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PubMed1995

[Virulence factors and 0 serogroups of Escherichia coli as a cause of community-acquired urinary infections].

BACKGROUND: The aim of this study was to determine the virulence factors and 0 serogroups of E. coli strains that cause community acquired urinary tract infections (UTI). METHODS: We examined 103 E. coli strains isolated from the urine of patients with UTI. The following virulence factors were investigated using phenotypic techniques: the alpha-haemolysin (Hly), the cytotoxic necrotizing factor type 1 (CNF-1) and the mannose-resistant haemagglutination (MRHA) types III, IVa and IVb expressed by P fimbriated E. coli. Serotyping of 0 antigen was carried out by means of a microtechnique using 163 antisera. RESULTS: Fifty-five (53%) of the 103 E. coli strains examined showed some of the virulence factors investigated in this study; 41% of the strains were Hly+, 28% were CNF-1+ and 48% expressed MRHA types III, IVa or IVb. The uropathogenic strains characterized belonged to 27 different 0 serogroups. However, 68% were from one of 10 serogroups (01, 02, 04, 06, 09, 018, 027, 073, 075 and 077) and 36% were from one of only 3 serogroups (02, 04 and 06). Furthermore, the virulence factors were concentrated in strains belonging to the 3 serogroups most frequently detected. Thus, 36 (97%) of the 37 strains of these 3 serogroups showed virulence factors, versus only 19 (29%) of 66 belonging to other serogroups (p < 0.001). CONCLUSIONS: Our results support the special pathogenicity theory and suggest that many cases of community acquired UTI may be caused by a limited number of uropathogenic E. coli strains that produce toxins (Hly+ and/or CNF-1+) and possess P fimbriae or P-related adhesins (with MRHA types III, IVa or IVb), and that usually belong to 02, 04 and 06 serogroups.

Community-Acquired Infections↗

PubMed1994

Effect of mutations causing overexpression of RNA polymerase alpha subunit on regulation of virulence factors in Bordetella pertussis.

In Bordetella pertussis, expression of virulence factors is controlled by the Bvg proteins, which comprise a sensor-regulator two-component signal transduction system. Previously, we described a mutant strain of B. pertussis that had reduced transcription of pertussis toxin and adenylate cyclase toxin genes, while other virulence factors were relatively unaffected. We obtained a B. pertussis clone that repaired the defect in both this strain and an independent mutant strain with a similar phenotype when introduced onto the chromosome by allelic exchange. Further analysis revealed that the mutations were just upstream of the translational start site of the rpoA gene encoding the alpha subunit of RNA polymerase. We confirmed that these mutations were responsible for the mutant phenotype by site-directed mutagenesis. Our hypothesis that these mutations cause an overexpression of rpoA was confirmed by Western immunoblotting and translational fusion analysis. Corroboration of this effect was obtained by overexpressing rpoA on a plasmid in wild-type B. pertussis, which caused the same phenotype as the mutants showed. Conclusions in regard to the identity of the transcription activator of the toxin genes are discussed.

Adenylate Cyclase Toxin↗

PubMed1996

Production of extracellular virulence factors by Pseudomonas aeruginosa isolates obtained from tracheal, urinary tract, and wound infections.

This study was conducted to determine the effect of the local environment within the host on the ability of P. aeruginosa to produce different extracellular virulence factors (elastase, phospholipase C, toxin A, and exoenzyme S). A total of 105 P. aeruginosa isolates was obtained from patients with tracheal, urinary tract, and wound infections. Quantitative analysis of the virulence factors was done by growing the isolates in vitro in different defined media. Single colonies of each isolate were inoculated from the primary isolation plates into the defined medium. All four virulence factors were produced by most isolates. However, depending on the location of their isolation, the isolates varied in the level of virulence factors they produced. High levels of elastase and phospholipase C were produced by most isolates obtained from trachea, urinary tract, and wounds. A significantly higher level of toxin A was produced by wound isolates, while a significantly higher level of exoenzyme S was produced by wound and urinary tract isolates. Some P. aeruginosa strains were frequently isolated from the same site of infection (persistent infection isolates). Comparative analysis of virulence factors produced by these isolates showed that, regardless of the isolation site, subsequent isolates produced higher levels of exoenzyme S. These results suggest that: (1) elastase, phospholipase C, toxin A, and exoenzyme S are produced by P. aeruginosa isolates from different sites of infection; (2) the production of higher levels of elastase and phospholipase C is important in all types of infections, while the production of toxin A and exoenzyme S is important in wound infection; (3) persistent infection with P.aeruginosa may enhance exoenzyme S production.

