locus of the Salmonella dublin plasmid pSDL2.

The virulence properties of various non-typhoid Salmonella serotypes depend on the presence of large plasmids 60-100 kb in size. We have shown previously that the virulence region on the 80 kb plasmid pSDL2 of Salmonella dublin Lane maps within a 14kb SalI fragment. In this report we show that an 8.2 kb region within this fragment is sufficient to express lethal disease in BALB/c mice. Sequence analysis of this segment revealed six sequential open reading frames designated vsdA-F, which encode putative proteins of 13-65kDa. Deletion analysis and location of Tn5-oriT inserts which abolish virulence suggest that vsdA, vsdC, vsdD and vsdE are essential for virulence expression. Downstream of vsdF we discovered a locus involved in stable plasmid maintenance. Deletion of that region resulted in plasmid multimerization and instability.

Amino Acid Sequence↗
PubMed1991

A site-specific DNA inversion in Bacteroides plasmid pBF4 is influenced by the presence of the conjugal tetracycline resistance element.

pBF4 is a 42-kb R plasmid from Bacteroides fragilis which transfers clindamycin resistance (Clr) independently of the chromosomal tetracycline resistance (Tcr) transfer element. We have found that this plasmid exists in two nonequimolar conformations, A and B. These forms differ by an inversion of approximately 11.5 kb which does not involve the repeated DNA sequences previously mapped on the plasmid. The presence of chromosomal tetracycline resistance conjugal elements influences the relative amounts of the two conformations: induction with tetracycline shifts the dominant form from B to A.

Bacteroides fragilis↗
PubMed1991

Growth regulation of a Salmonella plasmid gene essential for virulence.

The Salmonella dublin plasmid gene vsdC is essential for virulence. We have constructed a vsdC-lacZ translational fusion to demonstrate that vsdC is selectively expressed during the stationary phase of bacterial cell growth. This pattern of expression has been confirmed by mRNA hybridization studies. Carbon starvation is able to induce vsdC expression by limiting bacterial growth. The expression of vsdC is dependent upon an upstream gene, vsdA, whose gene product possesses significant amino-terminus homology with the LysR family of transcriptional activator proteins. We have further demonstrated that vsdC expression is not dependent upon the known Salmonella chromosomal virulence regulatory loci ompR, phoP, and cya-crp and that vsdC can be expressed in a range of nontyphoidal Salmonella serovars, including some serovars in which introduction of the virulence plasmid does not confer mouse virulence. The vsd system provides a model for the study of transcriptional activation, a basis for the development of new expression vectors, and a novel mechanism of virulence gene regulation. Bacterial growth limitation within the phagosomes of host phagocytic cells may be the environmental signal inducing plasmid-mediated virulence gene expression in salmonellae.

Blotting, Northern↗
PubMed1990

Correlation between the presence of sequences homologous to the vir region of Salmonella dublin plasmid pSDL2 and the virulence of twenty-two Salmonella serotypes in mice.

Large plasmids encoding important virulence properties have been found in several Salmonella serotypes. We have studied the relationship between the presence of a highly conserved 4-kilobase (kb) EcoRI fragment from the plasmid virulence region and pathogenicity for mice of 53 isolates representing 22 serotypes of Salmonella. Only strains possessing the homologous 4-kb region were virulent for mice. In addition, we transferred the virulence plasmid from S. dublin into nine different serotypes, including S. typhi and S. paratyphi A, that lack a native virulence plasmid. Only S. heidelberg and S. newport were rendered mouse virulent by the introduction of the S. dublin plasmid. This study demonstrates that plasmid-mediated virulence sequences are required for Salmonella virulence in mice, but many strains, including the agents of human typhoid fever, also lack chromosomal genes necessary to produce lethal systemic disease in mice. Since all the major Salmonella strains that are host-adapted to animals carry virulence plasmids, it appears that these plasmids are important in mediating systemic infection in animals and may contribute to septicemic, nontyphoid salmonellosis in humans.

Animals↗
PubMed1988

Physical and genetic mapping of the Salmonella dublin virulence plasmid pSDL2. Relationship to plasmids from other Salmonella strains.

