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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.

Abstract: Bacillus anthracis is the causative agent of anthrax that is characterized by septicemia and toxemia. Many vaccine strategies were described to counteract anthrax infection. In contrast with veterinary live vaccines, currently human vaccines are acellular with the protective antigen, a toxin component, as the main constituent. However, in animal models this vaccine is less efficient than the live vaccine. In this study, we analyzed the protection afforded by a single extractable surface element. The poly-γ-d-glutamate capsule is covalently linked to the peptidoglycan. A preparation of peptidoglycan-linked poly-γ-d-glutamate (GluPG) was tested for its immunogenicity and its protective effect. GluPG injection, in mice, elicited the production of specific antibodies directed against poly-glutamate and partially protected the animals against lethal challenges with a non-toxinogenic strain. When combined to protective antigen, GluPG immunization conferred full protection against cutaneous anthrax induced with a fully virulent strain. [Copyright &y& Elsevier]