ADP Ribose Transferases↗

PubMed1988

Dermonecrotic toxin and tracheal cytotoxin, putative virulence factors of Bordetella avium.

We examined Bordetella avium for virulence factors common to Bordetella pertussis, including pertussis toxin, filamentous hemagglutinin, adenylate cyclase, dermonecrotic toxin, and tracheal cytotoxin. B. avium produced a dermonecrotic toxin and a tracheal cytotoxin. The dermonecrotic toxin of B. avium is a 155,000-molecular-weight, heat-labile protein which was lethal for mice, guinea pigs, young chickens, and turkey poults and produced dermonecrosis when injected intradermally into guinea pigs, chickens, and turkey poults. High-pressure liquid chromatography of B. avium culture supernatant fluid revealed the presence of a tracheal cytotoxin chemically identical to that produced by B. pertussis. B. avium isolates were negative for B. pertussis-like filamentous hemagglutinin and pertussis toxin when assayed with antibody against B. pertussis filamentous hemagglutinin and pertussis toxin. Furthermore, B. avium failed to induce the clustered CHO cell morphology characteristic of pertussis toxin. Adenylate cyclase assays indicated that B. avium does not produce an extracytoplasmic adenylate cyclase, even after passage through embryonated turkey eggs. Since production of virulence proteins by B. pertussis is regulated by growth in media containing nicotinamide or MgSO4 or by growth at reduced temperatures, we determined the effect of these supplements and growth conditions on production of dermonecrotic toxin by B. avium. Production of dermonecrotic toxin in B. avium was not altered by growth in media containing 100 microM FeSO4 or 500 micrograms of nicotinamide per ml or by growth at 25 or 42 degrees C, but production was significantly decreased by growth in media containing 20 mM MgSO4 and slightly reduced by growth in media containing 500 micrograms of nicotinic acid per ml. These studies revealed that B. avium is similar to B. pertussis in that both species produce a dermonecrotic toxin and a tracheal cytotoxin and production of dermonecrotic toxin is regulated by nicotinamide and MgSO4. The presence of dermonecrotic toxin and tracheal cytotoxin in all Bordetella species indicates that these products may be important virulence factors in bordetellosis.

Adenylate Cyclase Toxin↗

PubMed2001

[Virulence factor of Escherichia coli strains isolated during asymptomatic bacteriura among patients treated by drugs with acetylcholine antagonistic activity in a psychiatric institute].

In two successive investigations on nosocomial infections in our hospital, wa have found that asymptomatic bacteriuria is closely related to age (over 50 years) and to treatment with acetylcholine antagonistic activity. We therefore searched for the presence and expression of genes coding for the virulence factors usually present in uropathogenic E. coli in our strains, in strains isolated during asymptomatic bacteriura related to neurologic bladder, and in strains isolated during symptomatic bacteriura. We found that strains from neurologic bladders rarely carried one or two virulence factors while 50% of our strains isolated from asymptomatic bacteriuria carriea at least 3 virulence factors commonly found in strains isolated from symptomatic urinary tract infection. Consequently, it appears important to look for urinary tract infection in patients (over 50 years of age) treated with such drugs, and to look for virulence factors in case of asymptomatic bacteriura. If the stains carry no virulence factors, no antibiotic treatment shoud be instituted but the patients should be invited to drink more water than usual in order to promote elimination of the strains in the urine. Inversely, if the strains carry virulence factors, an adpted antibiotic treatment should be started.

Bacteriuria↗

PubMed2004

Real-time characterization of virulence factor expression in Yersinia pestis using a GFP reporter system.

