Bordetella pertussis in Adult Pneumonia Patients1

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 11, No. 4, April 2005 639 each of the 5 routes. B. pseudomallei could be detected in the tissues of IVand IP-infected mice earlier and in higher numbers than in those of intranasally and orally-infected mice, despite the fact that all mice received equal numbers of bacteria. This finding reflects differences in the innate immune response, depending on the route of infection. Bacterial numbers in mice infected by the IV or IP route reached >106 CFU by day 2 postinfection, which indicates a failure of the innate immune response to control infection, leading to overwhelming sepsis and death. Bacterial loads in tissues after challenge with a lethal dose of highly virulent NCTC 13178 did not indicate any tropism for the lung after intranasal infection. As early as day 1, bacterial loads were greatest in the liver and spleen, not lungs, of C57BL/6 and BALB/c mice following intranasal challenge. This finding suggests a very early systemic spread of B. pseudomallei from the lungs to other organs. Bacteria were detected in the brains of all mice after infection by either the IV, IP, intranasal, or oral route. Colonies recovered from the brains of C57BL/6 mice infected by the intranasal or oral routes were mucoid in appearance. In comparison, bacteria recovered from brains of C57BL/6 mice that were challenged by the IV or IP route demonstrated the characteristic wrinkled shape on Ashdown agar and may have been a consequence of the overwhelming septicemia that spilled over to all organs. Variation in colonial morphology of B. pseudomallei has been documented previously (8), and biofilm formation may be an adaptation of B. pseudomallei that enables it to evade host immune responses or to survive within unfavorable environments (9,10). The variation in colonial morphology on Ashdown agar observed in bacteria isolated from brains of C57BL/6 mice infected by the intranasal or oral route may reflect a change to biofilm formation of B. pseudomallei in this tissue. In summary, the results of this study reiterate the validity of the mouse model for differential susceptibility to B. pseudomallei, regardless of the route of infection. The data also emphasize that virulence depends on the portal of entry of B. pseudomallei. Researchers should, therefore, be particularly cautious when comparing and extrapolating data from studies that use different methods of infection.