Bacillus Anthracis

INTRODUCTION

Bacillus anthracis has recently become popular as the causative agent of anthrax infections. Belonging to the bacillus species, the bacterium is considered, along with Bacillus cereus, to be of extreme medical importance. Until recently, the condition caused by the bacterium was rarely heard of. Although the bacterium is naturally found in the soil, its rare occurrences in humans have only been observed in those working with livestock or imported livestock products, therefore the disease was considered to be merely zoonotic.

HISTORICAL BACKGROUND

Although anthrax is not currently considered to be a common infection, we have found, through descriptions found in the early literature of Greeks, Romans, and Hindus, to have been affecting humans for thousands of years. It is now believed by many scientists to have been the source of both the fifth and sixth plagues described in the biblical book of Exodus.

B. anthracis is infamous in the history of bacteriology as being the first bacterium to have been identified as the cause of disease by, the German physician, Dr. Robert Koch. Also, it was with the help of early studies of the bacteria during 1876, that Dr. Koch developed his fabulous postulates! Louis Pasteur and his colleagues, independent of Dr. Koch, also found the bacteria to be the definitive cause of disease, and later observed that B. anthracis spores released from carcasses of animals that had died of anthrax were capable of returning to the soil surface through the action of earthworms.

MORPHOLOGY & CHARACTERISTICS

Bacillus anthracis is identified in the laboratory as being a large, aerobic, rod-shaped bacterium that is capable of producing spores under harsh environmental conditions. Each bacterium will produce a single ellipsoidal-shaped centrally-located spore that is capable of surviving several chemicals and extreme temperatures. Although the bacterium grows best in an aerobic environment, it has also been found to multiply under anaerobic conditions. The bacterium is both gram and catalase positive, non-motile, and will normally microscopically observed in chains. When cultured upon blood agar, the bacteria will form non-hemolytic gray or white colonies similar in structure to ground glass.

There are several microbiological differences used in differentiating B. anthracis bacilli from non-B. anthracis bacilli, otherwise known as pseudoanthrax bacilli. While B. anthracis bacilli will form a capsule on bicarbonate agar and show no growth on penicillin agar, the opposite is observed of pseudoanthrax bacilli. The most obvious difference between the differing types of bacilli would be the fact that B. anthracis bacilli will always be found to be non-motile, whereas pseudoanthrax bacilli is generally found to be mobile.

The bacterium’s specific species name, “anthracis” was derived from the Greek word “ anthrakos” meaning coal, referring to the indistinguishable black lesions, which occur in cutaneous anthrax cases. There have been several nicknames for the disease caused by the bacterium, anthrax, such as Black Bane during medieval times, Woolsorter’s Disease in England, and miltsiekte meaning “spleen sickness” in Africa.

STRUCTURE

The B. anthracis bacterium’s structure consists of four layers, which encapsulate its nucleus, and two of which contribute to the bacterium’s pathogenicity. The nucleus is surrounded by a plasma membrane, which is enclosed by a thick layer of peptidoglycan, the layer responsible for the gram positive-ness of the bacterium. Surrounding the peptidoglycan is a thin slime layer and capsule, which both contribute as a virulence factor of the bacterium. Both the slime layer and the capsule protect the bacterium from phagocytosis by defensive macrophages of the infected host.

The pathogenicity of B. anthracis heavily depends upon the exotoxin produced by the bacterium once it has found the proper environment to multiply. The toxin consists of three different proteins including the protective antigen, lethal factor, and edema factor. When the protective antigen has been activated by a receptor site on the host cell surface, a secondary binding site for either lethal or edema factor will be revealed. Following the adherence of either of the factors, the entire complex is endocytosed into the cell. At this point, the attached factor will be released from the complex and invade the cell.

Once within the cell, the edema factor will increase the concentration of camp, a molecule used in the regulation of cell functions, leading to the accumulation of fluids both between and within cells, resulting in the edema observed in cutaneous anthrax cases. On the other hand,