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PubMed2003

Helicobacter pylori virulence factors--one part of a big picture.

CONTEXT: At least half the world's population is infected with Helicobacter pylori, although only 10-20% of carriers develop gastric diseases, ranging from ulcer to MALT-lymphoma and adenocarcinoma (MALT is mucosa-associated lymphoid tissue). The clinical outcome of H pylori infection is determined by a complex interaction of environmental influences and host and microbial virulence factors. H pylori genotypes carrying the babA2 gene, encoding a bacterial adhesin mediating interaction with gastric epithelial cells, have enhanced pathogenicity. Moreover, coexistence of babA2 with other bacterial virulence factors further worsens clinical outcomes. STARTING POINT: To further elucidate the clinical relevance of babA2-genopositive H pylori strains, Carlo-Frederico Zambon and colleagues analysed the association of babA2 genotypes with gastritis, gastroduodenal ulcer disease, or intestinal metaplasia in 167 infected Italian individuals. The coexistence of babA2 with other potentially disease-related H pylori genes, such as cagA, vacA, or oipA, correlated with clinical outcome. 36% of H pylori strains were babA2(-) genopositive, and abundance of babA2 was associated with the genomic presence of the other potential virulence-factor genes. H pylori strains carrying babA2, cagA, and the vacA genotype s1m1 were associated with the highest risk of developing intestinal metaplasia, whereas this condition was rarely (<10%) associated with strains with a cagA-, babA2-, vacA s2m2 genotype. Whilst the risk of developing more serious gastric lesions increased as the number of virulence factor genes accumulated in a given H pylori strain, there was no indication of any one specific bacterial gene-pattern being associated with a particular clinical disease. WHERE NEXT? Identifying the factors responsible for the enhanced pathogenicity of H pylori leading to development of life-threatening diseases in a subset of infected individuals is a mandatory task for the future. Identification of virulence-associated H pylori genes and investigation of their clinical relevance in large prospective studies will help to define such strains with increased pathogenicity. The value of H pylori genotypes as predictors of disease outcome is limited, because the pathogenic impact of bacterial virulence factors is greatly influenced by coexisting environmental and host factors.

Genotype↗

PubMed2003

Role of virulence factors in resistance of avian pathogenic Escherichia coli to serum and in pathogenicity.

In chickens, colibacillosis is caused by avian pathogenic Escherichia coli (APEC) via respiratory tract infection. Many virulence factors, including type 1 (F1A) and P (F11) fimbriae, curli, aerobactin, K1 capsule, and temperature-sensitive hemagglutinin (Tsh) and plasmid DNA regions have been associated with APEC. A strong correlation between serum resistance and virulence has been demonstrated, but roles of virulence factors in serum resistance have not been well elucidated. By using mutants of APEC strains TK3, MT78, and chi7122, which belong to serogroups O1, O2, and O78, respectively, we investigated the role of virulence factors in resistance to serum and pathogenicity in chickens. Our results showed that serum resistance is one of the pathogenicity mechanisms of APEC strains. Virulence factors that increased bacterial resistance to serum and colonization of internal organs of infected chickens were O78 lipopolysaccharide of E. coli chi7122 and the K1 capsule of E. coli MT78. In contrast, curli, type 1, and P fimbriae did not appear to contribute to serum resistance. We also showed that the iss gene, which was previously demonstrated to increase resistance to serum in certain E. coli strains, is located on plasmid pAPEC-1 of E. coli chi7122 but does not play a major role in resistance to serum for strain chi7122.

Animals↗

PubMed1998

Virulence factors of Staphylococcus aureus strains causing infective endocarditis--a comparison with strains from skin infections.

