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PubMed1978

Factors affecting virulence in Escherichia coli urinary tract infections.

The prevalence of E. coli relative to other bacteria in the urinary tract is assumed to be the result of its proximity to and its close relationship with the gastrointestinal tract. Strains on E. coli may establish themselves more readily in the urinary tract, and/or invade the upper urinary tract, if they have a number of different virulence factors. The relative importance of these factors in the development of urinary tract infection, with or without renal involvement, is not clear. In addition, the means by which these factors may increase the virulence of E. coli are not understood, although there seems to be some evidence that the K antigens alter resistance to phagocytosis and serum bactericidal activity %9,10]. The main reason that certain E. coli serotypes are cultured from the urinary tract, however, still seems to be their dominance in the stool. The broader question of why certain O serotypes of E. coli dominate the bowel flora has not been examined adequately. The studies suggesting that the K antigen is a significant virulence factor seem to be in conflict with other studies indicating the dominance of certain serotypes of E. coli in the stool and in urinary tract infections. A resolution of this dilemma may possibly be found in the recent observations of Dr. Frits Orskov [20] and others discussed elsewhere at this meeting that the K and O serotypes appear to be interrelated.

Animals↗
PubMed1978

O antigen as virulence factor in mouse typhoid: effect of B-cell suppression.

Immunosuppression by cyclophosphamide was used to make mice incapable of B-lymphocyte responses; they could not make an antibody response to NIP-Ficoll. These mice, as well as untreated mice, were challenged intraperitoneally with graded doses of isogenic O-4,12 or O-6,7 Salmonella typhimurium derivatives. The 50% lethal dose of the O-6,7 strains was 35- to 70-fold higher than that of the O-4,12 strains, both in the normal and the immunosuppressed animals, although the latter were approximately 1,000-fold more susceptible to the infection by either challenge organism. We conclude that the O-antigen-dependent difference in the mouse virulence of these sister strains is not mediated through differences in their capacity to evoke B-lymphocyte-mediated immune responses.

Animals↗
PubMed1979

Experimental studies of the pathogenesis of infections due to Pseudomonas aeruginosa: extracellular protease and elastase as in vivo virulence factors.

The effects on mortality of supplemental injections of protease and elastase were determined in burned mice infected with non-lethal inocula of a toxin-producing but non-proteolytic-enzyme-producing strain of Pseudomonas aeruginosa. When a variety of solutions containing proteolytic enzyme were injected under these conditions, the mortality increased significantly. This did not occur when organisms other than P. aeruginosa were used. Injections of the enzyme solutions alone were non-lethal. Injection of a solution of alpha 2-macroglobulin, which was shown to inhibit proteolytic activity, together with a proteolytic enzyme--toxin producing strain of P. aeruginosa caused a significant delay in mortality when compared with controls. It was concluded that protease, elastase, and toxin production were necessary for P. aeruginosa to express full virulence in the burned mouse model.

Animals↗
PubMed1979

Virulence factors in Bacillus thuringiensis: purification and properties of a protein inhibitor of immunity in insects.

We have previously shown that Bacillus thuringiensis subsp. alesti, serotype 3, produces two extracellular inhibitors of the immune system of Saturniid pupae (designated inhibitors A and B; Edlund et al., 1976). Starting from the culture supernatant of a new mutant of B. thuringiensis with a decreased extracellular proteolytic activity, we have now purified immune inhibitor A(InA). The procedure described consists of three steps: ultrafiltration, precipitation with ammonium sulphate and chromatography on hydroxylapatite. Purified InA gave a single band on polyacrylamide gel electrophoresis using either a gel concentration of 7.5% (w/v) and reducing and denaturing conditions or a gradient gel and native conditions. In both cases the apparent molecular weight was 78 000. A certain amount of proteolytic activity was always co-purified with InA but the two activities could be dissociated by heat or EDTA treatment. Antiserum against purified InA gave only one sharp precipitation band on immunodiffusion against InA with or without EDTA. InA inhibited the in vitro killing of Escherichia coli by immune haemolymph but did not affect the killing of Bacillus subtilis. InA was toxic for Drosophila when injected into the abdomen of adult male flies.

