The English name for this disease comes from the Greek word for coal, a reference to the characteristic black skin lesions that form in cutaneous anthrax infections. This visual hallmark, a painless ulcer with a necrotic center surrounded by vivid red swelling, has been recognized since ancient times, with the first recorded use of the word anthrax in English appearing in a 1398 translation of Bartholomaeus Anglicus's work. Before the late 19th century, the disease was known by a wide variety of names including Siberian plague, Cumberland disease, and woolsorter's disease, reflecting its impact on specific vulnerable groups and locations. The infection typically occurs through contact with the bacterium's spores, which can survive in the soil for decades or even centuries, entering the body through the skin, lungs, or intestines. While the skin form presents with a small blister that turns into a black eschar, the inhalation form presents with fever, chest pain, and shortness of breath, often leading to rapid death if untreated. The first clinical descriptions of cutaneous anthrax were given by Maret in 1752 and Fournier in 1769, but it was the German scientist Robert Koch who first identified Bacillus anthracis as the causative bacterium in 1876, proving that microbes could cause disease and revolutionizing the field of medicine.
The Microscopic Assassin
Bacillus anthracis is a rod-shaped, Gram-positive bacterium that exists in two forms: the active vegetative state and the dormant spore state. The spores are incredibly hardy, capable of surviving harsh conditions for decades, and can be found on all continents, including Antarctica. When a host ingests or inhales these spores, they germinate into active bacilli that multiply rapidly, producing two powerful exotoxins and a lethal toxin that causes death. The bacterium's lethality is due to its poly-D-glutamic acid capsule, which protects it from being eaten by host neutrophils, and its tripartite protein toxin consisting of protective antigen, edema factor, and lethal factor. These toxins work together to cause tissue destruction, bleeding, and death. The infection of herbivores begins with inhaled spores being transported into the lungs, where they are picked up by scavenger cells and transported to the lymph nodes in the chest cavity. Once in the lymph nodes, the spores germinate and burst the macrophages, releasing bacilli into the bloodstream to be transferred to the entire body. The production of these toxins causes septic shock and death, and even if antibiotics eradicate the bacteria, the toxins may remain in the system at lethal dose levels, killing the host.The Wool Sorter's Plague
In the 19th century, anthrax posed a major economic challenge to industries dealing with animal products, particularly in Britain where it affected workers in the wool, worsted, hides, and tanning industries. John Henry Bell, a doctor based in Bradford, was the first to link the mysterious and deadly woolsorter's disease to anthrax in 1878, showing that they were one and the same. The disease was so feared that it led to the Anthrax Prevention Act of 1919, following research by German bacteriologist Friederich Wilhelm Eurich. The French scientist Louis Pasteur developed the first effective veterinary vaccine in 1881, performing a public experiment at Pouilly-le-Fort where he vaccinated half of a group of animals and left the other half unvaccinated. All the unvaccinated animals died, while all the vaccinated animals survived, a triumph that was widely reported in the press. Pasteur's work led to the establishment of Pasteur Institutes across Europe and Asia, though the vaccine was initially unsuccessful in the challenging climate of rural Australia. The human vaccine for anthrax became available in 1954, and an improved cell-free vaccine became available in 1970, providing protection for those at high risk of infection.