A real-time reporter system was developed to monitor the thermal induction of virulence factors in Yersinia pestis, the etiological agent of plague. The reporter system consists of a plasmid in Y. pestis in which the expression of green fluorescent protein (GFP) is under the control of the promoters for six virulence factors, yopE, sycE, yopK, yopT, yscN, and lcrE yopN, which are all components of the Type III secretion virulence mechanism of Y. pestis. Induction of the expression of these genes in vivo was determined by the increase in fluorescence intensity of GFP in real time, in 96-well format. Different basal levels of expression at 26 degrees C were observed for the Y. pestis promoters. Expressed as percentages of the level measured for the lac promoter (positive control), the basal expression levels before temperature shift were: yopE (15%), sycE (15%), yopK (13%), yopT (4%), lcrE (3.3%), and yscN (0.8%). Following the shift in temperature from 26 to 37 degrees C, the rates of expression of these genes increased with the yopE reporter showing the strongest degree of induction. The rates of induction of the other virulence factors after the temperature, expressed as percentages of yopE induction, were: yopK (57%), sycE (9%), yscN (3%), lcrE (3%), and yopT (2%). The thermal induction of each of these promoter fusions was repressed by calcium, and the ratios of the initial rates of thermal induction without calcium supplementation compared to the rate with calcium supplementation were: yopE (11-fold), yscN (7-fold), yopK (6-fold), lcrE (3-fold), yopT (2-fold), and sycE (1-fold). This work demonstrates a novel approach to quantify gene induction and provides a method to rapidly determine the effects of external stimuli on expression of Y. pestis virulence factors in real time, in living cells, as a means to characterize virulence determinants.

Adenosine Triphosphatases↗

PubMedDate not supplied

Comparative infectivity for axenic and specific-pathogen-free chickens of O2 Escherichia coli strains with or without virulence factors.

Adhesion to epithelial respiratory cells, iron acquisition, and production of K1 polysaccharide capsules have been proposed as potential virulence factors of avian Escherichia coli. These factors were studied by inoculating groups of axenic or specific-pathogen-free (SPF) chickens intratracheally with O2 E. coli strains after previous challenge with a wild strain of infectious bronchitis virus (IBV). In all experiments, the association between IBV and an E. coli strain endowed with the three virulence factors previously mentioned resulted in the most severe pathological effects, as measured by mortality, weight gains, lesions, and reisolation of E. coli from internal organs. An E. coli strain devoid of virulence factors was able only to induce mild pathological effects restricted to the respiratory tract when combined with IBV. Both E. coli strains were more invasive in axenic chickens than in SPF chickens. These results confirm the probable involvement of the three factors studied in the pathogenic properties of avian E. coli. This model can be used to assess the role of virulence factors, by comparing pairs of positive and negative isogenic strains.

Animals↗

PubMed1994

Virulence factors and O groups of Escherichia coli strains isolated from cultures of blood specimens from urosepsis and non-urosepsis patients.

Ninety-six Escherichia coli strains isolated from cultures of blood specimens taken from both urosepsis patients (n = 48) and non-urosepsis patients (n = 48) were examined for the production of alpha-haemolysin (Hly) and cytotoxic necrotizing factor type 1 (CNF1), the expression of P-fimbriae and mannose-resistant haemagglutination (MRHA). Twenty-seven (56%) of the E. coli strains from urosepsis showed some of the virulence factors investigated, whereas only 15 (31%) of the strains associated with non-urosepsis possessed virulence factors (P < 0.05). By contrast, only 16% (P < 0.001) of the faecal isolates from healthy individuals were virulent. Of the bacteremic E. coli strains, 56 (58%) belonged to one of 8 serogroups (O1, O2, O4, O6, O8, O9, O18 and O83). Virulence factors were concentrated in strains belonging to serogroups O2, O4, O6, O18 and O83. Thus, 23 (72%) of the 32 strains of these 5 groups showed virulence factors, but only 19 (30%) of the 64 strains belong to other serogroups (P < 0.001). The majority of bacteremic O2, O4, O6 and O83 E. coli strains were Hly+CNF1+ and expressed P-fimbriae or MRHA type III, whereas the strains of serogroup O18 were Hly+CNF1- and had P-fimbriae or MRHA type III, whereas the strains of serogroup O18 were Hly+CNF1- and had P-fimbriae. We conclude that strains from urosepsis show more virulence factors than bacteremic strains isolated from non-urosepsis.

Adolescent↗

PubMed2000

Virulence factors of Helicobacter pylori in Korean isolates do not influence proinflammatory cytokine gene expression and apoptosis in human gastric epithelial cells, nor do these factors influence the clinical outcome.

