Exposure from 2001 anthrax bioterrorism attacks was widespread

February 2007

Cellular immune responses to Bacillus anthracis, the bacterium that cause anthrax, were detected in people as far as a few city blocks away from the point of exposure after the October 2001 anthrax bioterrorism attack in Washington, D.C., according to a recent study.

The study examined clinical outcomes and immune responses, including hard-to-detect cell-mediated immune (CMI) responses, in people who were exposed to anthrax. Although there were several anthrax attacks during the autumn of 2001, this study focused specifically on the anthrax spore-laden envelope opened in Sen. Tom Daschle’s office on October 15, 2001. The office is in the Hart Senate Office Building, part of the larger 20-building Capitol complex.

Results showed that beyond the exposure zone, there were immune responses in people who worked throughout the Capitol, according to Daniel A. Freilich, MD, CDR, Medical Corps, USN. Freilich, Denise Doolan, PhD, and their colleagues wrote the study, which recently appeared in The Journal of Infectious Diseases.

Freilich said that although deemed hardy and viable, the bacteria appeared quickly thwarted by antibiotics or immune responses triggered by anthrax vaccine immunization. The significance of low-level exposure, however, should not be underestimated, he said.

“People who are looking at epidemiologic responses to bioterrorism exposures should add CMI to diagnostics,” Freilich told Infectious Disease News. “CMI might be a good way to add to the sensitivity of your outbreak investigation.”

Perimeter widened

Stratified on the basis of spore exposure, nasopharyngeal culture results and immunization status, participants (n=124) from the epidemiologically defined exposure zone were studied. Antibody and CMI responses to protective antigens were examined.

The original control group became a study group after antibody and CMI dose-exposure responses were detected in people outside the perimeter. “The biggest surprise of the study was the exposure of people outside the Hart Senate building. They were supposed to be our negative controls so we never expected responses,” Freilich said. “The anthrax got farther than was initially thought and many people mounted immune responses; therefore, one should have more caution. People appear to mount immune responses to even very small amounts of anthrax antigen.”

More than 6,000 people were tested for spore exposure within and outside the perimeter. In the absence of a definitive path for the far-reaching anthrax spread, researchers reported spores may have traveled on clothes or within nasal passages.

Anthrax spores primed cellular and possibly antibody immune responses in a dose-dependent manner and may have enhanced vaccine boost and recall responses, researchers said.

Despite high exposure, only 47.5% of people (n=59) in the two groups nearest the point of exposure had positive nasopharyngeal cultures. The results also showed that the greater the exposure, the more complete the immune response, according to the study.

Anti-protective antigen antibody and CMI responses were detected in 94% and 86% of the participants. Of the entire exposure group, 95% took antibiotics and no illness occurred.

HIV as model

Protective antigen and lethal factor specific cell-mediated immune responses were found in the absence of detectable antibodies, which researchers found consistent with HIV.

“The CDC published antibody data on more or less the same cohort, but they didn’t find much in terms of antibody responses. We weren’t surprised,” Freilich said.

Although antibodies were not detected, it did not mean that there were no specific immune responses to anthrax, he said.

“So the body knows it’s there, but is not making antibodies, most likely because of quantity,” Freilich said.

For the model basis, Freilich and his colleagues looked at data from health care workers accidentally exposed to HIV in the 1990s who were told they were not HIV positive due to favorable antibody profiles and because they did not seroconvert. The health care workers did have antigen-specific lipocyte responses to HIV.

“The HIV exposure was not enough to make an antibody response and was probably killed off quickly. We think that’s what happened here,” Freilich said. “From a vaccine point of view, it’s interesting because in theory the current vaccine formulation is not a lethal factor vaccine, but it doesn’t mean it doesn’t have a potentially effective amount of lethal factor antigen in it.”

For more information:

• Doolan D, Freilich D, Brice G, et al. The US Capitol anthrax exposures: clinical epidemiological and immunological characteristics. J Infect Dis. 2007:195:174-184.