Genome sequences of actinobacteriophages JorRay, Blocker23, Nibbles, and OlgasClover.

JorRay, Blocker23, Nibbles, and OlgasClover are actinobacteriophages belonging to clusters G1, B2, CT, and DJ, respectively. JorRay and Blocker23 were identified in host bacterium . Nibbles and OlgasClover were identified in host bacterium NRRL B-16540.

Genome Sequences of Gordonia rubripertincta Bacteriophages AnarQue and Figliar.

AnarQue and Figliar are bacteriophages identified from the host bacterium Gordonia rubripertincta NRRL B-16540. AnarQue is circularly permuted and has a length of 61,822 bp; it is assigned to cluster DR. Figliar has a 3' sticky overhang and a length of 61,147 bp; it is assigned to cluster DJ.

Genome Sequences of Bacteriophages Jodelie19, BlingBling, and Burnsey.

Jodelie19, BlingBling, and Burnsey are bacteriophages identified using host bacteria of the genus Jodelie19 is a lytic phage found in NRRL B-16540. The temperate phage BlingBling and lytic phage Burnsey were both isolated using the host bacterium 3612.

Genome Sequences of Gordonia rubripertincta Bacteriophages Jellybones and NHagos.

Jellybones and NHagos are bacteriophages that were identified in the host bacterium NRRL B-16540. Jellybones has a direct terminal repeat and was assigned to the CS2 subcluster with a length of 77,514 bp. NHagos is circularly permuted and was assigned to the DR cluster with a length of 59,580 bp.

Native or Proteolytically Activated NanI Sialidase Enhances the Binding and Cytotoxic Activity of Clostridium perfringens Enterotoxin and Beta Toxin.

Many strains produce NanI as their major sialidase. Previous studies showed that NanI could potentiate epsilon toxin cytotoxicity by enhancing the binding of this toxin to host cells. The present study first determined that NanI exerts similar cytotoxicity-enhancing effects on enterotoxin and beta toxin, which are also important toxins for diseases (enteritis and enterotoxemia) originating in the gastrointestinal (GI) tract.

Identification and characterization of Clostridium perfringens beta toxin variants with differing trypsin sensitivity and in vitro cytotoxicity activity.

By producing toxins, Clostridium perfringens causes devastating diseases of both humans and animals. C. perfringens beta toxin (CPB) is the major virulence determinant for type C infections and is also implicated in type B infections, but little is known about the CPB structure-function relationship.

Clostridium perfringens type A-E toxin plasmids.

Clostridium perfringens relies upon plasmid-encoded toxin genes to cause intestinal infections. These toxin genes are associated with insertion sequences that may facilitate their mobilization and transfer, giving rise to new toxin plasmids with common backbones. Most toxin plasmids carry a transfer of clostridial plasmids locus mediating conjugation, which likely explains the presence of similar toxin plasmids in otherwise unrelated C.

Synergistic effects of Clostridium perfringens enterotoxin and beta toxin in rabbit small intestinal loops.

The ability of Clostridium perfringens type C to cause human enteritis necroticans (EN) is attributed to beta toxin (CPB). However, many EN strains also express C. perfringens enterotoxin (CPE), suggesting that CPE could be another contributor to EN.

Towards an understanding of the role of Clostridium perfringens toxins in human and animal disease.

Clostridium perfringens uses its arsenal of >16 toxins to cause histotoxic and intestinal infections in humans and animals. It has been unclear why this bacterium produces so many different toxins, especially since many target the plasma membrane of host cells. However, it is now established that C.

Cysteine-scanning mutagenesis supports the importance of Clostridium perfringens enterotoxin amino acids 80 to 106 for membrane insertion and pore formation.

Clostridium perfringens enterotoxin (CPE) causes the gastrointestinal symptoms of the second most common bacterial food-borne illness. Previous studies suggested that a region named TM1, which has amphipathic characteristics and spans from amino acids 81 to 106 of the native CPE protein, forms a β-hairpin involved in β-barrel pore formation. To further explore the potential role of TM1 in pore formation, the single Cys naturally present in CPE at residue 186 was first altered to alanine by mutagenesis; the resultant rCPE variant, named C186A, was shown to retain cytotoxic properties.

The Campylobacter jejuni Dps homologue is important for in vitro biofilm formation and cecal colonization of poultry and may serve as a protective antigen for vaccination.

In this work, we investigated the Campylobacter jejuni dps (DNA binding protein from starved cells) gene for a role in biofilm formation and cecal colonization in poultry. In vitro biofilm formation assays were conducted with stationary-phase cells in cell culture plates under microaerophilic conditions. These studies demonstrated a significant (>50%) reduction in biofilm formation by the C.

A Campylobacter jejuni Dps homolog has a role in intracellular survival and in the development of campylobacterosis in neonate piglets.

Iron acquisition is an absolute requirement by most microorganisms for host survival. In this work, we investigated the Campylobacter jejuni iron binding Dps protein for a potential role in virulence. In vitro assays using J774A.

Virulence for chickens of Clostridium perfringens isolated from poultry and other sources.

Clostridium perfringens type A is the most common cause of poultry necrotic enteritis (NE). Of the four "major" toxins, type A strains produce only alpha toxin (CPA), which has long been considered a major factor in pathogenesis of NE. We investigated the virulence for poultry of type A strains from a variety of enteric sources.

Comparative metagenomics reveals host specific metavirulomes and horizontal gene transfer elements in the chicken cecum microbiome.

Background: The complex microbiome of the ceca of chickens plays an important role in nutrient utilization, growth and well-being of these animals. Since we have a very limited understanding of the capabilities of most species present in the cecum, we investigated the role of the microbiome by comparative analyses of both the microbial community structure and functional gene content using random sample pyrosequencing. The overall goal of this study was to characterize the chicken cecal microbiome using a pathogen-free chicken and one that had been challenged with Campylobacter jejuni.