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At least 199 records · Page 11Linked to original sources
PubMed2003

Shiga toxin-producing Escherichia coli in Montana: bacterial genotypes and clinical profiles.

The diseases and virulence genes associated with Shiga toxin-producing Escherichia coli (STEC) are characterized incompletely. We analyzed, by polymerase chain reaction, 82 STEC isolates collected prospectively in Montana and profiled associated illnesses by patient chart review. All E. coli O157:H7 contained stx2-group genes, as well as eae, iha, espA, and ehxA; 84% contained stx1. Non-O157:H7 STEC less frequently contained stx1 (P=.046), stx2 (P<.001), iha (P<.001), eae, and espA (P=.039 for both), were isolated less often from patients treated in emergency departments (P=.022), and tended to be associated less frequently with bloody diarrhea (P=.061). There were no significant associations between stx genotype and bloody diarrhea, but isolates containing stx2c or stx(2d-activatable) were recovered more often from patients who underwent diagnostic or therapeutic procedures (P=.033). Non-O157:H7 STEC are more heterogeneous and cause bloody diarrhea less frequently than do E. coli O157:H7. Bloody diarrhea cannot be attributed simply to the stx genotype of the infecting organism.

Adolescent↗
PubMed2002

Evaluation of DNA polymorphisms amplified by arbitrary primers (RAPD) as genetically associated elements to differentiate virulent and non-virulent Paracoccidioides brasiliensis isolates.

Randomly amplified polymorphic DNA (RAPD) analysis of 35 Paracoccidioides brasiliensis isolates was carried out to evaluate the correlation of RAPD profiles with the virulence degree or the type of the clinical manifestations of human paracoccidioidomycosis. The dendrogram presented two main groups sharing 64% genetic similarity. Group A included two isolates from patients with chronic paracoccidioidomycosis; group B comprised the following isolates showing 65% similarity: two non-virulent, six attenuated, five virulent, eight from patients with chronic paracoccidioidomycosis and two from patients with acute paracoccidioidomycosis. The virulent Pb18 isolate and six attenuated or non-virulent samples derived from it were genetically indistinguishable (100% of similarity). Thus, in our study, RAPD patterns could not discriminate among 35 P. brasiliensis isolates according to their differences either in the degree of virulence or in the type of the clinical manifestation of this fungal infection.

Animals↗
PubMed2004

Occurrence of virulence-associated genes in clinical Enterococcus faecalis strains isolated in Londrina, Brazil.

Epidemiological studies have reinforced the importance of Enterococcus faecalis in causing serious infections, and to date, our understanding of how certain virulence factors are involved in the pathogenesis of enterococcal infections is still limited. The aim of the present study was to examine the occurrence of known virulence determinants in a group of E. faecalis strains isolated from different clinical sources in Brazil. A total of 95 E. faecalis strains were investigated for the presence of nine virulence genes including aggA, cylA, cylB, cylM, eep, efaA, enlA, esp and gelE by using PCR. The data showed a relatively wide distribution of the virulence genes among the investigated strains. The clinical strains carried at least one and concomitantly up to as many as eight virulence markers, with two or three being the most common pattern. Most of the strains carried efaA (58.9 %), eep (58.9 %) and esp (57.9 %) genes, whereas the remaining virulence markers were detected in variable percentages ranging from 9.5 to 45 %. Simultaneous presence of virulence markers was observed among clinical strains regardless of their sources. In this study, the efaA+ esp+ gelE+ profile was the virulence genotype most frequently detected among E. faecalis strains. Finally, there was no significant association between virulence markers and clinical sources.

Antigens, Bacterial↗
PubMed2006

Comparative analysis of growth-phase-dependent gene expression in virulent and avirulent Streptococcus pneumoniae using a high-density DNA microarray.

The global pattern of growth-dependent gene expres-sion in Streptococcus pneumoniae strains was evalu-ated using a high-density DNA microarray. Total RNAs obtained from an avirulent S. pneumoniae strain R6 and a virulent strain AMC96-6 were used to compare the expression patterns at seven time points (2.5, 3.5, 4.5, 5.5, 6.0, 6.5, and 8.0 h). The expression profile of strain R6 changed between log and station-ary growth (the Log-Stat switch). There were clear differences between the growth-dependent gene ex-pression profiles of the virulent and avirulent pneumo-coccal strains in 367 of 1,112 genes. Transcripts of genes associated with bacterial competence and capsular polysaccharide formation, as well as clpP and cbpA, were higher in the virulent strain. Our data suggest that late log or early stationary phase may be the most virulent phase of S. pneumoniae.