Animals↗
PubMed1977

Virulence factors of enterotoxigenic Escherichia coli.

Further evidence for the role of enterotoxigenic Escherichia coli as an etiologic agent of diarrhea is presented. A retrospective study of 71 cases of diarrhea in Mexican children demonstrated that greater than 40% of them harbored E. coli that produced heat-labile and/or heat-stable enterotoxin. The antigenic surface-associated colonization factor of E. coli strain H-10407 has been further characterized: this pilus-like antigen is produced under conditions of growth that repress the production of common pili of E. coli. The E. coli H-10407-type colonization factor pilus has been identified as one of the antigens possessed by a strain of E. coli that produced only heat-stable enterotoxin and that was responsible for an outbreak of pediatric diarrhea.

Antigens, Bacterial↗
PubMed1977

Virulence factors of influenza A viruses: WSN virus neuraminidase required for plaque production in MDBK cells.

The genetic basis for the distinctive capacity of influenza A/WSN/33 (H0N1) virus (WSN virus) to produce plaques on bovine kidney (MDBK) cells was found to be related to virus neuraminidase. Recombinant viruses that derived only the neuraminidase of WSN virus were capable of producing plaques, whereas recombinant viruses identical to WSN except for neuraminidase did not produce plaques. With viruses that do not contain WSN neuraminidase, infectivity of virus yields from MDBK cells was increased approximately 1,000-fold after in vitro treatment with trypsin. In contrast, no significant increase in infectivity was observed after trypsin treatment of viruses containing WSN neuraminidase. In addition, polyacrylamide gel analysis of proteins of WSN virus obtained after infection of MDBK cells demonstrated that hemagglutinin was present in the cleaved form (HA1 + HA2), whereas only uncleaved hemagglutinin was obtained with a recombinant virus that derived all of its genes from WSN virus except its neuraminidase. These data are in accord with the hypothesis that neuraminidase may facilitate production of infectious particles by removing sialic acid residues and exposing appropriate cleavage sites on hemagglutinin.

Animals↗
PubMed2025

Quorum sensing and DNA methylation play active roles in clinical Burkholderia phase variation.

Phenotypic diversity in bacteria often results from adaptation to changing environmental conditions, exemplified by variable colony morphotypes. In Burkholderia pseudomallei, discrete genomic alterations and modulation of gene expression facilitate adaptation. Adapted variants of species within the Burkholderia cepacia complex (Bcc) often lose the pC3 virulence megaplasmid, impacting their colony morphology and their production of virulence factors. In this study, we characterize variants arising in Burkholderia ambifaria clinical isolates using proteomics and phenotypic tests and show that some of them have retained the pC3, indicating a distinct phase variation mechanism at play in this Bcc species. Interestingly, variants of B. ambifaria strains CEP0996 (pC3-null) and HSJ1 (pC3-positive) still share similarities in phenotypes controlled by the Cep quorum-sensing (QS) system. We further investigated the role of QS in B. ambifaria HSJ1 phase variation and confirmed that the Cep QS system is important for the emergence of variants. Given that DNA methylation is a key epigenetic factor regulating virulence factors in Burkholderia cenocepacia, we hypothesized that adenosine DNA methylation also governs phase variation in B. ambifaria HSJ1. By deleting the genes encoding putative adenosine DNA methyltransferases, we discovered that an orphan type II DNA methyltransferase inhibits the emergence of phase variants. This study is the first to demonstrate that quorum sensing and adenosine DNA methylation are two antagonistic systems independently controlling phase variation in B. ambifaria.IMPORTANCESome Burkholderia species are pathogenic to plants, animals, or humans. In immunocompromised individuals, and people suffering from cystic fibrosis, infection from the Burkholderia cepacia complex (Bcc) can lead to "cepacia syndrome." In northern Australia and southeast Asia, melioidosis caused by Burkholderia pseudomallei is prevalent among native population, particularly among people with diabetes, chronic lung or kidney disease or alcoholism. Burkholderia's phenotypic plasticity, including colony morphotype variation (CMV), enables rapid adaptation to diverse environments, enhancing its survival and pathogenicity. This study reveals phase variation as a new CMV mechanism within the Bcc group and is the first to report that quorum sensing and DNA methylation are involved in phase variation. Understanding the underlying mechanisms of CMV could lead to the development of targeted therapies against these highly antibiotic-tolerant bacteria.