The objective was to study potential bacterial virulence factors in S. aureus endocarditis. S. aureus strains isolated from patients with well-classified episodes of infective endocarditis (IE) (n=26) were compared with control S. aureus strains from consecutive patients with skin infections (n=30). The potential virulence factors studied were Staphylococcal enterotoxin A-D (SEA, SEB, SEC, SED) and toxic shock syndrome toxin-1 (TSST-1) production and binding capacity to the extracellular matrix proteins: fibronectin, collagen type I, collagen type II and bone sialoprotein (BSP). None of the potential virulence factors studied was more prevalent among the IE strains. BSP binding was more often found in the control group with skin infections. Endocarditis patients with previous damage of the heart valves were more often infected by strains not producing any enterotoxin. No correlation was found between the potential bacterial virulence factors studied and IE. Concerning the toxins known to act as superantigens (SEA-E and TSST-1), the tendencies in this and other studies indicate that a larger study group might identify them as pathogenic factors in a subgroup of staphylococcal endocarditis.

Adolescent↗

PubMed2001

Microarray analysis of microbial virulence factors.

Hybridization with oligonucleotide microchips (microarrays) was used for discrimination among strains of Escherichia coli and other pathogenic enteric bacteria harboring various virulence factors. Oligonucleotide microchips are miniature arrays of gene-specific oligonucleotide probes immobilized on a glass surface. The combination of this technique with the amplification of genetic material by PCR is a powerful tool for the detection of and simultaneous discrimination among food-borne human pathogens. The presence of six genes (eaeA, slt-I, slt-II, fliC, rfbE, and ipaH) encoding bacterial antigenic determinants and virulence factors of bacterial strains was monitored by multiplex PCR followed by hybridization of the denatured PCR product to the gene-specific oligonucleotides on the microchip. The assay was able to detect these virulence factors in 15 Salmonella, Shigella, and E. coli strains. The results of the chip analysis were confirmed by hybridization of radiolabeled gene-specific probes to genomic DNA from bacterial colonies. In contrast, gel electrophoretic analysis of the multiplex PCR products used for the microarray analysis produced ambiguous results due to the presence of unexpected and uncharacterized bands. Our results suggest that microarray analysis of microbial virulence factors might be very useful for automated identification and characterization of bacterial pathogens.

Bacterial Proteins↗

PubMed2006

[Susceptibility of 36 Helicobacter pylori clinical isolates to four first-line antibiotics and virulence factors].

Helicobacter pylori possess various virulence factors, including cagA and vacA genes, that are associated with more aggressive symptoms such as bleed-ing ulcer and gastric cancer. Although there are different treatment regimens, there is still a failure rate of up to 20% due to antibiotic resistance, among other causes. In our country resistance to metronidazole and clarithromycin is increasing, especially in children, although they are still susceptible to amoxicillin and tetracycline. In order to determine the susceptibility pattern to these antibiotics 36 H. pylori clinical isolates were studied. MIC was determined by agar diffusion and agar dilution, and vacA and cagA genes were detected by conventional PCR. All isolates were susceptible to amoxicillin and tetracycline. Resistance to metronidazole by diffusion or dilution tests was 35.7% and 36.1%, respectively, and to clarithromycin, 21.4% and 22.3%, respectively. There was one strain that showed intermediate resistance to clarithromycin (MIC 0.38 mg/l), using agar diffusion, and that was included among the resistant strains. Three discrepancies were observed between the diffusion and dilution methods. The vacA s1 allele was detected in 17.2% of the strains, and vacA s2 in 82.8%; 51.7% of the total were cagA+. In conclusion, all strains tested in our study were susceptible to amoxicillin and tetracycline, allowing them to be considered as first-line antibiotics, while clarithromycin and metronidazole maintain a slight increase in their resistance level. The cagA+ strains were detected in expected quantities, while the s1 allele of the vacA gene was detected in lower quantities.

Adult↗

PubMed2006

Identification and characterization of msa (SA1233), a gene involved in expression of SarA and several virulence factors in Staphylococcus aureus.

