ArticleInfection and immunity2009
Discriminating virulence mechanisms among Bacillus anthracis strains by using a murine subcutaneous infection model.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Decoding Virulence Mechanisms ofMicroorganisms · 2026Article
- Current Status and Trends in Prophylaxis and Management of Anthrax Disease.Pathogens (Basel, Switzerland) · 2020Review
- Distinct Contribution of the HtrA Protease and PDZ Domains to Its Function in Stress Resilience and Virulence ofFrontiers in microbiology · 2019Article
- Galactosylation of the Secondary Cell Wall Polysaccharide of Bacillus anthracis and Its Contribution to Anthrax Pathogenesis.Journal of bacteriology · 2018Article
- Using Telemetry Data to Refine Endpoints for New Zealand White Rabbits Challenged withJournal of the American Association for Laboratory Animal Science : JAALAS · 2017Article
- Global metabolomic analysis of a mammalian host infected with Bacillus anthracis.Infection and immunity · 2015Article
- Lethal factor, but not edema factor, is required to cause fatal anthrax in cynomolgus macaques after pulmonary spore challenge.The American journal of pathology · 2014Article
- Vaccine protection against Bacillus cereus-mediated respiratory anthrax-like disease in mice.Infection and immunity · 2013Article
- Bacillus anthracis co-opts nitric oxide and host serum albumin for pathogenicity in hypoxic conditions.Frontiers in cellular and infection microbiology · 2013Article
- Differential contribution of Bacillus anthracis toxins to pathogenicity in two animal models.Infection and immunity · 2012Article
- Expression of either lethal toxin or edema toxin by Bacillus anthracis is sufficient for virulence in a rabbit model of inhalational anthrax.Infection and immunity · 2012Article
- Sortase-conjugation generates a capsule vaccine that protects guinea pigs against Bacillus anthracis.Vaccine · 2012Article
- Anthrax edema toxin impairs clearance in mice.Infection and immunity · 2012Article
- Anthrax vaccine antigen-adjuvant formulations completely protect New Zealand white rabbits against challenge with Bacillus anthracis Ames strain spores.Clinical and vaccine immunology : CVI · 2012Article
- Article
- Cellular and physiological effects of anthrax exotoxin and its relevance to disease.Frontiers in cellular and infection microbiology · 2012Review
- Bacillus cereus G9241 makes anthrax toxin and capsule like highly virulent B. anthracis Ames but behaves like attenuated toxigenic nonencapsulated B. anthracis Sterne in rabbits and mice.Infection and immunity · 2011Article
- Multigenic control and sex bias in host susceptibility to spore-induced pulmonary anthrax in mice.Infection and immunity · 2011Article
- Noninvasive imaging technologies reveal edema toxin as a key virulence factor in anthrax.The American journal of pathology · 2011Article
- Two capsular polysaccharides enable Bacillus cereus G9241 to cause anthrax-like disease.Molecular microbiology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Bacillus anthracis strains harboring virulence plasmid pXO1 that encodes the toxin protein protective antigen (PA), lethal factor, and edema factor and virulence plasmid pXO2 that encodes capsule biosynthetic enzymes exhibit different levels of virulence in certain animal models. In the murine model of pulmonary infection, B. anthracis virulence was capsule dependent but toxin independent. We examined the role of toxins in subcutaneous (s.c.) infections using two different genetically complete (pXO1(+) pXO2(+)) strains of B. anthracis, strains Ames and UT500. Similar to findings for the pulmonary model, toxin was not required for infection by the Ames strain, because the 50% lethal dose (LD(50)) of a PA-deficient (PA(-)) Ames mutant was identical to that of the parent Ames strain. However, PA was required for efficient s.c. infection by the UT500 strain, because the s.c. LD(50) of a UT500 PA(-) mutant was 10,000-fold higher than the LD(50) of the parent UT500 strain. This difference between the Ames strain and the UT500 strain could not be attributed to differences in spore coat properties or the rate of germination, because s.c. inoculation with the capsulated bacillus forms also required toxin synthesis by the UT500 strain to cause lethal infection. The toxin-dependent phenotype of the UT500 strain was host phagocyte dependent, because eliminating Gr-1(+) phagocytes restored virulence to the UT500 PA(-) mutant. These experiments demonstrate that the dominant virulence factors used to establish infection by B. anthracis depend on the route of inoculation and the bacterial strain.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.