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Cesar A Arias

Publications and source records attributed to Cesar A Arias.

11 recordsLinked to original sources
PubMed2026

First-line fecal microbiota transplantation for the management of immune checkpoint inhibitor-mediated diarrhea and colitis.

Immune checkpoint inhibitor (ICI) therapy commonly leads to adverse events such as ICI-mediated diarrhea and colitis (IMDC). Fecal microbiota transplantation (FMT) remains an option for patients with refractory colitis. We report a multi-omics profiling of patients receiving first-line FMT for IMDC. In our preliminary analysis, 10 (76.9%) patients achieve clinical response, with a median time to clinical improvement of 1.5 (1-10.5) days. Among responder patients with baseline and follow-up samples, 6 (75%) show an increase in alpha-diversity post-FMT. Pre-FMT samples show an increase in the abundance scores of plasma cells, neutrophils, macrophages (M1 and M2), memory activated and resting memory CD4+ T cells, CD8+ T cells, T follicular helper (Tfh) cells, and regulatory T cells (Tregs), all of which decrease post-FMT. In a small cohort of patients, we identify potential mechanisms for FMT response and demonstrate that first-line FMT in patients with IMDC (NCT04038619) can be effective.

FMT↗
PubMed2026

A Duty to Act.

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healthcare↗
PubMed2026

A Duty to Act.

Explore the source record for details and available documents.

healthcare↗
PubMed2026

Loss of O-antigen due to wbbL mutations is common and associated with increased mortality in Escherichia coli bloodstream infections.

Escherichia coli bloodstream infections are common and associated with high mortality. A key feature of E. coli is the lipopolysaccharide (LPS) O-antigen, which contributes to immune evasion during invasive infection. We analyzed serial isolates from patients with relapsed E. coli bacteremia and identified frequent disruption of O-antigen synthesis due to mutations in wbbL, resulting in a rough LPS phenotype. Rough LPS isolates were more serum sensitive and less pathogenic in mice. Despite this apparent attenuation, 11 of 61 (18%) E. coli sequence type 131 bloodstream isolates in our cohort harbored disruptive wbbL mutations and were associated with significantly worse clinical outcomes, including septic shock and mortality. Using a murine model of recurrent bacteremia, we show that rough LPS isolates partially evade protective immunity generated against smooth LPS E. coli, highlighting the importance of host immune context in invasive disease.

O Antigens↗
PubMed2006

Rapid identification of Enterococcus hirae and Enterococcus durans by PCR and detection of a homologue of the E. hirae mur-2 Gene in E. durans.

During an evaluation of PCR for identification of isolates of Enterococcus hirae, a homologue with 82% identity to E. hirae mur-2 was identified in Enterococcus durans and was named mur-2(ed). PCR using primers for two genes (copY and murG) of E. hirae strains showed amplification with E. hirae strains only. PCR (under high-stringency conditions) with primers for the mur-2(ed) gene gave the expected amplification product only with E. durans strains. A combination of murG and mur-2(ed) primers in a multiplex PCR assay differentiated E. hirae from E. durans in all cases. PCR using these primers appears to be a rapid alternative for identification of E. hirae and E. durans isolates.

Bacterial Outer Membrane Proteins↗
PubMed2005

Transcriptional analysis of the vanC cluster from Enterococcus gallinarum strains with constitutive and inducible vancomycin resistance.

The vanC glycopeptide resistance gene cluster encodes enzymes required for synthesis of peptidoglycan precursors ending in D-Ala-D-Ser. Enterococcus gallinarum BM4174 and SC1 are constitutively and inducibly resistant to vancomycin, respectively. Analysis of peptidoglycan precursors in both strains indicated that UDP-MurNAc-tetrapeptide and UDP-MurNAc-pentapeptide[D-Ser] were synthesized in E. gallinarum SC1 only in the presence of vancomycin (4 microg/ml), whereas the "resistance" precursors accumulated in the cytoplasm of BM4174 cells under both inducing and noninducing conditions. Northern hybridization and reverse transcription-PCR experiments revealed that all the genes from the cluster, vanC-1, vanXY(C), vanT, vanR(C), and vanS(C), were transcribed from a single promoter. In the inducible SC1 isolate, transcriptional regulation appeared to be responsible for inducible expression of resistance. Promoter mapping in E. gallinarum BM4174 revealed that the transcriptional start site was located 30 nucleotides upstream from vanC-1 and that the -10 promoter consensus sequence had high identity with that of the vanA cluster. Comparison of the deduced sequence of the vanS(C) genes from isolates with constitutive and inducible resistance revealed several amino acid substitutions located in the X box (R200L) and in the region between the F and G2 boxes (D312N, D312A, and G320S) of the putative sensor kinase proteins from isolates with constitutive resistance.

Amino Acid Sequence↗
PubMed2003

Tolerance to vancomycin in a multiresistant, Colombian isolate of Streptococcus pneumoniae.