The staphylococcal accessory regulator (sarA) plays a central role in the regulation of virulence in Staphylococcus aureus. To date, studies involving sarA have focused on its activity as a global regulator that modulates transcription of a wide variety of genes (>100) and its role in virulence. However, there is also evidence to suggest the existence of accessory elements that modulate SarA production and/or function. A reporter system was developed to identify such elements, and a new gene, msa (SA1233), mutation of which results in reduced expression of SarA, was identified and characterized. Additionally, it was shown that mutation of msa resulted in altered transcription of the accessory gene regulator (agr) and the genes encoding several virulence factors including alpha toxin (hla) and protein A (spa). However, the impact of mutating msa was different in the laboratory strain RN6390 and the clinical isolate UAMS-1. For instance, mutation of msa caused a decrease in spa and hla transcription in RN6390 but had a different effect in UAMS-1. The strain-dependent effects of the msa mutation were similar to those observed previously, which suggests that msa may modulate the production of specific virulence factors through its impact on sarA. Interestingly, sequence analysis of Msa suggests that it is a putative membrane protein with three membrane-spanning regions, indicating that Msa might interact with the environment. The findings show that msa is involved in the expression of SarA and several virulence factors.

Bacterial Proteins↗

PubMed1999

Pseudomonas aeruginosa killing of Caenorhabditis elegans used to identify P. aeruginosa virulence factors.

We reported recently that the human opportunistic pathogen Pseudomonas aeruginosa strain PA14 kills Caenorhabditis elegans and that many P. aeruginosa virulence factors (genes) required for maximum virulence in mouse pathogenicity are also required for maximum killing of C. elegans. Here we report that among eight P. aeruginosa PA14 TnphoA mutants isolated that exhibited reduced killing of C. elegans, at least five also exhibited reduced virulence in mice. Three of the TnphoA mutants corresponded to the known virulence-related genes lasR, gacA, and lemA. Three of the mutants corresponded to known genes (aefA from Escherichia coli, pstP from Azotobacter vinelandii, and mtrR from Neisseria gonorrhoeae) that had not been shown previously to play a role in pathogenesis, and two of the mutants contained TnphoA inserted into novel sequences. These data indicate that the killing of C. elegans by P. aeruginosa can be exploited to identify novel P. aeruginosa virulence factors important for mammalian pathogenesis.

Animals↗

PubMedDate not supplied

Virulence factors of Clostridium difficile.

In addition to the two major toxins of Clostridium difficile--toxins A and B, which represent the major virulence factors--a number of other putative virulence factors have been described. These factors include fimbriae and the ability to associate with gut cells/mucus, the production of a capsule, the secretion of a range of hydrolytic enzymes, the production of other toxins (such as an actin-specific ADP-ribosyltransferase by some strains), and the controversial possibility of the production of a second enterotoxin. The extent to which these additional putative virulence factors are involved in the pathogenesis of C. difficile-related gut disease remains to be elucidated.

Bacterial Adhesion↗

PubMed2000

Expression of virulence factors among Escherichia coli isolated from the periurethra and urine of children with neurogenic bladder on intermittent catheterization.

BACKGROUND: Patients with neurogenic bladder caused by spinal cord injury or myelomeningocele empty their bladder several times a day by intermittent catheterization. Bacteriuria without symptoms of infection is frequently present in these patients. Occasionally a clone of Escherichia coli that has been carried for weeks without symptoms causes a symptomatic urinary tract infection. Virulence factors are commonly expressed among E. coli causing infection in patients with normal urinary tracts. However, it is unknown whether expression of virulence factors by an E. coli clone colonizing the neurogenic bladder increases the risk of subsequent infection. In this study we examined the prevalence of virulence factor expression among E. coli isolated from the periurethra and urine of patients with neurogenic bladder. METHODS: The prevalence of virulence factors was examined among E. coli isolated from the periurethra and urine in patients with neurogenic bladder who received intermittent catheterization and were followed for 6 months. Representative isolates from the 37 clonal types of E. coli detected in the periurethra and urine of children with neurogenic bladder were assessed for O antigen, hemolysin, aerobactin, serum resistance and type I and P-adhesin. RESULTS: All clones were serum-resistant and expressed type I adhesin, none expressed aerobactin and two expressed hemolysin. The presence of P-adhesin was not unique to clones associated with symptomatic infection. The presence of P-adhesin carried for weeks in a clone did not predict subsequent infection in the neurogenic bladder. CONCLUSION: Bacterial virulence factors did not predict infection of the neurogenic bladder.

