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We describe a case of bacterial aortitis caused by Burkholderia pseudomallei. This patient presented with prolonged fever and hoarseness of voice. Aneurysm removal with Dacron graft replacement was performed, followed by a prolonged course of antibiotics. The patient has progressed satisfactorily without recurrence of symptoms. Previous case reports are summarized.
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We recently managed 4 patients with cystic fibrosis who had acquired Burkholderia pseudomallei infection after exposure in a region of endemicity. Person-to-person transmission between 2 siblings may have occurred; otherwise, the evidence suggests that cystic fibrosis may increase the likelihood of infection with this organism, and patients should be warned of this possibility and cautioned to avoid high-risk activities.
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Antigen-specific T cells are important sources of interferon (IFN)-gamma for acquired immunity to intracellular pathogens, but they can also produce IFN- gamma directly via a "bystander" activation pathway in response to proinflammatory cytokines. We investigated the in vivo role of cytokine- versus antigen-mediated T cell activation in resistance to the pathogenic bacterium Burkholderia pseudomallei. IFN-gamma, interleukin (IL)-12, and IL-18 were essential for initial bacterial control in infected mice. B. pseudomallei infection rapidly generated a potent IFN-gamma response from natural killer (NK) cells, NK T cells, conventional T cells, and other cell types within 16 h after infection, in an IL-12- and IL-18-dependent manner. However, early T cell- and NK cell-derived IFN-gamma responses were functionally redundant in cell depletion studies, with IFN-gamma produced by other cell types, such as major histocompatibility complex class II(int) F4/80(+) macrophages being sufficient for initial resistance. In contrast, B. pseudomallei-specific CD4(+) T cells played an important role during the later stage of infection. Thus, the T cell response to primary B. pseudomallei infection is biphasic, an early cytokine-induced phase in which T cells appear to be functionally redundant for initial bacterial clearance, followed by a later antigen-induced phase in which B. pseudomallei-specific T cells, in particular CD4(+) T cells, are important for host resistance.
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BACKGROUND: Bacterial pathogens and their products are potential agents of biological terrorism and biological warfare. These agents can be deployed through simple aerosol delivery systems and thereby cause widespread disease and death. METHODS: This report is a review of bacterial species that have been employed for development of biological terrorism, relying on a system for classification of their threat developed by the Centers for Disease Control. RESULTS: Physicians must understand how to recognize early signs and symptoms caused by bacterial agents. Clinical findings often seen on presentation are emphasized along with a summary of therapeutic approaches. CONCLUSIONS: Initiation of immediate therapy and supportive care provides the best chance for survival from these potentially lethal and devastating infections. A high index of suspicion must be maintained, especially in the setting of a sudden influx of cases with what are often relatively nonspecific symptoms.
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Pseudomonas pseudomallei was recovered from urine specimens of two patients who acquired the organism after they were admitted to a hospital in a region in which it is endemic. Both patients were diabetic and both had urethral catheters passed while they were hospitalized. samples of soil taken from the hospital grounds yielded an isolate of P. pseudomallei that was identical biochemically and by antibiogram to the two isolates recovered from the urine specimens of the two patients. The two patients stayed in wards located in separate hospital blocks, which were geographically distinct but connected by a walkway. The relevant clinical histories of the two patients and the epidemiologic and microbiologic characteristics of the P. pseudomallei isolates were studied. Sera from both patients showed a significant rise in titers of antibody specific for P. pseudomallei. These two patients are considered to represent the first reported cases of hospital-acquired infection due to P. pseudomallei.
We report three cases of corneal ulcer caused by Pseudomonas pseudomallei. In all cases corneal trauma preceded the development of extensive ulcers, subconjunctival abscesses, and hypopyon. Treatment for a total of 8 weeks with topical and/or parenteral ceftazidime followed by amoxicillin-clavulanic acid produced resolution of infection in each case.
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