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Bacillus anthracis as an agent of bioterrorism: a review emphasizing surgical treatment

Binkley, Charles E; Cinti, Sandro; Simeone, Diane M; Colletti, Lisa M
OBJECTIVE: To familiarize surgeons with the specific complications of cutaneous, gastrointestinal, inhalation, and systemic infection with Bacillus Anthracis, which may require surgical treatment. SUMMARY BACKGROUND DATA: The recent cases of intentional exposure to Bacillus Anthracis in the United States make familiarity with the basic microbiology, clinical manifestations, diagnosis, treatment, and control of this disease essential if mortality and morbidity is to be minimized, particularly following mass exposure. Although the treatment of Bacillus Anthracis infection is primarily medical, there are specific surgical complications with which the surgeon should be familiar. METHODS: A review of the literature was undertaken, utilizing electronic databases on infection with Bacillus Anthracis, as well as consultation with experts in this field. Emphasis was placed on the diagnosis and treatment of complications of infection that might require surgical intervention. RESULTS: Cutaneous anthrax infection results in eschar formation and massive soft tissue edema. When involving the extremities, increased compartment pressure requiring fasciotomy may result. Primary infection of the gastrointestinal tract may result in oropharyngeal edema and respiratory compromise requiring a surgical airway. Direct involvement of the lower gastrointestinal tract can result in intestinal ulceration, necrosis, bleeding, and perforation, which would require surgical exploration and resection of affected segments. Systemic sepsis, most often associated with inhalation anthrax, can cause massive ascites, electrolyte derangements, and profound shock requiring aggressive fluid resuscitation and careful hemodynamic monitoring and respiratory support. Systemic anthrax infection can also lead to gastrointestinal involvement by hematogenous dissemination, resulting in complications and requiring surgical management similar to direct gastrointestinal infection. CONCLUSIONS: Cutaneous, gastrointestinal, inhalation and systemic infection with Bacillus Anthracis can result in complications which would require familiarity with the pathogenesis and manifestations of this disease in order to recognize and treat promptly and successfully by surgical intervention.
PMCID:1422543
PMID: 12131080
ISSN: 0003-4932
CID: 2418072

Connecting islet development and developing useful islets

Burant, Charles F; Simeone, Diane M
PMID: 11854014
ISSN: 1043-2760
CID: 2418082

NF-kappaB activation in pancreas induces pancreatic and systemic inflammatory response

Chen, Xueqing; Ji, Baoan; Han, Bing; Ernst, Stephen A; Simeone, Diane; Logsdon, Craig D
BACKGROUND & AIMS/OBJECTIVE:The role of nuclear factor kappaB (NF-kappaB) activation in acute pancreatitis is uncertain. The transcription factor NF-kappaB is activated early in acute pancreatitis, and NF-kappaB is widely considered a key element in inflammatory responses based on its ability to regulate the expression of inflammatory mediators in vitro. However, its role in vivo in specific diseases remains unclear, and the current data on the role of NF-kappaB in acute pancreatitis is primarily correlative. METHODS:In this study, NF-kappaB was directly activated within the pancreas using adenoviral-mediated transfer of an active subunit, RelA/p65 (Adp65), delivered by intraductal injection. RESULTS:Administration of Adp65 led to the infection of a population of acinar cells within the pancreas, the activation of NF-kappaB, the expression of NF-kappaB target genes, and an inflammatory response. Administration of Adp65 increased the infiltration of neutrophils to the pancreas and lung and caused widespread damage to pancreatic acinar cells. In contrast, at the same titer, control adenovirus (AdGFP) had no effect on these parameters. The level of NF-kappaB activation and the severity of inflammation were reduced when an adenovirus bearing the inhibitory subunit IkappaB-alpha was coadministered with Adp65. CONCLUSIONS:Thus, activation of NF-kappaB within the pancreas was sufficient for the initiation of an inflammatory response in this model. These results help define the specific role of NF-kappaB activation in acute pancreatitis.
PMID: 11832459
ISSN: 0016-5085
CID: 5080452