The cytotoxin-associated gene (cagA) and vacuolating cytotoxin (Vac) production have been reported to be major virulence factors of Helicobacter pylori. However, there have been some disputes regarding the correlation between these virulence factors and clinical outcomes. We evaluated whether the cagA-positive genotype and Vac production might be correlated with various gastroduodenal diseases in Korea and whether this correlation could be due to differences in proinflammatory cytokine gene expression and apoptosis of gastric epithelial cells in vitro. The presence of the cagA gene was examined by the polymerase chain reaction (PCR), and Vac production was detected using the bacterial culture supernatant and HeLa cells after H. pylori was isolated from Korean patients. Gastric epithelial cells were infected with cagA+Vac+, cagA+Vac-, or cagA-Vac- strains, after which cytokine gene expression was evaluated, using quantitative reverse transcription (RT)-PCR. Apoptosis and caspase-3 activation were measured in H. pylori-infected gastric epithelial cells. There was no significant correlation between the presence of these virulence factors in H. pylori isolates and peptic ulcer or gastric cancer. Upregulation of cytokine gene expression, including that of interleukin (IL)-1alpha, IL-8, granulocyte macrophage colony-stimulating factor (GM-CSF), and monocyte chemotactic protein (MCP)-1, as well as apoptosis and caspase-3 activation, were similar in infections with cagA-positive and cagA-negative strains, but were not correlated with the production of Vac. These results suggest that the lack of correlation between virulence factors of isolated H. pylori strains and serious gastroduodenal disease entities in Korea may be due to the similar capacity for proinflammatory cytokine gene expression and apoptosis caused by infection with each of the H. pylori strains.

Antigens, Bacterial↗

PubMedDate not supplied

Virulence factors of Escherichia coli contribute to acute renal failure.

BACKGROUND: The development of acute renal failure (ARF) significantly enhances the mortality of patients with Gram-negative septic shock. The role of specific bacterial virulence factors different from lipopolysaccharides (LPS) in the deterioration of renal function in septic shock remains to be determined. METHODS: An Escherichia coli wild-type strain (536/21 WT, O6:K15:H31) was isolated from a patient suffering from a urinary tract infection. The strain expresses various virulence factors (e.g. hemolysin, fimbriae) genetically encoded by pathogenicity islands. The spontaneous deletion mutant 536/21 Del lacks the expression of these virulence factors. Isolated rat kidneys were perfused with a suspension (5 x 10(4)/ml) of the respective strain or control perfusion medium and the renal functional parameters were analyzed. Intrarenal deposition of E. coli was detected by immunohistology and Gram staining. RESULTS: The perfusion of the isolated perfused rat kidney with a uropathogenic E. coli wild-type strain (536/21 WT) caused an acute deterioration of renal function which was not observed in kidneys exposed to a deletion mutant of E. coli 536/21 lacking the expression of virulence factors. The glomerular filtration rate and the urine flow rate significantly decreased only in kidneys perfused with the E. coli wild-type strain, while there was no change versus controls in kidneys perfused with the deletion mutant. CONCLUSIONS: Distinctive bacterial virulence factors different from LPS such as hemolysin and the presence of different fimbriae may contribute to the development of ARF in sepsis induced by E. coli. Anti-LPS strategies may not be sufficient to reduce the risk of ARF in Gram-negative septic shock.

Acute Kidney Injury↗

PubMed1999

Evolution of virulence factors in Shiga-toxin-producing Escherichia coli.

The major demonstrated or putative virulence factors of Shiga-toxin-producing Escherichia coli (STEC) are the Shiga toxins, products of the locus of enterocyte effacement, and products encoded by the EHEC-hemolysin plasmid. Molecular analysis shows that STEC acquired the majority of these virulence factors by horizontal transfer of genetic material. In the case of Shiga toxins, the phages encoding them are probably responsible for this transfer. For the locus of enterocyte effacement, however, it is not clear how often this transfer took place and which parts of the locus were involved in this transfer. The large EHEC-hemolysin plasmid is clearly a mosaic structure, which arose from multiple recombination events with foreign DNA. Two lineages of this plasmid can be distinguished, one of which is associated with chromosomally encoded virulence factors. Despite the wealth of information available, further comparative studies are needed to decipher definitively the evolution of virulence in STEC.