Gene Expression Profiling↗
PubMed2026

Genomic Characterization of Aeromonas dhakensis Isolated From a Fatal Dolphin Case.

Aeromonas dhakensis has emerged as a significant pathogen affecting both aquatic animals and humans; however, genomic data for isolates from marine mammals remain scarce. In this study, we characterised the genome of A. dhakensis strain KDL-001, isolated from a fatal dolphin case, using whole-genome sequencing and comparative genomics. Taxonomic analyses, including MLST and average nucleotide identity (ANI), confirmed the isolate as A. dhakensis. Core-genome phylogeny further revealed that KDL-001 is closely related to strains derived from fish and aquatic environments. Notably, in silico screening of virulence-associated genes showed that the virulence-associated gene profile of the dolphin isolate was broadly comparable to those of other A. dhakensis strains, with no isolate-specific virulence-associated genes being identified within the limits of this analysis. These findings demonstrate that the dolphin-derived isolate is genomically comparable to previously described A. dhakensis strains and possesses conserved virulence-associated genes commonly found within the species.

Animals↗
PubMed2006

Quorum sensing affects virulence-associated proteins F1, LcrV, KatY and pH6 etc. of Yersinia pestis as revealed by protein microarray-based antibody profiling.

Protein microarray that consists of virulence-associated proteins of Yersinia pestis is used to compare antibody profiles elicited by the wild-type and quorum sensing (QS) mutant strain of this bacterium to define the immunogens that are impacted by QS. The results will lead the way for future functional proteomics studies. The antibody profile that was induced by the QS mutant differed from that of the parent strain. Detailed comparison of the antibody profiles, according to the proteins' functional annotations, showed that QS affects the expression of many virulence-associated proteins of Y. pestis. The antibodies to many virulence-associated proteins were not detected or lower titers of antibodies to many proteins were detected in the sera of rabbits immunized with the QS mutant, relative to those of the wild type, which indicated that these proteins were not expressed or expressed at relatively lower levels in the QS mutant. The results demonstrated that antibody profiling by protein microarrays is a promising high-throughput method for revealing the interactions between pathogens and the host immune system.

Animals↗
PubMed2001

Nef triggers a transcriptional program in T cells imitating single-signal T cell activation and inducing HIV virulence mediators.

Gene expression profiling was used to explore the role of Nef in HIV. Nef induces a transcriptional program in T cells that is 97% identical to that of anti-CD3 T cell activation. This program is inhibited in the presence of cyclosporin. A requirement for TCR zeta and ZAP-70 is demonstrated for formation of the complete profile. Among eight factors particular to the anti-CD3 activation profile are IL16 and YY1, negative regulators of HIV transcription. In contrast, Nef exclusively upregulates factors positively regulating HIV, including Tat-SF1, U1 SNRNP, and IRF-2. New genes associated with Nef include CDK9, the induction of which enhances Tat function. Thus, Nef acts as a master switch early in the viral life cycle, forcing an environment conducive to dynamic viral production.

Cyclin-Dependent Kinase 9↗
PubMed1980

Minor base sequence differences between the genomes of two strains of murine cytomegalovirus differing in virulence.

Two strains of murine cytomegalovirus (MCMV), differing in virulence towards mice, were compared for possible genetic differences. The two strains behaved identically in cell cultures, although the virulent strain gave higher yields of infectious virus in salivary glands. The viral DNAs displayed identical reassociation kinetics, but minor differences in their base sequences were revealed by restriction endonuclease profiles. The endonuclease profile of the "virulent" strain was conserved during serial high multiplicity infection in vitro.

Animals↗
PubMed2005

Insights on evolution of virulence and resistance from the complete genome analysis of an early methicillin-resistant Staphylococcus aureus strain and a biofilm-producing methicillin-resistant Staphylococcus epidermidis strain.

