Inhaled non-capsulated Bacillus anthracis in A/J mice: nasopharynx and alveolar space as dual portals of entry, delayed dissemination, and specific organ targeting.

Abstract

Bacillus anthracis virulence is dependent on toxins and capsule. Encapsulation is associated with dissemination. We hypothesized that eliminating capsule would modify the portal of entry and the spread of bacteria. Using a bioluminescent model of inhalational anthrax, we demonstrated that aerosolized spores of a capsule-deficient strain administered at moderate doses initiated infection in the nasopharynx. Dissemination beyond the nasopharynx was delayed for at least 24h and then targeted the kidneys. Interestingly, high intranasal doses led to spore germination in the alveoli. We conclude that eliminating capsule while maintaining toxin production alters dissemination, but allows infection initiation in the lungs.