1700s
1881
1918
Some scholars believe that
in Moses’ time, during the
10 plagues, anthrax may have
caused what was known as the
fifth plague, affecting horses,
cattle, sheep, camels and oxen.
The first clinical
descriptions of
cutaneous anthrax were
given by Maret in 1752
and Fournier in 1769.
During the first World War
there is evidence that the
German army used anthrax to
secretly infect livestock and animal
feed traded to the Allied Nations by
neutral partners.
Louis Pasteur tried to fully prove
how anthrax was spread and how
it made people or animals sick.
Pasteur successfully created a
vaccine for anthrax.
A comparatively less threatening but more
common infection route is through the skin,
known as
cutaneous anthrax
. 80-90% of lesions
recover without causing systemic infection
or complications [2]. Anthrax can also enter
through ingestion of contaminated meat.
Endospores enter the body through breaches in
the mucous lining, causing systemic infection.
Systemic anthrax infection occurs when a
number of organs are infected: the toxins
cause large-scale edema and tissue necrosis in
the body, leading to organ failure, heavy loss
of blood, loss of fluids and electrolyte, as well
as shock.
Inhalational anthrax is, however, the most
lethal, even after diagnosis and antibiotic
treatment. According to the Centre of Disease
Control and Prevention (CDC), the rate of
fatality among the most recent eighteen cases
of inhalational anthrax was more than 85%.
Inhaled endospores enter the lungs and trigger
macrophages to surround the foreign body
and phagocytosis (an initial immune response
whereby phagocy tes engu l f the foreign
body). Instead of dying, however, the bacteria
germinate inside the cells and are eventually
carried to lymph nodes and the blood stream,
hence, increasing the lethality of the infection
[3].
Antibiotics are the common cour se of
treatment for an anthrax infection, but it must
be administered in the early stages before
the bacter ia are able to secrete enough
toxins when the infection reaches a point of
“no return”. Thus, its efficacy as a bioweapon
comes from the infection’s nonspecific initial
symptoms, causing misdiagnosis and delayed
treatment. Scientists have been investigating
the possibility of creating antibodies that
bind to and inhibit the three toxin-forming
proteins. Cur rently, they have successfully
targeted edema factor (one of the proteins
responsible for the production of toxins that
disrupt signaling pathways) with a drug called
Adefovir, originally designed for Hepatitis B. The
pursuit is however only at its infancy and much
more remai