Staphylococcus aureus is an opportunistic pathogen and the major causative agent of numerous hospital- and community-acquired infections. Staphylococcus epidermidis has emerged as a causative agent of infections often associated with implanted medical devices. We have sequenced the approximately 2.8-Mb genome of S. aureus COL, an early methicillin-resistant isolate, and the approximately 2.6-Mb genome of S. epidermidis RP62a, a methicillin-resistant biofilm isolate. Comparative analysis of these and other staphylococcal genomes was used to explore the evolution of virulence and resistance between these two species. The S. aureus and S. epidermidis genomes are syntenic throughout their lengths and share a core set of 1,681 open reading frames. Genome islands in nonsyntenic regions are the primary source of variations in pathogenicity and resistance. Gene transfer between staphylococci and low-GC-content gram-positive bacteria appears to have shaped their virulence and resistance profiles. Integrated plasmids in S. epidermidis carry genes encoding resistance to cadmium and species-specific LPXTG surface proteins. A novel genome island encodes multiple phenol-soluble modulins, a potential S. epidermidis virulence factor. S. epidermidis contains the cap operon, encoding the polyglutamate capsule, a major virulence factor in Bacillus anthracis. Additional phenotypic differences are likely the result of single nucleotide polymorphisms, which are most numerous in cell envelope proteins. Overall differences in pathogenicity can be attributed to genome islands in S. aureus which encode enterotoxins, exotoxins, leukocidins, and leukotoxins not found in S. epidermidis.

Biofilms↗
PubMed2001

Streptococcus iniae virulence is associated with a distinct genetic profile.

Streptococcus iniae causes meningoencephalitis and death in commercial fish species and has recently been identified as an emerging human pathogen producing fulminant soft tissue infection. As identified by pulsed-field gel electrophoresis (PFGE), strains causing disease in either fish or humans belong to a single clone, whereas isolates from nondiseased fish are genetically diverse. In this study, we used in vivo and in vitro models to examine the pathogenicity of disease-associated isolates. Strains with the clonal (disease-associated) PFGE profile were found to cause significant weight loss and bacteremia in a mouse model of subcutaneous infection. As little as 10(2) CFU of a disease-associated strain was sufficient to establish bacteremia, with higher inocula (10(7)) resulting in increased mortality. In contrast, non-disease-associated (commensal) strains failed to cause bacteremia and weight loss, even at inocula of 10(8) CFU. In addition, disease-associated strains were more resistant to phagocytic clearance in a human whole blood killing assay compared to commensal strains, which were almost entirely eradicated. Disease-associated strains were also cytotoxic to human endothelial cells as measured by lactate dehydrogenase release from host cells. However, both disease-associated and commensal strains adhered to and invaded cultured human epithelial and endothelial cells equally well. While cellular invasion may still contribute to the pathogenesis of invasive S. iniae disease, resistance to phagocytic clearance and direct cytotoxicity appear to be discriminating virulence attributes of the disease-associated clone.

Animals↗
PubMed2025

Mycobacterium tuberculosis complex Lineage 1: A neglected cause of tuberculosis.

The Mycobacterium tuberculosis complex (MTBC) phylogenetic lineages 1-4 (L1-L4) are the main causes of human tuberculosis (TB). Until now, most of the focus in the TB field has been on MTBC L2 and L4, as these two lineages are geographically widespread and have been repeatedly associated with multidrug resistance. By comparison, MTBC L1 has received little attention, partially because of its restricted geographical range that mainly includes low- to middle-income countries in South and Southeast Asia, and East Africa. However, recent estimates indicate that MTBC L1 is in fact the most common cause of human TB in terms of absolute numbers of TB patients, particularly among several high TB burden countries. As more L1 strains are being sampled in L1-endemic countries, the high genetic diversity of this geographically restricted MTBC lineage is slowly uncovered. This discovery has also impacted L1 nomenclature, which has been modified as new distinct L1 clades were identified. In parallel to the genomic discoveries ushered by progress in whole genome sequencing, clinical researchers have also studied several phenotypes that better describe L1 TB disease. L1 strains have been shown to have increased vulnerability to oxidative stress, which was associated with decreased virulence in animal and in vitro models. L1 infection also shows possible association with extrapulmonary TB and asymptomatic TB. However, despite belonging to the same lineage, L1 strains display phenotypic diversity that can be attributed to high within-lineage genetic diversity and possibly the interaction of different L1 genotypes with different human host genotypes. Among the clinical phenotypes that show heterogeneity are bacterial factors, immune profiles, and clinical virulence. The traditional view regarding the reduced transmissibility in L1 is now being challenged by new data indicating that L1 may be as transmissible as L2 or L4. Lastly, although historically referred to as being negatively associated with drug resistance, there is indication that the contribution of L1 to TB drug resistance is significant and that it may evolve drug resistance in ways distinct from those of other MTBC lineages.

Mycobacterium tuberculosis↗
PubMed2002

Comparative profiles of intramacrophage behavior of Mycobacterium tuberculosis and Mycobacterium avium complex with different levels of virulence.

