Anthrax Lethal Factor

Introduction

Lethal Factor (LF) is one of the enzyme components belonging to the Anthrax Toxin . Anthrax toxin is a three protein exotoxin secreted by the bacterium Bacillus anthracis made up of a binding protein known as the protective antigen (PA) and two enzyme components known as edema factor (EF) and lethal factor (LF).

Human Interaction

Anthrax is primarily a disease of domesticated and wild animals. Herbivores, such as cattle, sheep, horses, mules and goats are primarily affected because these animals maybe grazing on soils contaminated with Bacillus anthracis endospores.^[1][2] The blood of an animal that dies of anthrax can contain upward of 109 vegetative bacteria per milliliter. As the carcass decays, the bacteria form highly infectious endospores, which contaminate the local environment and can remain viable for long time periods. ^[1] The endosopres produced by Bacillus Anthracis remains viable for lengthy periods do to the poly-D- glutamic acid capsule, which itself is nontoxic. This capsule functions to protect the endospore from complement and other bactericidal components found in serum against phagocytic engulfment and destruction. This capsule plays an important role during the infection of anthrax, but is not important during the disease phase, which is primarily caused by PA, EF, LF. Genes encoding this plasmid are located on plasmid pX02.^[1][3].

Anthrax is not common is for humans. Humans become infect by be exposed to farm animal s or contaminated animal products such as wool, hides, flesh and blood. There are three ways in which Anthrax can be transmitted to humans:

Cutaneous Anthrax which is the most common form of the disease. This usually occurs when the endospores enter the body through injured skin and germinate. In most cases the bacteria remain contain at the site of infection and present as a lesion. A main characteristic of this type of infection is gelatinous edema at the site infection. As the infection advances, the site of infection goes through multiple stages. Next a papule (solid elevation of the skin) develops which turns into a vesicle (a small fluid-filled blister). The vesicle then develops into a pustule (pus-filled blister). The finally stage is the formation of a necrotic ulcer. In rare case, the infection could spread to the blood stream and cause septicemia.

Treatments

Structure

Function

References