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Bacillus anthracis

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Title: Bacillus anthracis  
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Subject: Anthrax, Bacillus, 2001 anthrax attacks, List of infectious diseases, Anthrax toxin
Collection: Anthrax, Bacillus, Bacteria with Sequenced Genomes
Publisher: World Heritage Encyclopedia

Bacillus anthracis

Bacillus anthracis
Photomicrograph of Bacillus anthracis (fuchsin-methylene blue spore stain)
Scientific classification
Domain: Bacteria
Phylum: Firmicutes
Class: Bacilli
Order: Bacillales
Family: Bacillaceae
Genus: Bacillus
Species: B. anthracis
Binomial name
Bacillus anthracis
Cohn 1872

Bacillus anthracis is the etiologic agent of anthrax — a common disease of livestock and, occasionally, of humans — and the only obligate pathogen within the genus Bacillus.[1] B. anthracis is a Gram-positive, endospore-forming, rod-shaped bacterium, with a width of 1.0–1.2 µm and a length of 3–5 µm.[1] It can be grown in an ordinary nutrient medium under aerobic or anaerobic conditions.[2]

B. anthracis belongs to the B. cereus group of strains.
Structure of B. anthracis

It is one of few bacteria known to synthesize a protein capsule (poly-D-gamma-glutamic acid). Like Bordetella pertussis, it forms a calmodulin-dependent adenylate cyclase exotoxin known as (edema factor), along with lethal factor. It bears close genotypical and phenotypical resemblance to Bacillus cereus and Bacillus thuringiensis. All three species share cellular dimensions and morphology. All form oval spores located centrally in an unswollen sporangium. B. anthracis spores, in particular, are highly resilient, surviving extremes of temperature, low-nutrient environments, and harsh chemical treatment over decades or centuries.

The spore is a dehydrated cell with thick walls and additional layers that form inside the cell membrane. It can remain inactive for many years, but if it comes into a favorable environment, it begins to grow again. It is sometimes called an endospore because it initially develops inside the rod-shaped form. Features such as the location within the rod, the size and shape of the endospore, and whether or not it causes the wall of the rod to bulge out are characteristic of particular species of Bacillus. Depending upon the species, the endospores are round, oval, or occasionally cylindrical. They are highly refractile and contain dipicolinic acid. Electron micrograph sections show they have a thin outer spore coat, a thick spore cortex, and an inner spore membrane surrounding the spore contents. The spores resist heat, drying, and many disinfectants (including 95% ethanol).[3] Because of these attributes, B. anthracis spores are extraordinarily well-suited to use (in powdered and aerosol form) as biological weapons. Such weaponization has been accomplished in the past by at least five state bioweapons programs — those of the United Kingdom, Japan, the United States, Russia, and Iraq — and has been attempted by several others.[4]


  • Historical background 1
  • Genome structure 2
    • pXO1 plasmid 2.1
    • pXO2 plasmid 2.2
  • Strains 3
  • Evolution 4
    • Nearest neighbors 4.1
    • Pseudogene 4.2
  • Clinical aspects 5
    • Pathogenesis 5.1
    • Manifestations in human disease 5.2
    • Prevention and treatment 5.3
  • Laboratory research 6
    • Recent research 6.1
  • Host interactions 7
  • References 8
  • External links 9

Historical background

CapD protein crystal structure of B. anthracis

French physician Casimir Davaine (1812-1882) demonstrated the symptoms of anthrax were invariably accompanied by the microbe B. anthracis.[5] German physician Aloys Pollender (1799–1879) is also credited for this discovery. B. anthracis was the first bacterium conclusively demonstrated to cause disease, by Robert Koch in 1876.[6] The species name anthracis is from the Greek anthrax (ἄνθραξ), meaning "coal" and referring to the most common form of the disease, cutaneous anthrax, in which large, black skin lesions are formed.

