Bacillus anthracis is a gram-positive and rod-shaped bacterium that causes anthrax, a deadly disease to livestock and, occasionally, to humans.

It forms a protective layer called endospore by which it can remain inactive for many years and suddenly becomes infective under suitable environmental conditions.

Fatal symptoms include a flu-like fever, chest discomfort, diaphoresis (excessive sweating), and body aches.

On agar plates, they form large colonies several millimeters across that are generally white or cream colored.

[4] It is one of few bacteria known to synthesize a weakly immunogenic and antiphagocytic protein capsule (poly-D-gamma-glutamic acid) that disguises the vegetative bacterium from the host immune system.

The difference in capsule composition is also significant because poly-g-D-glutamic acid has been hypothesized to create a negative charge which protects the vegetative phase of the bacteria from phagocytosis by macrophages.

[6] The capsule is degraded to a lower molecular mass and released from the bacterial cell surface to act as a decoy to protect the bacteria from complement.

B. anthracis endospores, in particular, are highly resilient, surviving extremes of temperature, low-nutrient environments, and harsh chemical treatment over decades or centuries.

[8] Because of these attributes, B. anthracis endospores are extraordinarily well-suited to use (in powdered and aerosol form) as biological weapons.

Expression of the capsule operon is activated by the transcriptional regulators AcpA and AcpB, located in the pXO2 pathogenicity island (35 kb).

A contributing factor to the reconstruction is B. anthracis being monomorphic, meaning it has low genetic diversity, including the absence of any measurable lateral DNA transfer since its derivation as a species.

The lack of diversity is due to a short evolutionary history that has precluded mutational saturation in single nucleotide polymorphisms.

During the B. anthracis lifecycle, it spends a significant amount of time in the soil spore reservoir stage, in which DNA replication does not occur.

[11] B. cereus is a soil-dwelling bacterium which can colonize the gut of invertebrates as a symbiont[14] and is a frequent cause of food poisoning[15] It produces an emetic toxin, enterotoxins, and other virulence factors.

[11] B. thuringiensis is an microrganism pathogen and is characterized by production of parasporal crystals of insecticidal toxins Cry and Cyt.

[19] In B. anthracis, however, the plcR gene contains a single base change at position 640, a nonsense mutation, which creates a dysfunctional protein.

[21][22] The papR gene encodes a small protein which is secreted from the cell and then reimported as a processed heptapeptide forming a quorum-sensing system.

[citation needed] The symptoms in anthrax depend on the type of infection and can take anywhere from 1 day to more than 2 months to appear.

All types of anthrax have the potential, if untreated, to spread throughout the body and cause severe illness and even death.

[citation needed] Components of tea, such as polyphenols, have the ability to inhibit the activity both of B. anthracis and its toxin considerably; spores, however, are not affected.

[27] Activity against the B. anthracis in the laboratory does not prove that drinking tea affects the course of an infection, since it is unknown how these polyphenols are absorbed and distributed within the body.

These methods include multiple-locus variable-number tandem repeat analysis (MLVA) and typing systems using canonical single-nucleotide polymorphisms.

Due to the high pathogenecity and sequence similarity to the Ames Ancestor, H9401 will be used as a reference for testing the efficacy of candidate anthrax vaccines by the Republic of Korea.

[29] As a result the enzymatic mechanism of polysaccharide de-acetylases is being investigated, that catalyze the removal of an acetyl group from N-acetyl-glucosamine and N-acetyl-muramic acid, components of the peptidoglycan layer.

[citation needed] As with most other pathogenic bacteria, B. anthracis must acquire iron to grow and proliferate in its host environment.

However, rather than being degraded, the anthrax spores hijack the function of the macrophage to evade recognition by the host immune system.

CD14, an extracellular protein embedded in the host membrane, binds to rhamnose residues of BclA, a glycoprotein of the B. anthracis exosporium, which promotes inside-out activation of the integrin Mac-1, enhancing spore internalization by macrophages.