Adolescent↗

PubMed2001

Interference with Pseudomonas quinolone signal synthesis inhibits virulence factor expression by Pseudomonas aeruginosa.

Pseudomonas aeruginosa is an opportunistic pathogen that controls numerous virulence factors through intercellular signals. This bacterium has two quorum-sensing systems (las and rhl), which act through the intercellular signals N-(3-oxododecanoyl)-l-homoserine lactone (3-oxo-C(12)-HSL) and N-butyryl-l-homoserine lactone (C(4)-HSL), respectively. P. aeruginosa also produces a third intercellular signal that is involved in virulence factor regulation. This signal, 2-heptyl-3-hydroxy-4-quinolone [referred to as the Pseudomonas quinolone signal (PQS)], is a secondary metabolite that is part of the P. aeruginosa quorum-sensing hierarchy. PQS can induce both lasB (encodes LasB elastase) and rhlI (encodes the C(4)-HSL synthase) in P. aeruginosa and is produced maximally during the late stationary phase of growth. Because PQS is an intercellular signal that is part of the quorum-sensing hierarchy and controls multiple virulence factors, we began basic studies designed to elucidate its biosynthetic pathway. First, we present data that strongly suggest that anthranilate is a precursor for PQS. P. aeruginosa converted radiolabeled anthranilate into radioactive PQS, which was bioactive. We also found that an anthranilate analog (methyl anthranilate) would inhibit the production of PQS. This analog was then shown to have a major negative effect on elastase production by P. aeruginosa. These data provide evidence that precursors of intercellular signals may provide viable targets for the development of therapeutic treatments that will reduce P. aeruginosa virulence.

Anthranilate Synthase↗

PubMed1994

Virulence factors in anaerobes.

Among the broad spectrum of species of anaerobic bacteria in the normal flora of humans, a few exhibit marked pathogenic potential and are responsible for the majority of infections. The factors that determine the virulence of particular species are varied and probably interrelated. Just as most anaerobic infections are polymicrobial and depend on interactions of a combination of species, the virulence of a species probably depends on a combination of properties, including surface structures, metabolic functions, ability to avoid the host's defenses, and capacity to damage tissues. Thus, the production of each virulence factor--adhesins that attach to epithelial and red blood cells and to other bacteria, producing metabolically interdependent ecosystems; capsules that protect against phagocytosis and induce abscess formation; lipopolysaccharide; proteases, including those that degrade immunoglobulins and complement components; and other hydrolytic enzymes--represents only a component of virulence, but a consideration of these factors in combination begins to clarify the mechanisms by which anaerobes cause disease.

Animals↗

PubMed2006

Effects of various growth conditions in a chemostat on expression of virulence factors in Porphyromonas gingivalis.

Porphyromonas gingivalis, one of the gram-negative organisms associated with periodontal disease, possesses potential virulence factors, including fimbriae, proteases, and major outer membrane proteins (OMPs). In this study, P. gingivalis ATCC 33277 was cultured in a chemostat under hemin excess and presumably peptide-limiting conditions to better understand the mechanisms of expression of the virulence factors upon environmental changes. At higher growth rates, the amounts of FimA and the 75-kDa protein, forming long and short fimbriae, respectively, increased significantly, whereas gingipains decreased in amount and activity. In a nutrient-limited medium, lesser amounts of the above two fimbrial proteins were observed, whereas clear differences were not found in the amounts of gingipains. In addition, two-dimensional electrophoresis revealed that proteins in cells were generally fewer in number during nutrient-limited growth. Under aeration, a considerable reduction in gingipain activity was found, whereas several proteins associated with intact cells significantly increased. However, the expression of major OMPs, such as RagA, RagB, and the OmpA-like proteins, was almost constant under all conditions tested. These results suggest that P. gingivalis may actively control expression of several virulence factors to survive in the widely fluctuating oral environment.

