A new study shows that more people were at risk of anthrax infection in the Oct. 2001 attack on U.S. Sen. Tom Daschle’s office than previously known. The research is published in the January 15 issue of The Journal of Infectious Diseases, now available online. On the other hand, the study shows, prompt intervention with antibiotics and vaccination appeared to be highly effective against the disease.
In October of 2001, a letter containing spores of Bacillus anthracis, the bacterium that causes the deadly disease anthrax, was opened in Daschle’s office at the Hart Senate Office Building in Washington, DC. Those in or near Daschle’s office, judged likely to have been exposed to the spores, received antibiotics or a vaccine, as did others within or outside the building, and no deaths resulted from this act of bioterrorism. According to the new study of the event, however, people in areas assumed to be at minimal risk of exposure showed immune responses suggesting they had been exposed.
The researchers, Denise L. Doolan, PhD, MPH, Daniel A. Freilich, MD, and coworkers of the Naval Medical Research Center, Silver Spring, MD, and elsewhere, prospectively studied clinical outcomes and immune responses in 123 subjects including 83 people who were nearby when the letter containing the anthrax spores was opened; 20 who were outside the building and presumed to be unexposed; and, for comparison, six individuals vaccinated against B. anthracis, two confirmed to have had anthrax, and 12 with no known B. anthracis exposure.
The results: Immune responses occurred not only in subjects in or near the Daschle office but also in those elsewhere in the Hart building, or even outside the building; the extent of exposure was thus greater than predicted. No associations were seen between exposure levels and immune responses or symptoms, but the most-exposed subjects were the only ones to have high-magnitude responses. Low-level exposure did not appear to trigger an antibody response, but did induce a response by cells of the immune system, Intermediate exposure induced both. Finally, cellular immune responses declined with post-exposure use of antibiotics, suggesting that the intervention impeded spore germination and implying that it may reduce the incidence of both subclinical and clinical B. anthracis infection.
In an accompanying editorial, James L. Hadler, MD, MPH, of the Infectious Diseases Section of the Connecticut Department of Public Health, commented that the study by Doolan and coworkers is “one of the few studies of the immune response to high-level, naturally occurring anthrax exposure in humans, and may be the first to describe cell-mediated responses to this pathogen.” Dr. Hadler said that the study’s data suggest that cell-mediated responses in B. anthracis infection may be more sensitive than antibody responses, and he recommended that future studies of anthrax vaccines investigate cellular immunity’s role in inhibiting the pathogen.