Bacillus anthracis is a spore-forming bacterium that causes anthrax in humans and animals. It is a zoonaotic disease in that it is normally transmitted by handling of animal carcases. Human are an accidental host. Transmission may also be via aerosol which encounter breaks in the skin (cutaneous anthrax) or get into the lungs (pulmonary anthrax). B. anthracis is hemalysis negative and catalase positive. Sporulation does not occur in vivo and the spores can remain in the environment for years. The spores can plasmids and a chromosome. Calcium dipicolinate stabilizes the spore. 

The endospores of Bacillus anthracis are the infectious particles of anthrax. Spores are dormant bacterial morphotypes able to withstand harsh environments for decades, which contributes to their ability to be formulated and dispersed as a biological weapon. See Liu. See UCLA

Types of Anthrax: 

The least severe but most common anthrax is called  cutaneous anthrax where spores are deposited in an abrasion. Infection begins as an erythematous macule or papule which enlarges. The most severe form of anthrax is inhalation anthrax (Woolsorter’s Disease) where spores are inhaled and deposited in terminal alveoli. They are then engulfed by macrophages and transported to regional lymph nodes where they germinate. Case fatality rate is about 85% even with treatment.  Gastrointestinal anthrax is the least common anthrax and results from ingestion of contaminated meat or food where organisms or spores penetrate the intestinal mucosa. CFR is about 50%. 

The incidence (1-2 cases of cutaneous disease per year) of naturally acquired anthrax is rare in the United States. In fall 2001, intentional contamination of mail resulted in 22 cases of anthrax, of which 11 were inhalation and 11 cutaneous.

Pathology/Virulence:

The two major factors responsible for virulence are presence of the capsule and toxin production. 

Capsule:

The capsule (slime layer) is a polymer of amino acids (D-glutamate), unlike most other bacteria which have polysaccharide capsules. The cells excrete the capsule for protection and virulence. The capsule and the S-layer are compatible, but they can both be formed independently (without the presence of the other). A characteristic mucoid or “smooth” colony variant is correlated with capsule production ability. Virulent strains all form the capsule, and “rough” colony capsules are avirulent. Growth in atmospheric CO₂ cause the antiphagocytic capsule and anthrax toxin proteins to be synthesized. The nontoxic capsule has an important role in infection establishment, while the end disease phases are mediated by the toxin. See Microbe Wiki

The capsule of Bacillus anthracis, composed of poly-D-glutamic acid, serves as one of the principal virulence factors during anthrax infection. By virtue of its negative charge, the capsule is purported to inhibit host defence through inhibition of phagocytosis of the vegetative cells by macrophages. In conjunction with lethal toxin and oedema toxin, whose target cells include macrophages and neutrophils, respectively, the capsule allows virulent anthrax bacilli to grow virtually unimpeded in the infected host. See Ezzell

Exotoxins: 

Two B anthracis toxiins, lethal toxin (LT) and edema toxin (ET) are primary mediators of disease. LT and ET each consist of two components, an enzymatic activity, lethal factor (LF) and I. edema factor (EF), respectively, and a shared cofactor,  protective antigen. The protective antigen is responsible for getting the other 2 toxins into the cell. Thus if you have protection against this toxin you have immunity to the other two toxins. 

The three exotoxin compoents (PA, letal factor, and edema factor) are encoded on virulence plasmid pX01, which is 185.5 kilobase pairs (kbp) in size. The other virulence plasmid, pX02, is 95.3 kbp and codes for 3 genes (cap!, capB, and capC) associated with the synthesis of the polyglutamyl capsule, which inhibits phagocytosis of vegetative antrhax bacilli.

–Edema Toxin: consists of protective antigen (PA), which permits entry of the toxin into the host cell, and edema factor, a calmodulin-dependent adenylate cyclase that increases intracellular levels of cyclic adenosine monophospate, upsetting water homeostasis.

–Lethal toxin: consists of PA and lethal factor, a zinc metalloprotease that ininactivates mitogen-actived protein kinase in vtiro (It has been shown to cleave the N Terminus of MKKs 1, 2, 3, 4, 6, and 7 and thereby suppress phosphorylation of downstream mitogen-activated protein kinases (MAP kinases) including ERK, p38 and JNK/SAPK. ) and stimulates macrophages to release tumor necrosis factor alpha and interleukin 1beta.

Symptoms

During the first stage of inhaled anthrax illness, the symptoms are similar to influenza, including fever, coughing, sore throat, fatigue, sweating, vomiting, diarrhea, headache, nausea, chest pain, and shortness of breath. Symptoms are much more extreme in the second stage, which can result in death in 2-48 hours. 

Detection: 

Laboratory diagnosis of anthrax involves identifcation of B. anthracis microbiologically, serologically, or by use of more sensitive molecular technieques. B. anthracis forms rough gra-white colonies with characteristic “comet-tail” protrusions on sheep blood agar. It is aerobic, Gram-positive, spore-forming, and nonmotile.

Treatment: 

Treatment of B. anthracis includes penicillin, doxycycline and ciprofloxacin. Antibiotics are used against anthrax but must be administered before the bacterial load has reached 3 x 108 CFU.

Treatment of any form of anthrax infection is generally the same: aggressive antibiotics and supportive care. Intravenous ciprofloxacin or deoxycycline is recommended for treatment of anthrax, usually as part of a cocktail of antibiotics.