CD14 and Mac-1 work together to increase the macrophage internalization of B. anthracis spores. (a) CD14 and TLR2 work in close proximity to propagate the activation signal. Mac-1 starts in a closed conformation which keeps the integrin from binding the spores, keeping them out of the cell. (b) CD14 binds the rhamnose residues on the BclA of the exosporium leading to TLR2-mediated activation of PI3K. (c) Activation of PI3K pushes Mac-1 into its open conformation so the spore can be bound and internalized (information from Oliva

CapD protein crystal structure of B. anthracis

Koch in c. 1900

The Anthrax Disease Cycle. Anthrax particles live in a vegetative state until exposed to oxygen, where they form many infectious spores. They can live in the soil and be consumed by herbivores. Large herbivores, like cows, are most susceptible to anthrax disease, and humans are affected by animal waste, fecal matter, or corpses, from these herbivores. Anthrax infection is spread to humans when spores gain entry into the body, whether that is from inhalation, open wounds, or another method of entrance. Once inside, the spores are activated, allowing the bacteria to multiply and spread their toxins. Another spread of infection is through biting flies, like mosquitoes, that come in contact with the blood and feces of herbivores, preceded by contact with human flesh (information from Bergman

Koch's drawing of tuberculosis bacilli in 1882 (from Die Ätiologie der Tuberkulose)

Photograph of Koch (third from the right) and other members of the German Cholera Commission in Egypt, 1884