Quorum Sensing↗
PubMed2026

Whole-Genome Sequencing Reveals Virulence and Antimicrobial Resistance Determinants of Lactococcus garvieae Causing Lactococcosis in Cage-Cultured Nile Tilapia (Oreochromis niloticus) in Thailand.

Lactococcosis is an important bacterial disease affecting farmed fish worldwide and is primarily associated with Lactococcus garvieae, Lactococcus petauri, and Lactococcus formosensis. In Thailand, information on L. garvieae infection in tilapia remains limited, particularly regarding genome-based identification, virulence determinants, and antimicrobial resistance profiles. This study characterized two L. garvieae isolates, AAHM-LG2501 and AAHM-LG2509, recovered from a lactococcosis outbreak in cage-cultured Nile tilapia (Oreochromis niloticus) in Ubon Ratchathani province, Thailand. Both isolates exhibited typical phenotypic characteristics of L. garvieae, including Gram-positive cocci, alpha hemolysis, positive capsule staining, and positive carbohydrate fermentation. Whole-genome sequencing confirmed both isolates as L. garvieae, with genome sizes of approximately 1.95 Mb and a G + C content of 38.9%. Genome-based taxonomic analysis supported species identification based on dDDH and ANI values, and both isolates were assigned to sequence type ST95 and serotype I. Virulence factor analysis identified 288 virulence-associated genes representing 97 virulence factors across 14 functional categories. Capsule-associated genes were prominent, together with genes involved in heme uptake, adhesion, hemolysis, stress survival, biofilm formation, and host adaptation. Ten capsule biosynthesis genes, including cpsABCFGKO, cps4A, and cps4I, as well as LPxTG cell wall anchor protein genes, were detected. Antimicrobial susceptibility testing showed resistance to nalidixic acid, oxolinic acid, and oxacillin, while reduced inhibition zones were observed for enrofloxacin and sulfamethoxazole-trimethoprim. Genome analysis identified predicted antimicrobial resistance determinants, including lsaD, vanT, vanY, and mdtA. Resistance-associated protein variants were detected in gyrA and gyrB, suggesting that target alteration may contribute to fluoroquinolone resistance. Overall, this study provides genome-level evidence of virulence and antimicrobial resistance determinants in L. garvieae from Thai tilapia and highlights the importance of whole-genome sequencing for accurate diagnosis, epidemiological surveillance, and disease management in aquaculture.

Animals↗
PubMed2025

Genome-wide mapping of cAMP receptor protein binding in enteroaggregative Escherichia coli reveals targeting of virulence-associated genes.

Bacterial pathogens employ a diverse array of virulence factors to colonize and subsequently elicit disease in their host. These factors are often subject to extensive regulation at the transcriptional level to ensure that their expression is timely. Although many pathogens use bespoke transcription factors that primarily target virulence genes, global transcription factors also sometimes play a role in controlling these genes. Enteroaggregative Escherichia coli (EAEC) is a significant cause of watery and mucoid diarrhoea globally. The organism colonizes the small intestine before producing toxins that elicit disease, using a multitude of virulence factors that are encoded both chromosomally and on virulence plasmids. In this work, we have studied the cAMP receptor protein (CRP), a well-characterized bacterial global transcription factor, focusing on its role in the pathogenicity of the prototype EAEC strain 042. We show that, although most functional CRP binding sites on the chromosome are conserved between E. coli K-12 and 042, CRP has been co-opted to couple the expression of some virulence genes to the nutritional state of the cell. We report novel mechanisms for CRP-dependent regulation of genes whose products contribute to the maturation of a bacterial antibiotic, export of a polysaccharide capsule and production of a putative adhesin.