Genome structure

B. anthracis has a single chromosome which is a circular, 5,227,293-bp DNA molecule.[7] It also has two circular, extrachromosomal, double-stranded DNA plasmids, pXO1 and pXO2. Both the pXO1 and pXO2 plasmids are required for full virulence and represent two distinct plasmid families.[8]

Feature Chromosome pXO1 pXO2
Size (bp) 5,227,293 181,677 94,829
Number of genes 5,508 217 113
Replicon coding (%) 84.3 77.1 76.2
Average gene length (nt) 800 645 639
G+C content (%) 35.4 32.5 33.0
rRNA operons 11 0 0
tRNAs 95 0 0
sRNAs 3 2 0
Phage genes 62 0 0
Transposon genes 18 15 6
Disrupted reading frame 37 5 7
Genes with assigned function 2,762 65 38
Conserved hypothetical genes 1,212 22 19
Genes of unknown function 657 8 5
Hypothetical genes 877 122 51

pXO1 plasmid


pXO2 plasmid



The 89 known strains of B. anthracis include:

    • Ames Ancestor
    • Ames Florida
  • H9401, isolated from human patient in Korea; used in investigational anthrax vaccines[9]




Nearest neighbors


B. cereus is a soil-dwelling bacterium which can colonize the gut of invertebrates as a symbiont[11] and is a frequent cause of food poisoning[12] It produces an emetic toxin, enterotoxins, and other virulence factors.[13] The enterotoxins and virulence factors are encoded on the chromosome, while the emetic toxin is encoded on a 270-kb plasmid, pCER270.[8]

B. thuringiensis is an insect pathogen and is characterized by production of parasporal crystals of insecticidal toxins Cry and Cyt.[14] The genes encoding these proteins are commonly located on plasmids which can be lost from the organism, making it indistinguishable from B. cereus.[8]



The plcR gene is part of a two-gene operon with papR.[17][18] The papR gene encodes a small protein which is secreted from the cell and the reimported as a processed heptapeptide forming a quorum-sensing system.[18][19] The lack of PlcR in B. anthracis is a principle characteristic differentiating it from other members of the B. cereus group. While B. cereus and B. thuringiensis depend on the plcR gene for expression of their virulence factors, B. anthracis relies on the pXO1 and pXO2 plasmids for its virulence.[8]

Clinical aspects


B. anthracis possesses an antiphagocytic capsule essential for full virulence. The organism also produces three plasmid-coded exotoxins: edema factor, a calmodulin-dependent adenylate cyclase, causes elevation of intracellular cAMP, and is responsible for the severe edema usually seen in B. anthracis infections; lethal toxin is responsible for tissue necrosis; protective antigen (so named because of its use in producing protective anthrax vaccines) mediates cell entry of edema factor and lethal toxin.

Manifestations in human disease

Three forms of human anthrax disease are recognized based on their portal of entry.

  • Cutaneous, the most common form (95%), causes a localized, inflammatory, black, necrotic lesion (eschar).
  • Pulmonary, the highly fatal form, is characterized by sudden, massive chest edema followed by cardiovascular shock.
  • Gastrointestinal, a rare but also fatal (causes death to 25%) type, results from ingestion of spores.

Prevention and treatment

A number of anthrax vaccines have been developed for preventive use in livestock and humans. Infections with B. anthracis can be treated with β-lactam antibiotics such as penicillin, and others which are active against Gram-positive bacteria.[20] Penicillin-resistant B. anthracis can be treated with fluoroquinolones such as ciprofloxacin or tetracycline antibiotics such as doxycycline.

