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Title:   Author  item
                                            Sacco, Randyitem
                                            Kunkle, Robertitem
                                            Palmer, Mitchellitem
                                            Rimler, Richard

                                                         - *Rick*
  Submitted to: Research Workers in Animal Diseases Conference Proceedings
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 10/7/1999
                                    Publication  Date: N/A
                                    Citation: N/AInterpretive Summary:
                                Technical Abstract: Members of the genus Bordetella cause upper respiratory infections in a number of animal species.  While these organisms produce a number of virulence factors, only endotoxin, tracheal cytotoxin, and dermonecrotic toxin (DNT) are common to all pathogenic Bordetella species.  The role of DNT in the pathogenesis of Bordetella infections has yet to be elucidated.  In the present study, DNT was purified from Bordetella avium.  B. avium DN had an isoelectric point in the range of pH 6.3-6.7 and a molecular size of approximately 155 kDa.  Mice were given an intraperitoneal injection of one of several doses of purified B. avium DNT.  At the time of necropsy, tissue samples from mice were collected for histopathological evaluation.  The most remarkable lesions were seen in lymphoid tissues, including spleen, thymus, mesenteric lymph node (MLN), and ileal Peyer's patches (PP).  MLN and PP had prominent germinal centers primarily composed of lymphoblasts.  In addition, there was a moderate to marked apoptosis in splenic white pulp, thymic cortex, MLN, and PP as characterized by discreet multifocal accumulations of pyknotic cells and cellular debris, and by immuno- histochemical staining using a terminal dUTP end labeling (TUNEL) method.  Thus, DNT may modulate the host leukocyte repertoire by deletion of subsets via an apoptotic pathway.


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