to those of cutaneous anthrax, but injection anthrax can spread throughout the body faster and can be harder to recognize and treat compared to cutaneous anthrax. symptoms include, fever, chills, a group of small bumps or blisters that may itch, appearing where the drug was injected. a painless sore with a black center that appears after the blisters or bumps. swelling around the sore. abscesses deep under the skin or in the muscle where the drug was injected. this type of entry has never been found in the us. prevention and treatment a number of anthrax vaccines have been developed for preventive use in livestock and humans. anthrax vaccine adsorbed (ava) may protect against cutaneous and inhalation anthrax. however, this vaccine is only used for at-risk adults before exposure to anthrax and has not been approved for use after exposure. infections with b. anthracis can be treated with β-lactam antibiotics such as penicillin, and others which are active against gram-positive bacteria. penicillin-resistant b. anthracis can be treated with fluoroquinolones such as ciprofloxacin or tetracycline antibiotics such as doxycycline. laboratory research 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. the addition of milk to the tea completely inhibits its antibacterial activity against anthrax. 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. b. anthracis can be cultured on plet agar, a selective and differential media designed to select specifically for b. anthracis. recent research advances in genotyping methods have led to improved genetic analysis for variation and relatedness. these methods include multiple-locus variable-number tandem repeat analysis (mlva) and typing systems using canonical single-nucleotide polymorphisms. the ames ancestor chromosome was sequenced in 2003 and contributes to the identification of genes involved in the virulence of b. anthracis. recently, b. anthracis isolate h9401 was isolated from a korean patient suffering from gastrointestinal anthrax. the goal of the republic of korea is to use this strain as a challenge strain to develop a recombinant vaccine against anthrax. the h9401 strain isolated in the republic of korea was sequenced using 454 gs-flx technology and analyzed using several bioinformatics tools to align, annotate, and compare h9401 to other b. anthracis strains. the sequencing coverage level suggests a molecular ratio of pxo1:pxo2:chromosome as 3:2:1 which is identical to the ames florida and ames ancestor strains. h9401 has 99.679% sequence homology with ames ancestor with an amino acid sequence homology of 99.870%. h9401 has a circular chromosome (5,218,947 bp with 5,480 predicted orfs), the pxo1 plasmid (181,700 bp with 202 predicted orfs), and the pxo2 plasmid (94,824 bp with 110 predicted orfs). as compared to the ames ancestor chromosome above, the h9401 chromosome is about 8.5 kb smaller. 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. since the genome of b. anthracis was sequenced, alternative ways to battle this disease are being endeavored. bacteria have developed several strategies to evade recognition by the immune system. the predominant mechanism for avoiding detection, employed by all bacteria is molecular camouflage. slight modifications in the outer layer that render the bacteria practically invisible to lysozymes. three of these modifications have been identified and characterized. these include (1) n-glycosylation of n-acetyl-muramic acid, (2) o-acetylation of n-acetylmuramic acid and (3) n-deacetylation of n-acetyl-glucosamine. research during the last few years has focused on inhibiting such modifications. 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. host interactions as with most other pathogenic bacteria, b. anthracis must acquire iron to grow and proliferate in its host environment. the most readily available iron sources for pathogenic bacteria are the heme groups used by the host in the transport of oxygen. to scavenge heme from host hemoglobin and myoglobin, b. anthracis uses two secretory siderophore proteins, isdx1 and isdx2. these proteins can separate heme from hemoglobin, allowing surface proteins of b. anthracis to transport it into the cell. b. anthracis must evade the immune system to establish a successful infection. b. anthracis spores are immediately phagocytosed by macrophages and dendritic cells once they enter the host. the dendritic cells can control the infection through effective intracellular elimination, but the macrophages can transport the bacteria directly inside the host by crossing a thin layer of epithelial or endothelial cells to reach the circulatory system. normally, in the phagocytosis process, the pathogen is digested upon internalization by the macrophage. however, rather than being degraded, the anthrax spores hijack the function of the macrophage to evade recognition by the host immune system. phagocytosis of b. anthracis spores begins when the transmembrane receptors on the extracellular membrane of the phagocyte interacts with a molecule on the surface of the spore. 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. this cascade results in phagocytic cellular activation and induction of an inflammatory response. sampling the presence of b. anthracis can be determined through samples taken on non-porous surfaces. 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. german physician aloys pollender (1799–1879) is credited for discovery. b. anthracis was the first bacterium conclusively demonstrated to cause disease, by robert koch in 1876. 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. throughout the 19th century, anthrax was an infection that involved several very important medical developments. the first vaccine containing live organisms was louis pasteur's veterinary anthrax vaccine.