Topic
Bacillus anthracis
About: Bacillus anthracis is a research topic. Over the lifetime, 3994 publications have been published within this topic receiving 128122 citations.
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TL;DR: To immunize successfully against anthrax toxin or spore challenge, attenuated, live strains of B. anthracis must produce the toxin components specified by the pXO1 plasmid.
Abstract: Live, attenuated strains of Bacillus anthracis lacking either the capsule plasmid pXO2, the toxin plasmid pXO1, or both were tested for their efficacy as vaccines against intravenous challenge with anthrax toxin in Fischer 344 rats and against aerosol or intramuscular challenge with virulent anthrax spores in Hartley guinea pigs. Animals immunized with toxigenic, nonencapsulated (pXO1+, pXO2-) strains survived toxin and spore challenge and demonstrated postimmunization antibody titers to the three components of anthrax toxin (protective antigen, lethal factor, and edema factor). Immunization with two nontoxigenic, encapsulated (pXO1-, pXO2+), Pasteur vaccine strains neither provided protection nor elicited titers to any of the toxin components. Therefore, to immunize successfully against anthrax toxin or spore challenge, attenuated, live strains of B. anthracis must produce the toxin components specified by the pXO1 plasmid.
170 citations
TL;DR: Results suggested that the antibody response, as determined by the quantitative anti-rPA IgG ELISA and toxin neutralizing antibody (TNA) assay, were significant predictors of protection against a B. anthracis aerosol spore challenge in rabbits.
168 citations
TL;DR: The key genes required for Bacillus anthracis to cause anthrax have been acquired recently by horizontal gene transfer and its chromosome does not appear to be exceptional on a macroscopic scale compared with close relatives.
Abstract: The key genes required for Bacillus anthracis to cause anthrax have been acquired recently by horizontal gene transfer. To understand the genetic background for the evolution of B. anthracis virulence, we obtained high-redundancy genome sequences of 45 strains of the Bacillus cereus sensu lato (s.l.) species that were chosen for their genetic diversity within the species based on the existing multilocus sequence typing scheme. From the resulting data, we called more than 324,000 new genes representing more than 12,333 new gene families for this group. The core genome size for the B. cereus s.l. group was ∼1750 genes, with another 2150 genes found in almost every genome constituting the extended core. There was a paucity of genes specific and conserved in any clade. We found no evidence of recent large-scale gene loss in B. anthracis or for unusual accumulation of nonsynonymous DNA substitutions in the chromosome; however, several B. cereus genomes isolated from soil and not previously associated with human disease were degraded to various degrees. Although B. anthracis has undergone an ecological shift within the species, its chromosome does not appear to be exceptional on a macroscopic scale compared with close relatives.
167 citations
TL;DR: It is shown that a strain carrying both virulence plasmids but deleted specifically for capBCAD is highly attenuated in a mouse model for inhalation anthrax, indicating that acpA and acpB are not true functional homologs and that acPB may play a larger role in virulence than originally suspected.
Abstract: Bacillus anthracis, the agent of anthrax, produces a poly-D-glutamic acid capsule that has been implicated in virulence. Many strains missing pXO2 (96 kb), which harbors the capsule biosynthetic operon capBCAD, but carrying pXO1 (182 kb) that harbors the anthrax toxin genes, are attenuated in animal models. Also, noncapsulated strains are readily phagocytosed by macrophage cell lines, whereas capsulated strains are resistant to phagocytosis. We show that a strain carrying both virulence plasmids but deleted specifically for capBCAD is highly attenuated in a mouse model for inhalation anthrax. The parent strain and capsule mutant initiated germination in the lungs, but the capsule mutant did not disseminate to the spleen. A mutant harboring capBCAD but deleted for the cap regulators acpA and acpB was also significantly attenuated, in agreement with the capsule-negative phenotype during in vitro growth. Surprisingly, an acpB mutant, but not an acpA mutant, displayed an elevated LD50 and reduced ability to disseminate, indicating that acpA and acpB are not true functional homologs and that acpB may play a larger role in virulence than originally suspected.
167 citations
Journal Article•
TL;DR: The similarity of this bacterial adenylate cyclase to calmodulin-dependent eucaryotic adenYLate cyclases suggests that EF may have originated as a eucARYotic enzyme, which may eventually be established through comparison of the antigenic and genetic properties of the enzymes.
Abstract: Studies on the mechanism of action of anthrax toxin have led to the discovery that the edema factor component is a calmodulin-dependent adenylate cyclase. This enzyme can be obtained in milligram amounts at high purity from culture supernatants of avirulent B. anthracis strains. The cyclase binds to and probably enters eucaryotic cells to cause large, unregulated increases in cyclic AMP concentrations, an effect that may decrease an animal's ability to limit B. anthracis infection. The similarity of this bacterial adenylate cyclase to calmodulin-dependent eucaryotic adenylate cyclases suggests that EF may have originated as a eucaryotic enzyme. Such a relationship may eventually be established through comparison of the antigenic and genetic properties of the enzymes or by demonstrating that the genes have related DNA sequences. Even if such a relationship is not found, the edema factor cyclase will be a useful model for study of the properties of calmodulin-dependent enzymes.
167 citations