Aerobiosis↗

PubMed2006

Weapons of mass destruction: virulence factors of the global killer enterotoxigenic Escherichia coli.

Enterotoxigenic Escherichia coli (ETEC) is the most common cause of food and water-borne E. coli-mediated human diarrhoea worldwide. The incidence in developing countries is estimated at 650 million cases per year, resulting in 800 000 deaths, primarily in children under the age of five. ETEC is also the most common cause of diarrhoea among travellers, including the military, from industrialized nations to less developed countries. In addition, ETEC is a major pathogen of animals, being responsible for scours in cattle and neonatal and postweaning diarrhoea in pigs and resulting in significant financial losses. Studies on the pathogenesis of ETEC infections have concentrated on the plasmid-encoded heat-stable and heat-labile enterotoxins and on the plasmid-encoded antigenically variable colonization factors. Relatively little work has been carried out on chromosomally encoded virulence factors. Here, we review the known virulence factors of ETEC and highlight the future for combating this major disease.

Animals↗

PubMed2000

Pseudomonas aeruginosa virulence factors delay airway epithelial wound repair by altering the actin cytoskeleton and inducing overactivation of epithelial matrix metalloproteinase-2.

To investigate the role of P. aeruginosa virulence factors in the repair of human airway epithelial cells (HAEC) in culture, we evaluated the effect of stationary-phase supernatants from the wild-type strain PAO1 on cell migration, actin cytoskeleton distribution, epithelial integrity during and after repair of induced wounds, and the balance between matrix metalloproteinases (MMP) and their tissue inhibitors (TIMP). PAO1 supernatant altered wound repair by slowing the migration velocity in association with altered actin cytoskeleton polymerization in the lamellipodia of migrating airway epithelial cells and delaying or inhibiting the restoration of epithelial integrity after wound closure. PAO1 virulence factors overactivated two of the gelatinolytic enzymes, MMP-2 and MMP-9, produced by HAEC during repair. During HAEC repair in the presence of PAO1 virulence factors, enhanced MMP-2 activation was associated with decreased rates of its specific inhibitor TIMP-2, whereas enhanced MMP-9 activation was independent of changes of its specific inhibitor TIMP-1. These inhibitory effects were specific to P. aeruginosa elastase-producing strains (PAO1 and lipopolysaccharide-deficient AK43 strain); supernatants from P. aeruginosa strain elastase-deficient PDO240 and Escherichia coli strain DH5alpha had no inhibitory effect. To mimic the effects of P. aeruginosa, we further analyzed HAEC wound closure in the presence of increasing concentrations of activated MMP-9 or MMP-2. Whereas increasing concentrations of active MMP-9 accelerated repair, excess activated MMP-2 generated a lower migration velocity. All these data demonstrate that P. aeruginosa virulence factors, especially elastase, may impede airway epithelial wound closure by altering cell motility and causing an imbalance between pro- and activated forms of MMP-2.

Actins↗

PubMed2006

Streptococcus pneumoniae virulence factors and their clinical impact: An update.

The morbidity and mortality rates associated with Streptococcus pneumoniae remain very high worldwide. The virulence of this bacterium is largely dependent on its polysaccharide capsule, which is quite heterogeneous and represents a serious obstacle for designing effective vaccines. However, it has been demonstrated that numerous protein virulence factors are involved in the pathogenesis of pneumococcal disease. An important related finding from experimental animal models is that non-capsulated strains of pneumococci are protective against capsulated ones. Hence, new vaccine designs are focused on the surface proteins (e. g., PspA and PspC) and on the cytolysin, pneumolysin. Moreover, several virulence factors have potential value for pneumococcal diagnosis by urinalysis. In this paper, we review the virulence factors involved in bacteria-host interactions, and the new developments in vaccines and diagnostic methods.

Humans↗

PubMed2002

Virulence factors of uropathogens.

