Anthrax Bacillus BETTER

Bacillus anthracis is a gram-positive and rod-shaped bacterium that causes anthrax, a deadly disease to livestock and, occasionally, to humans. It is the only permanent (obligate) pathogen within the genus Bacillus. Its infection is a type of zoonosis, as it is transmitted from animals to humans.[1] It was discovered by a German physician Robert Koch in 1876, and became the first bacterium to be experimentally shown as a pathogen. The discovery was also the first scientific evidence for the germ theory of diseases.[2]

anthrax bacillus

Untreated B. anthracis infection is usually deadly. Infection is indicated by inflammatory, black, necrotic lesions (eschars). The sores usually appear on the face, neck, arms, or hands. Fatal symptoms include a flu-like fever, chest discomfort, diaphoresis (excessive sweating), and body aches. The first animal vaccine against anthrax was developed by French chemist Louis Pasteur in 1881. Different animal and human vaccines are now available. The infection can be treated with common antibiotics such as penicillins, quinolones, and tetracyclines.

Like Bordetella pertussis, it forms a calmodulin-dependent adenylate cyclase exotoxin known as anthrax edema factor, along with anthrax lethal factor. It bears close genotypic and phenotypic 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 endospores, in particular, are highly resilient, surviving extremes of temperature, low-nutrient environments, and harsh chemical treatment over decades or centuries.[citation needed]

The pXO1 plasmid (182 kb) contains the genes that encode for the anthrax toxin components: pag (protective antigen, PA), lef (lethal factor, LF), and cya (edema factor, EF). These factors are contained within a 44.8-kb pathogenicity island (PAI). The lethal toxin is a combination of PA with LF and the edema toxin is a combination of PA with EF. The PAI also contains genes which encode a transcriptional activator AtxA and the repressor PagR, both of which regulate the expression of the anthrax toxin genes.[11]

The plcR gene is part of a two-gene operon with papR.[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.[22][23] 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.[11] Bacillus cereus biovar anthracis, i.e. B. cereus with the two plasmids, is also capable of causing anthrax.

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

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.[24]

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.[25] Infections with B. anthracis can be treated with β-lactam antibiotics such as penicillin, and others which are active against Gram-positive bacteria.[26] Penicillin-resistant B. anthracis can be treated with fluoroquinolones such as ciprofloxacin or tetracycline antibiotics such as doxycycline.

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.[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. B. anthracis can be cultured on PLET agar, a selective and differential media designed to select specifically for B. anthracis.

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[10] 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.[12]

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).[12] 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.[12]

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.[31] 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.[32]

A bioterrorism attack using anthrax spores is a possibility. In 2001, a U.S. military researcher mailed envelopes containing anthrax spores to members of Congress and the media. Five of the 22 people who developed cutaneous or inhalation anthrax died. Federal agencies continue to work to prevent a future anthrax attack.

Bacillus anthracis bacteria cause anthrax. The bacteria produce spores that can live in the ground for years. Wild animals like deer, and livestock such as cattle or sheep, can inhale or ingest the dormant (inactive) spores while grazing.

After mixing with bodily fluids, anthrax bacteria activate, multiply and spread throughout the body. The bacteria cause a toxic, potentially deadly reaction. The same process happens to people who inhale, ingest or come into skin contact with the spores.

A diagnosis of anthrax is rare in the United States. People who work in certain professions or who travel to developing countries are more likely to be exposed to the bacteria that cause anthrax. If you work in a high-risk field, talk to your healthcare provider about getting the anthrax vaccine. Most people infected with anthrax recover after receiving prompt treatment with antibiotics or other therapies. Inhalation anthrax is deadlier and more difficult to treat. For these reasons, inhalation anthrax is considered a potential bioterrorism threat.

Anthrax is a serious infectious disease caused by gram-positive, rod-shaped bacteria known as Bacillus anthracis. It occurs naturally in soil and commonly affects domestic and wild animals around the world. People can get sick with anthrax if they come in contact with infected animals or contaminated animal products. Anthrax can cause severe illness in both humans and animals.

This can happen when people breathe in spores, eat food or drink water contaminated with spores, or get spores in a cut or scrape in the skin. It is very uncommon for people in the United States to get infected with anthrax.

Domestic and wild animals can become infected when they breathe in or ingest spores in contaminated soil, plants, or water. These animals can include cattle, sheep, goats, antelope, and deer. In areas where domestic animals have had anthrax in the past, routine vaccination can help prevent outbreaks. 041b061a72