Mycobacterium tuberculosis (MTB) and M. avium complex (MAC) strains with different levels of virulence in mice were examined for profiles of interaction with murine peritoneal macrophages (Mphis). Their growth rates in Mphis were in these orders: H37Ra strain (attenuated) > H37Rv strain (virulent) for MTB, and N-260 strain (moderate virulence) > MAC N-444 strain (low virulence) for MAC. MTB but not MAC caused the necrotic death of host Mphis in terms of increased release of lactate dehydrogenase from infected Mphis. The MTB H37Ra strain induced a greater production of reactive nitrogen intermediates (RNI) by Mphis than the MTB H37Rv strain did. However, this phenomenon was not observed with MAC, implying less important roles of RNI in the expression of Mphi antimicrobial activity against MAC organisms.

Animals↗
PubMed2006

Quinolone, fluoroquinolone and trimethoprim/sulfamethoxazole resistance in relation to virulence determinants and phylogenetic background among uropathogenic Escherichia coli.

INTRODUCTION: The goal of this study was to assess how resistance to quinolones, fluoroquinolones and trimethoprim/sulfamethoxazole relates to the virulence potential and phylogenetic background of clinical Escherichia coli isolates. METHODS: Among 150 uropathogens (21% resistant to quinolones, 12% resistant to fluoroquinolones and 29.3% resistant to trimethoprim/sulfamethoxazole), E. coli phylogenetic group, 15 virulence-associated genes and 7 O antigens were analysed. Clonal group A (CGA) and genomic PCR profiles were studied among trimethoprim/sulfamethoxazole-resistant isolates. RESULTS: Isolates susceptible to the three antimicrobial agents were significantly associated with phylogenetic group B2, whereas resistant isolates exhibited shifts to non-B2 groups (quinolone and fluoroquinolone-resistant isolates to group A; trimethoprim/sulfamethoxazole-resistant isolates to group D). Diverse virulence traits, including UTI-associated O antigens, were significantly less frequent among resistant isolates, particularly those resistant to fluoroquinolones (median score, 3.9 virulence factors/strain) and also to quinolones (5.2) or trimethoprim/sulfamethoxazole (6.4), as compared with the corresponding drug-susceptible isolates (median scores of 7.9, 8.6 and 7.9, respectively). Among 44 trimethoprim/sulfamethoxazole-resistant isolates, 3 (6.8%) belonged to CGA. All these 3 CGA strains caused pyelonephritis (P=0.02) and exhibited the consensus virulence profile of previously described CGA strains from abroad. CONCLUSIONS: E. coli isolates resistant to quinolones, trimethoprim/sulfamethoxazole and especially fluoroquinolones were associated with reductions in virulence traits and shifts to non-B2 phylogenetic groups. Moreover, fluoroquinolone resistance usually occurred in low-virulence E. coli group A isolates rather than in isolates from groups B2 and D which had lost virulence traits. CGA accounted for 23% of trimethoprim/sulfamethoxazole-resistant E. coli producing pyelonephritis.

Adult↗
PubMed1998

Unusual species of campylobacters isolated in the Siena Tuscany area, Italy.

From January 1989 to December 1990, stool samples from 288 children with enteritis were examined for the presence of unusual campylobacters which represented about 20% of all campylobacteria isolated when the filtration technique was used. The isolation percentage was the following: C. jejuni ss. jejuni 6.9%; C. coli 2%; C. jejuni ss. doylei, C. upsaliensis and C. concisus each 0.7%. The atypical Campylobacter isolates were examined for their virulence characteristics. Toxin profiles based on cytotonic, cytotoxic and cytolethal distending factors were determined after analysis responses in Vero, CHO and HeLa cells. Adhesivity and invasivity tests were performed on Intestine 407 cells. No strain was cytotoxic. C. jejuni ss. doylei and C. concisus induced an elongation of CHO cells (a cytotonic-like effect). C. upsaliensis strains provoked a cytolethal distending effect. No strain adhered to cells in vitro. Our results suggest that the filtration technique is excellent for the isolation of atypical campylobacters and indicate that the unusual Campylobacter isolates could be potentially virulent.

Animals↗
PubMed2004

Structure of Pseudomonas aeruginosa populations analyzed by single nucleotide polymorphism and pulsed-field gel electrophoresis genotyping.