Escherichia coli↗
PubMed2026

Comprehensive profiling of antibiotic resistance genes and functional clusters of orthologous groups annotation of gut microbiota in Indonesian Kedu chickens.

Antibiotic resistance is a growing global health concern, with poultry systems acting as important reservoirs of antibiotic resistance genes (ARGs). However, resistome and functional profiles of indigenous chickens raised under traditional systems remain underexplored. This study aimed to characterize the antibiotic resistome, virulence factor genes, and metabolic potential of gut microbiota in Indonesian Kedu chickens using a shotgun metagenomic approach. Digesta samples from five gastrointestinal segments of 21 healthy adult chickens were analyzed through high-throughput sequencing. ARGs were identified using the Comprehensive Antibiotic Resistance Database (CARD) and Antibiotic Resistance Genes Databases (ARDB), while virulence factors and functional genes were annotated using Virulence Factor Database (VFDB), Clusters of Orthologous Groups (COG), and Carbohydrate-Active EnZymes (CAZy) databases. Results revealed a diverse resistome dominated by multidrug resistance and efflux pump mechanisms, with prominent genes associated with fluoroquinolone, tetracycline, β-lactam, and glycopeptide resistance. The detection of clinically relevant ARGs suggests that genetic determinants associated with antimicrobial resistance are present in the gut microbiota of traditionally raised Kedu chickens, although metagenomic data alone cannot determine whether these genes are actively expressed or confer phenotypic resistance. Virulence factor analysis showed functions related to adherence, immune evasion, iron acquisition, quorum sensing, and efflux activity, reflecting strong microbial adaptability. Functional profiling demonstrated enrichment in translation, carbohydrate and amino acid metabolism, genome maintenance, and cell envelope biogenesis. Additionally, CAZyme analysis indicated a high capacity for complex polysaccharide degradation, supporting efficient utilization of fiber-rich traditional diets. In conclusion, this study provides a comprehensive metagenomic overview of antibiotic resistance and functional potential in Kedu chicken gut microbiota, emphasizing the importance of incorporating indigenous poultry into antimicrobial resistance surveillance within a One Health framework.

Antibiotic resistance genes↗
PubMed2025

Genome-wide mapping of cyclic AMP receptor protein binding in Enteroaggregative Escherichia coli reveals targeting of virulence-associated genes.

Bacterial pathogens use a wide array of virulence factors to colonise and subsequently elicit disease in their host. These factors are often subject to extensive regulation at the transcriptional level, to ensure that their expression is timely. Although many pathogens use bespoke transcription factors that primarily target virulence genes, global transcription factors also sometimes play a role in controlling these genes. Enteroaggregative Escherichia coli (EAEC) is a significant cause of watery and mucoid diarrhoea globally. The organism colonises the small intestine before producing toxins that elicit disease, using a multitude of virulence factors that are encoded both chromosomally and on virulence plasmids. In this work, we have studied the cAMP Receptor Protein (CRP), a well-characterised bacterial global transcription factor, focusing on its role in pathogenicity of the prototype EAEC strain 042. We show that, although most functional CRP binding sites on the chromosome are conserved between E. coli K-12 and 042, CRP has been co-opted to couple the expression of some virulence genes to the nutritional state of the cell. We report novel mechanisms for CRP-dependent regulation of genes, whose products contribute to adhesion, production of a bacterial antibiotic, and export of a polysaccharide capsule.

CRP↗