Plasmids of approximately 80 kb in size are found in nearly all clinical isolates of Salmonella dublin and are believed to be essential for virulence. We have shown previously that the 80-kb plasmid pSDL2 is required for the S. dublin Lane strain to establish a lethal systemic infection in BALB/c mice after oral or intraperitoneal inoculation. We now present a physical and genetic characterization of pSDL2. We have established a complete restriction endonuclease cleavage map of pSDL2 for five enzymes: Xba I, Bam HI, Xho I, Sal I, and Hind III. The region specifying autonomous replication has been localized to a 10.5-kb region of the Sal I A fragment by subcloning on the vector pBR322. Using transposon insertion mutagenesis with Tn5-oriT, a region encoding the virulence phenotype has been mapped within a 6.4-kb portion of the Sal I B fragment. Deletions generated by partial Eco RI restriction digestion demonstrate that at least 50 kb of the plasmid DNA are not required for replication or virulence functions, confirming the map location of these phenotypes. Plasmids of different sizes and restriction patterns were found in mouse virulent strains of S. dublin Vi+, S. enteritidis, and S. choleraesuis. By Southern hybridization, these putative virulence plasmids share a common 4-kb Eco RI fragment with the virulence region of pSDL2, and the plasmids from S. dublin Vi+ and S. enteritidis were shown to express mouse virulence comparable to pSDL2.

Cloning, Molecular↗
PubMed1985

Determination of the activity on Legionella of eight macrolides and related agents by comparative testing on three media.

It has proved difficult to develop a standard method for the determination of minimum inhibitory concentrations (MICs) of antibiotics against the Legionellaceae. A major obstacle has been the inactivation of certain antibiotics by components of Charcoal Yeast Extract agar, especially charcoal. To determine the MICs of eight macrolides and related agents (erythromycin, spiramycin, oleandomycin, josamycin, midecamycin, lincomycin, clindamycin and pristinamycin) for 36 strains of Legionella, we used two charcoal-free media: Buffered Yeast Extract agar and Buffered Antibiotic Medium no. 1 (BAM1), the latter having been developed in our own laboratory. The inhibitory effect of charcoal was most marked on josamycin and pristinamycin. This effect was absent on the charcoal-free media, which both, however, inhibited spiramycin. BAM1 agar seemed the better of the two charcoal-free media as it gave more consistent growth. The most active agents were josamycin (0.06-0.25 mg/l), pristinamycin (0.06-0.5 mg/l) and erythromycin (0.12-0.5 mg/l). Midecamycin (0.12-1 mg/l) and spiramycin (1-5 mg/l) also had useful activity.

Anti-Bacterial Agents↗
PubMed1982

[Practical problems raised by antibiotic minimal inhibitory concentration determination in Legionella species (author's transl)].

Because of culture medium constitution and growth conditions of Legionella species, antibiotic Minimal inhibitory Concentration (MIC) determination is difficult and does not fit with the accepted standards. The following strains have been tested : references strains : Staphylococcus aureus Oxford CNCM 53154, S. aureus 209P CNCM 53156, E. coli CNCM A224, E. coli CNCM 7324. L. pneumophila, 9 strains representative of the 6 serogroups. L. micdadei, L. dumoffii. 5 clinical isolates of L. pneumophila serogroup 1 (3 isolated in our Laboratory and 2 in Belgium). MIC of 17 antibiotics have been determined, among them macrolids not tested before. The method used was the Agar Dilution Method, with several media compared. MIC values are different in function of the various media tested Charcoal yeast extract medium, which is recommended for Legionella growth, does not inhibit activity of penicillin G, cefalotin, cefoxitin, amikacin, erythromycin and lincosamins, in contrast of tetracyclin, gentamicin, dibekacin, chloramphenicol, oleandomycin, pristinamycin, spiramycin and rifampicin. Charcoal, ferric pyrophosphate and L-cystein present in the culture medium are inactivating factors. However our results confirm good activity of rifampicin, erythromycin, cefoxitin, chloramphenicol, gentamicin and amikacin. Among the others macrolids tested, pristinamycin is the most active.

Anti-Bacterial Agents↗