Escherichia coli↗

PubMed2004

Assessment of virulence-factor activity relationships (VFARs) for waterborne diseases.

Virulence-factor activity relationship (VFAR) is a concept that was developed as a way to relate the architectural and biochemical components of a microorganism to its potential to cause human disease. Development of these relationships requires specialised bioinformatics databases that do not exist at present. A pilot-scale VFAR database was designed for three different waterborne organisms: Escherichia coli, Norovirus and Cryptosporidium, to evaluate VFAR relationships. For the web-based database, each organism has separate pages containing virulence genes, occurrence genes, primer sets and probes, taxonomy, outbreaks, and serotype/species/genogroup/genotype. As the database continues to grow, it will be possible to relate the occurrence and prevalence of certain genes in various microorganisms to outbreak data and, subsequently, to establish the utility of using a combination of specific genes as markers of virulence and in establishing virulence-factor activity relationships (VFARs). The database and the VFARs established will be of use to the regulatory community as a way to assist with prioritising those organisms, which need to be regulated.

Animals↗

PubMed1990

[Clinico-bacteriological studies on the etiology of bacterial prostatitis. II. Virulence factors of E. coli in bacterial prostatitis].

The virulence factors of E. coli in bacterial prostatitis were studied using 59 E. coli isolated from uncomplicated prostatitis. O-antigens of prostatitis-derived E. coli belonged to some specific serotypes such as 0-4, 6, 18, 22 and the haemolysin production was positive in 64.4%. With regard to the fimbriae, the majority of the strains had type 1 fimbriae (81.4%). Mannose resistant (MR) fimbriae were also positive in 59.3% and both type 1 and MR fimbriae were positive in 55.9%. Among MR strains, P-fimbriated and S-fimbriated strains were present in 25.7% and 28.6%, respectively, indicating that these two MR fimbriae were not always specific for the prostatitis-derived E. coli. Although the specific adhesion of E. coli onto the human prostatic epithelium mediated by MR-fimbriae was equivocal, that mediated by type 1 fimbriae was observed clearly. Therefore, type 1 fimbriae was thought to be one of the most significant virulence factors in the pathogenesis of prostatitis caused by E. coli.

Bacterial Adhesion↗

PubMed2003

Bacterial virulence factors targeting Rho GTPases: parasitism or symbiosis?

In the past few years, an important question in microbiology has arisen from reports indicating that several pathogenic bacteria have evolved virulence factors directed towards a Ras subfamily of GTPases, namely the Rho GTPases. Progress made in studying both the virulence factors and the signaling pathways involving Rho GTPases has shed light on this crosstalk. One central question is raised by the findings that both activating and inactivating virulence factors that target Rho GTPases coexist in some pathogenic bacteria. Further studies on this peculiar aspect of the bacteria-host cell interactions, which leads to the outbreak of infectious diseases, might clarify whether this aspect of Rho GTPase activation or inactivation represents a finely adapted response of the pathogen for its own benefit or might lead to a reaction of the host against the bacteria.

Bacteria↗

PubMed2006

Role of several Staphylococcus aureus virulence factors on the inflammatory response in bovine mammary gland.

Staphylococcus aureus causes many serious diseases in humans and animals, and it is the most common aetiologic agent of contagious bovine mastitis. The bacteria produce several virulence factors and the importance of evaluating the combination of these virulence factors has been recently emphasized. In study, the combination of several virulence factors: coagulase gene (coa), protein A gene (spa), collagen-binding protein gene (cna), fibrinogen-binding protein gene (efb), Panton-Valentin leukocydin gene (pvl) and enterotoxins (sea,seb, sec, sed, see, seg, seh, sei, sej) was considered. The analysis of the relationship between presence/absence of the different genes and the udder inflammatory response measured by milk somatic cell counts was performed by general linear models and logistic regression. The classification of isolates in clusters by virulence genes combinations showed that at least one cluster induced a higher inflammatory response. Moreover, the analysis of the association between virulence genes and the presence of a subclinical mastitis showed the role of spa and sej gene as risk factors. These results support that the development of subclinical mastitis could be related to strains characteristics and to the expression of specific combinations of the virulence factors.

Animals↗

PubMed1999

PlcR is a pleiotropic regulator of extracellular virulence factor gene expression in Bacillus thuringiensis.