Pseudomonas aeruginosa has a wide ecological distribution that includes natural habitats and clinical settings. To analyze the population structure and distribution of P. aeruginosa, a collection of 111 isolates of diverse habitats and geographical origin, most of which contained a genome with a different SpeI macrorestriction profile, was typed by restriction fragment length polymorphism based on 14 single nucleotide polymorphisms (SNPs) located at seven conserved loci of the core genome (oriC, oprL, fliC, alkB2, citS, oprI, and ampC). The combination of these SNPs plus the type of fliC present (a or b) allowed the assignment of a genetic fingerprint to each strain, thus providing a simple tool for the discrimination of P. aeruginosa strains. Thirteen of the 91 identified SNP genotypes were found in two or more strains. In several cases, strains sharing their SNP genotype had different SpeI macrorestriction profiles. The highly virulent CHA strain shared its SNP genotype with other strains that had different SpeI genotypes and which had been isolated from nonclinical habitats. The reference strain PAO1 also shared its SNP genotype with other strains that had different SpeI genotypes. The P. aeruginosa chromosome contains a conserved core genome and variable amounts of accessory DNA segments (genomic islands and islets) that can be horizontally transferred among strains. The fact that some SNP genotypes were overrepresented in the P. aeruginosa population studied and that several strains sharing an SNP genotype had different SpeI macrorestriction profiles supports the idea that changes occur at a higher rate in the accessory DNA segments than in the conserved core genome.

Electrophoresis, Gel, Pulsed-Field↗
PubMed2006

Genomic approaches to understanding bacterial virulence.

The genomic sequences of bacterial pathogens and of the host species they infect have greatly increased the understanding of host-pathogen interactions. Sequences of bacterial genomes have led to the identification of virulence factors through the use of bioinformatics, targeted mutant library construction, screening approaches combining transposon mutagenesis and microarray technology, and through the expression of libraries of bacterial proteins within model organisms such as yeast. Host genomic information has also yielded insights into bacterial virulence through transcriptional profiling of host responses to infection and identification of host proteins required for bacterial pathogenicity using knockdown of host gene product expression during infection. Research using genomic approaches to bacterial pathogenesis is a rapidly growing field and will expand further as additional bacterial genome sequences become available and techniques for conducting high-throughput analysis are refined.

Bacteria↗
PubMed2002

Prevalence of serogroups and virulence genes in Escherichia coli associated with postweaning diarrhoea and edema disease in pigs and a comparison of diagnostic approaches.

Identification of Escherichia coli causing porcine postweaning diarrhoea (PWD) or edema disease (ED) requires knowledge regarding the prevalent pathotypes within a given region. This study was undertaken to determine the present distribution of serogroups, hemolytic activity and virulence factor gene profiles among porcine pathogenic E. coli isolates in Denmark and to compare detection of these characteristics as diagnostic approaches. Five hundred and sixty-three E. coli were serogrouped using E. coli O-antisera and investigated for hemolytic activity. Of these, 219 isolates were further characterized using a 5'-nuclease PCR assay detecting genes for adhesion factors, enterotoxins and verocytotoxin 2e (VT2e). Forty-two different serogroups were found. The most prevalent serogroup was O149 accounting for 49.9% of all isolates, followed by O138 (14.9%), O139 (6.9%), O141 (4.1%) and O8 (3.7%). Hemolytic activity was detected in 87.7% of all isolates. Virulence factor genes detected were F4 (44.7%), F18 (39.3%), intimin (1.4%), F6 (0.9%), STb (77.6%), EAST1 (65.8%), LT (61.6%), STa (26.5%) and VT2e (16.4%). Six pathotypes accounted for 65.7% of all isolates investigated. Using possession of virulence factor genes as reference, O-serogrouping employing a selection of antisera representing common pig pathogenic serogroups and detection of hemolysis were evaluated as epidemiological markers for pathogenicity. Both criteria were associated with pathogenicity (P<0.001, for both), however, both methods also resulted in false classifications regarding pathogenicity for 11.9 and 13.2% of isolates, respectively. Detection of adhesion factor genes F4, F18 and intimin is suggested as an operational alternative when diagnosing PWD and ED.

5'-Nucleotidase↗
PubMed1997

In vitro virulence factors of Arcobacter butzleri strains isolated from superficial water samples.

Eighteen isolates of A. butzleri from river water samples were examined for their biotype, serogroup and putative virulence characteristics. Toxin profiles based on cytotonic, cytotoxic and cytolethal distending factors were determined after analysis responses in Vero and CHO cells Adhesivity and invasivity tests were performed on HeLa and Intestine 407 cells. Six biotypes and five serogroups were determined in our isolates. All strains but one induced cytotoxic effects on cells in culture. The cytotoxic negative strain caused elongation of CHO cells (a cytotonic-like effect). This strain was the only one which adhered to cells in vitro. Invasiveness was never observed. Our results show a phenotypic heterogeneity of arcobacters isolated from environmental sources, and indicate that some strains could be potentially virulent.

Animals↗