Urinary tract infections are among the most frequent infections encountered in developed countries. The vast majority of community-acquired urinary tract infections are caused by Escherichia coli. However, other bacterial species play an important role in nosocomial urinary tract infections. All these species are equipped with a variety of virulence factors. The best characterized are those from Escherichia coli. Among the first virulence factors that come into play during establishment of a urinary tract infection are adhesins. Besides their primary function as adhesin molecules several other additional functions can now be attributed to these organelles. Adhesins may also function as invasins, promote biofilm formation and transmit signals to epithelial cells resulting in inflammation. Furthermore, subunit proteins of adhesins seem to be promising vaccines. Later in infection, toxins seem to enhance virulence. However, for cytotoxic necrotizing factor type 1 this is controversial. Many virulence factors of uropathogenic bacteria are encoded by foreign DNA stretches inserted into the core genome. These pathogenicity islands or islets were obviously acquired via horizontal gene transfer creating new pathotypes more efficient in establishing infection. The role of new virulence factors and the new functions of already known virulence factors will be discussed as well as the concept of the composite genome of uropathogenic Escherichia coli.

Adhesins, Escherichia coli↗

PubMed1990

Molecular analysis of two group B streptococcal virulence factors.

Molecular biology has provided new technology for evaluating the traits of bacterial pathogens that are important in the pathogenesis of infections. The ability to derive isogenic strains that differ by a single trait provides a powerful tool for investigating the interaction of a putative virulence factor with the host at any of the various steps in pathogenesis. Recombinant DNA techniques afford the opportunity to clone the genes involved in the biosynthesis of a particular virulence factor. Once the gene(s) are cloned, a vast amount of information can be learned about their composition, structure, and regulation, and similarity with genes in other organisms. Understanding the molecular biology of a virulence factor also provides information about potential targets for future therapies and preventive modalities. The molecular analysis of two virulence factors from the type III group B streptococcus has been reviewed to provide specific examples of how these techniques can be used. The data has shown that the capsular polysaccharide is an essential factor in GBS virulence. The structural influence of sialic acid on the capsule plays a major role in its virulence properties. The importance of the capsule has been tested in several assays to identify its role in pathogenesis. Its primary role appears to be evading host phagocytic mechanisms, but it does not appear to be essential in the vascular response observed during GBS sepsis. Using the isogenic strains, we have also learned that the capsule does not mask a fibronectin receptor on GBS. In contrast to the capsule, the beta-hemolysin of GBS does not appear to be essential for systemic disease once the organism has invaded. Its role in the initial invasive steps in GBS pathogenesis has not been tested, but the availability of isogenic mutants in beta-hemolysin production will allow this question to be answered once the model systems are available.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMed1994

Studies on the bacterial flora of fish which are potential pathogens for human. Virulence factors of potential human pathogen isolated.

Tests for various virulence factors, such as production of haemolysin on sheep blood agar plate, cytotoxin on HeLa cell line and enterotoxin in GM-1 ELISA and suckling mouse assay model, were done among the various strains of Aeromonas spp., Vibrio spp., Plesiomonas shigelloides and Esch. coli isolated from fresh water fish samples. Invasive properties of the isolates were also seen by using Sereny test. Haemolysin production was observed in 85.7% of Aeromonas, all (100%) of Vibrios, 13.3% of Esch. coli and none (0%) of P. shigelloides strains. Cytotoxin production was demonstrated in 60.8% of Aeromonas, 38.4% of Vibrios and none (0%) of P. shigelloides and Esch. coli strains. About 8% of Vibrio spp., were found positive for LT in GM-1 ELISA method whereas, none of the Aeromonas spp., Plesiomonas and Esch. coli. strains were found positive for LT and ST in GM-1 ELISA. By suckling mouse assay model 43.4% strains of Aeromonas were found positive for enterotoxin production whereas, strains of Vibrio spp., Plesiomonas and Esch. coli yielded negative results. Sereny test for invasive property was found negative in all the strains tested. The isolates from fish possess various virulence factors which contributes for pathogenicity in order to cause various diseases to susceptible individual.

Animals↗