Anthrax Structure and Its Key Components
An overview of the cellular and molecular adaptations of *Bacillus anthracis* that enable its environmental survival and pathogenesis within a host.
An overview of the cellular and molecular adaptations of *Bacillus anthracis* that enable its environmental survival and pathogenesis within a host.
The bacterium Bacillus anthracis is the causative agent of the disease anthrax. Its ability to survive and cause illness is a direct result of several highly specialized structures. These components are distinct in form and function, contributing to how the bacterium operates both inside a host and in the external environment.
The active, growing form of Bacillus anthracis is the vegetative cell, which is responsible for multiplying within a host. This microbe is a large rod, typically measuring 3 to 5 micrometers in length, and individual cells often link together to form long, chain-like filaments.
A defining feature is its classification as a Gram-positive bacterium, which refers to its thick cell wall made of peptidoglycan. This robust layer provides structural integrity and retains the violet dye used in Gram staining, a fundamental technique for bacterial identification.
Encasing the vegetative cell is a capsule that serves as a primary defense mechanism within a host. Its main purpose is to shield the bacterium from the host’s immune system by preventing phagocytosis, a process where immune cells engulf and destroy it.
The capsule’s composition is highly unusual. While most bacterial capsules are made from polysaccharides (complex sugars), the B. anthracis capsule is a polypeptide composed of poly-D-glutamic acid. The genetic instructions for producing this protective capsule are carried on a small, circular piece of DNA called the pXO2 plasmid.
When environmental conditions become unfavorable, Bacillus anthracis transforms into a dormant structure called an endospore. This is not a reproductive cell but a hardened, non-replicating survival pod designed to protect the bacterium’s genetic material from extreme environmental challenges.
The endospore’s resilience comes from its complex, multi-layered anatomy. At its center is the core, which houses the cell’s DNA and ribosomes, surrounded by a thick cortex made of specialized peptidoglycan. The entire structure is encased in a protein-rich spore coat, which acts as a barrier against chemical disinfectants, UV radiation, and heat.
This durability allows anthrax spores to remain viable in soil for many years. The endospore is the form of the bacterium that initiates an infection. Once spores enter the body, favorable conditions trigger their germination back into active vegetative cells.
The severe symptoms of anthrax are caused not by the bacteria themselves, but by a powerful three-part toxin they secrete. This tripartite toxin is assembled from three separate proteins that are individually non-toxic. They only become active and cause cellular damage when they combine on the surface of a host’s cells. The genes for these proteins are located on a plasmid known as pXO1.
The three protein components are Protective Antigen (PA), Edema Factor (EF), and Lethal Factor (LF). The process begins when the PA protein binds to receptors on a host cell. Multiple PA molecules then assemble into a ring-shaped structure called a heptamer, which functions as a docking platform for the other two components.
Once the PA heptamer is formed, it can bind with either EF or LF proteins. The host cell then draws the entire complex inside through endocytosis. Inside the cell, the PA heptamer acts as a channel, releasing the EF or LF components into the cell’s interior where they carry out their damaging functions.
The combination of Protective Antigen and Edema Factor creates Edema Toxin. Edema Factor works by disrupting the water balance within cells, leading to a massive fluid buildup in surrounding tissues, which manifests as severe swelling, or edema.
The combination of Protective Antigen with Lethal Factor forms Lethal Toxin. This toxin targets and destroys specific signaling proteins inside cells, which triggers cell death and leads to tissue necrosis.