Members of the Bacillus cereus group (B. anthracis, B. cereus, B. mycoides and B. thuringiensis) are well-known pathogens of mammals (B. anthracis and B. cereus) and insects (B. thuringiensis). The specific diseases they cause depend on their capacity to produce specific virulence factors, such as the lethal toxin of B. anthracis and the Cry toxins of B. thuringiensis. However, these Bacillus spp. also produce a variety of proteins, such as phospholipases C, which are known to act as virulence factors in various pathogenic bacteria. Few genes encoding these virulence factors have been characterized in pathogenic Bacillus spp. and little is known about the regulation of their expression. We had previously reported that in B. thuringiensis expression of the phosphatidylinositol-specific phospholipase C gene is regulated by the transcriptional activator PlcR. Here we report the identification of several extracellular virulence factor genes by the virtue of their PlcR-regulated expression. These PlcR-regulated genes encode degradative enzymes, cell-surface proteins and enterotoxins. The PlcR-regulated genes are widely dispersed on the chromosome and therefore do not constitute a pathogenic island. Analysis of the promoter region of the PlcR-regulated genes revealed the presence of a highly conserved palindromic region (TATGNAN4TNCATA), which is presumably the specific recognition target for PlcR activation. We found that the plcR gene is also present in and probably restricted to all the members of the B. cereus group. However, although the polypeptide encoded by the B. cereus PlcR gene is functionally equivalent to the B. thuringiensis regulator, the polypeptide encoded by the B. anthracis gene is truncated and not active as a transcriptional activator. PlcR is the first example described of a pleiotropic regulator involved in the control of extracellular virulence factor expression in pathogenic Bacillus spp. These results have implications for the taxonomic relationships among members of the B. cereus group, the virulence properties of these bacteria and the safety of B. thuringiensis-based biopesticides.

Amino Acid Sequence↗

PubMed1990

[Detection of bacterial virulence factors].

Several newly developed methods, including immunological and DNA hybridization techniques, have been recently introduced in clinical diagnosis. Target molecules for these detection methods are either avirulent materials or virulence factors specific to the individual causative pathogen. Examples requiring the detection of bacterial virulence factors for the accurate identification of causative agents are increasing; for example differentiation of enterotoxigenic Escherichia coli from nonpathogenic E. coli, and identification of cholera toxin-producing (or non-producing) V. cholerae 01. Recent progress in the detection of virulence factors is described. Advantages and disadvantages of various detection methods of bacterial virulence factors are also discussed.

Bacteria↗

PubMed1988

Aerobactin and other virulence factor genes among strains of Escherichia coli causing urosepsis: association with patient characteristics.

To assess the role of aerobactin as a virulence factor among uropathogenic Escherichia coli, we determined the prevalence, location, and phenotypic expression of aerobactin determinants among 58 E. coli strains causing bacteremic urinary tract infections. We correlated the presence of the aerobactin system with antimicrobial-agent resistance, the presence and phenotypic expression of other uropathogenic virulence factor determinants (P fimbriae, hemolysin, and type 1 fimbriae), and characteristics of patients. Colony and Southern hybridization of total and plasmid DNA with DNA probes for each virulence factor showed that aerobactin determinants were present in 78% of the strains and were plasmid associated in 21%, whereas P fimbria, hemolysin, and type 1 fimbria determinants were present in 74, 43, and 98% of the strains, respectively, and were always chromosomal. Chromosomal aerobactin, P fimbria, and hemolysin determinants occurred together on the chromosome more often in strains from patients without predisposing urological or medical conditions (P = 0.04). Strains with plasmid-encoded aerobactin lacked determinants for P fimbriae (P = 0.004) and hemolysin (P = 0.0004), were resistant to multiple antimicrobial agents (P = 0.0001), and were found only in compromised patients. Mating experiments demonstrated that some aerobactin plasmids also encoded antimicrobial-agent resistance. These findings suggest that the determinants for aerobactin, P fimbriae, and hemolysin are conserved on the chromosome of the antimicrobial-agent-susceptible uropathogenic strains of E. coli which invade noncompromised patients. In contrast, these chromosomal virulence factors are often absent from E. coli strains causing urosepsis in compromised hosts; these strains may acquire plasmid aerobactin in conjunction with antimicrobial-agent resistance genes.

Chromosomes, Bacterial↗