Laboratory research


Recent research



Host interactions



  1. ^ a b Spencer, RC (March 2003). "Bacillus anthracis.". Journal of clinical pathology 56 (3): 182–7.  
  2. ^ Holt, J. G., N. R. Krieg, P. H. A. Sneath, J. T. Staley, and S. T. Williams. 1994. Group 17: gram-positive cocci, p. 527–558. In W. R. Hensyl (ed.), Bergey's manual of determinative bacteriology, 9th ed. Williams and Wilkins, Baltimore, Md.
  3. ^ Bergey's Manual of Systematic Bacteriology, vol. 2, p. 1105, 1986, Sneath, P.H.A.; Mair, N.S.; Sharpe, M.E.; Holt, J.G. (eds.); Williams & Wilkins, Baltimore, Maryland, USA
  4. ^ Zilinskas, Raymond A. (1999), "Iraq's Biological Warfare Program: The Past as Future?", Chapter 8 in: Lederberg, Joshua (editor), Biological Weapons: Limiting the Threat (1999), The MIT Press, pp 137-158.
  5. ^ Théodoridès, J (April 1966). "Casimir Davaine (1812-1882): a precursor of Pasteur". Medical history 10 (2): 155–65.  
  7. ^ a b Read, TD; Peterson, SN; Tourasse, N; Baillie, LW; Paulsen, IT; Nelson, KE; Tettelin, H; Fouts, DE; Eisen, JA; Gill, SR; Holtzapple, EK; Okstad, OA; Helgason, E; Rilstone, J; Wu, M; Kolonay, JF; Beanan, MJ; Dodson, RJ; Brinkac, LM; Gwinn, M; DeBoy, RT; Madpu, R; Daugherty, SC; Durkin, AS; Haft, DH; Nelson, WC; Peterson, JD; Pop, M; Khouri, HM; Radune, D; Benton, JL; Mahamoud, Y; Jiang, L; Hance, IR; Weidman, JF; Berry, KJ; Plaut, RD; Wolf, AM; Watkins, KL; Nierman, WC; Hazen, A; Cline, R; Redmond, C; Thwaite, JE; White, O; Salzberg, SL; Thomason, B; Friedlander, AM; Koehler, TM; Hanna, PC; Kolstø, AB; Fraser, CM (May 1, 2003). "The genome sequence of Bacillus anthracis Ames and comparison to closely related bacteria.". Nature 423 (6935): 81–6.  
  8. ^ a b c d e f g Kolstø, Anne-Brit; Tourasse, Nicolas J.; Økstad, Ole Andreas (1 October 2009). "What Sets Apart from Other Species?". Annual Review of Microbiology 63 (1): 451–476.  
  10. ^ a b Keim, Paul; Gruendike, Jeffrey M.; Klevytska, Alexandra M.; Schupp, James M.; Challacombe, Jean; Okinaka, Richard (1 December 2009). "The genome and variation of Bacillus anthracis". Molecular Aspects of Medicine 30 (6): 397–405.  
  11. ^ Jensen, G. B.; Hansen, B. M.; Eilenberg, J.; Mahillon, J. (18 July 2003). "The hidden lifestyles of Bacillus cereus and relatives". Environmental Microbiology 5 (8): 631–640.  
  12. ^ Drobniewski, FA (October 1993). "Bacillus cereus and related species.". Clinical Microbiology Reviews 6 (4): 324–38.  
  13. ^ Stenfors Arnesen, Lotte P.; Fagerlund, Annette; Granum, Per Einar (1 July 2008). "From soil to gut: and its food poisoning toxins". FEMS Microbiology Reviews 32 (4): 579–606.  
  14. ^ Schnepf, E; Crickmore, N; Van Rie, J; Lereclus, D; Baum, J; Feitelson, J; Zeigler, DR; Dean, DH (September 1998). "Bacillus thuringiensis and its pesticidal crystal proteins.". Microbiology and molecular biology reviews : MMBR 62 (3): 775–806.  
  15. ^ Agaisse, H; Gominet, M; Okstad, OA; Kolstø, AB; Lereclus, D (June 1999). "PlcR is a pleiotropic regulator of extracellular virulence factor gene expression in Bacillus thuringiensis.". Molecular microbiology 32 (5): 1043–53.  
  16. ^ Slamti, L; Perchat, S; Gominet, M; Vilas-Bôas, G; Fouet, A; Mock, M; Sanchis, V; Chaufaux, J; Gohar, M; Lereclus, D (June 2004). "Distinct mutations in PlcR explain why some strains of the Bacillus cereus group are nonhemolytic.". Journal of bacteriology 186 (11): 3531–8.  
  17. ^ Okstad, OA; Gominet, M; Purnelle, B; Rose, M; Lereclus, D; Kolstø, AB (November 1999). "Sequence analysis of three Bacillus cereus loci carrying PIcR-regulated genes encoding degradative enzymes and enterotoxin.". Microbiology (Reading, England) 145 (11): 3129–38.  
  18. ^ a b Slamti, L; Lereclus, D (Sep 2, 2002). "A cell-cell signaling peptide activates the PlcR virulence regulon in bacteria of the Bacillus cereus group.". The EMBO Journal 21 (17): 4550–9.  
  20. ^ Barnes JM (1947). "Penicillin and B. anthracis". J Path Bacteriol 194: 113–125.  
  21. ^ "Anthrax and tea". Society for Applied Microbiology. 2011-12-21. Retrieved 2011-12-21. 

External links

  • Bacillus anthracis genomes and related information at PATRIC, a Bioinformatics Resource Center funded by NIAID
  • Bacillus anthracisHazards in Animal Research Database -
  • ResourceBacillusPathema-