The present study was set up to determine vancomycin tolerance in Colombian, multiresistant, invasive, paediatric isolates of Streptococcus pneumoniae. A total of seven clinical isolates of penicillin-resistant S. pneumoniae, serotype 14, corresponding to the Spain(9v)-3 clone, were studied. Isolates were grown in Todd Hewitt broth at 37 degrees C. Growth (A(595)) and cell viability (cfu/ml) were monitored hourly for 4 h after addition of vancomycin at 10x MIC. S. pneumoniae R6 was used as a control for growth. For R6, the mean decrease in A(595) and cell viability (log(10) cfu/ml) after 4 h of vancomycin treatment (in 10 independent experiments) was 95.1% and 4.2 log(10), respectively. Six out of seven isolates exhibited similar behaviour. In contrast, for S. pneumoniae E239, the mean decrease in A(595) and cell viability was 48.5% and 2.2 log(10) after 4 h of vancomycin exposure, which suggested the presence of tolerance to vancomycin. The emergence of vancomycin-tolerant strains is of great concern in Colombia, owing to the alarming increase in resistance to penicillin.

Colombia↗
PubMed2003

Surveillance of surgical site infections: decade of experience at a Colombian tertiary care center.

A protocol for surveillance of surgical site infections (SSIs) was established in a tertiary care center in 1991 in Bogota, Colombia and followed for 10 years. Wounds were classified according to the Centers for Disease Control guidelines. The National Nosocomial Infection Surveillance and Study of the Efficacy of Nosocomial Infection Control scores for risk factors were included from June 1999. A total of 33027 surgical procedures were followed by the surveillance team. The overall infection rate was 2.6%. Most surgical procedures (70.6%) were classified as clean; 25.3%, 3.8%, and 0.26% were classified as clean/contaminated, contaminated, and dirty, respectively. Infection rates according to wound classification were 1.28%, 3.9%, 15.4%, and 38.4% for clean, clean/contaminated, contaminated, and dirty procedures, respectively. Escherichia coli and coagulase-negative staphylococci were the most frequently isolated microorganisms from SSI: 23.9% and 22.8% of isolates, respectively. A program of surveillance of SSIs has been successfully implemented in a country with limited resources and has maintained the infection rate within international standards.

Colombia↗
PubMed2002

D-Ala:D-Ala ligase gene flanking the vanC cluster: evidence for presence of three ligase genes in vancomycin-resistant Enterococcus gallinarum BM4174.

An open reading frame located 230 nucleotides downstream from the stop codon of vanS(c) and in the opposite direction relative to the other genes of the vanC cluster was identified in Enterococcus gallinarum BM4174. This gene (designated ddl2) encoded a protein of 343 amino acids that had significant predicted structural similarity to D-Ala:D-Ala ligases and displayed 33 and 35% amino acid identity to VanC-1 and the previously reported partial sequence of Ddl from E. gallinarum, respectively. Biochemical characterization by thin-layer chromatography confirmed that Ddl2 is a D-Ala:D-Ala ligase with no detectable D-Ala:D-Ser ligase activity. The vancomycin dependence of Enterococcus faecalis BM4320 (ddl mutant) was lost on electroporation of a plasmid construct expressing ddl2 constitutively. The latter strain was able to grow in the absence of vancomycin, and peptidoglycan precursor analysis under the same conditions indicated the synthesis of pentapeptide[D-Ala] as the main precursor, confirming the activity of Ddl2 in vivo. Expression of ddl and ddl2 in BM4174 was tested by reverse transcription-PCR: results suggested that both D-Ala:D-Ala ligases were expressed concomitantly. Our findings indicate that vancomycin-resistant E. gallinarum BM4174 is likely to express one D-Ala:D-Ser and two D-Ala:D-Ala ligase genes.

Amino Acid Sequence↗
PubMed2000

Serine and alanine racemase activities of VanT: a protein necessary for vancomycin resistance in Enterococcus gallinarum BM4174.

Vancomycin resistance in Enterococcus gallinarum results from the production of UDP-MurNAc-pentapeptide[D-Ser]. VanT, a membrane-bound serine racemase, is one of three proteins essential for this resistance. To investigate the selectivity of racemization of L-Ser or L-Ala by VanT, a strain of Escherichia coli TKL-10 that requires D-Ala for growth at 42 degrees C was used as host for transformation experiments using plasmids containing the full-length vanT from Ent. gallinarum or the alanine racemase gene (alr) of Bacillus stearothermophilus: both plasmids were able to complement E. coli TKL-10 at 42 degrees C. No alanine or serine racemase activities were detected in the host strain E. coli TKL-10 grown at 30, 34 or 37 degrees C. Serine and alanine racemase activities were found almost exclusively (96%) in the membrane fraction of E. coli TKL-10/pCA4(vanT): the alanine racemase activity of VanT was 14% of the serine racemase activity in both E. coli TKL-10/pCA4(vanT) and E. coli XL-1 Blue/pCA4(vanT). Alanine racemase activity was present mainly (95%) in the cytoplasmic fraction of E. coli TKL-10/pJW40(alr), with a trace (1.6%) of serine racemase activity. Additionally, DNA encoding the soluble domain of VanT was cloned and expressed in E. coli M15 as a His-tagged polypeptide and purified: this polypeptide also exhibited both serine and alanine racemase activities; the latter was approximately 18% of the serine racemase activity, similar to that of the full-length, membrane-bound enzyme. N-terminal sequencing of the purified His-tagged polypeptide revealed a single amino acid sequence, indicating that the formation of heterodimers between subunits of His-tagged C-VanT and endogenous alanine racemases from E. coli was unlikely. The authors conclude that the membrane-bound serine racemase VanT also has alanine racemase activity but is able to racemize serine more efficiently than alanine, and that the cytoplasmic domain is responsible for the racemase activity.

Alanine Racemase↗