Browsing School, Graduate by Author "Johnson, Judith A. (Judith Ann), 1957-"
The capsular polysaccharide of Vibrio cholerae O139 Bengal: Induction and modulation of host-cell mediated immune responsesTrigiani-Fernandez, Ellen Ruth; Johnson, Judith A. (Judith Ann), 1957-; Powell, Jan L. (2001)Cholera is a severe and sometimes lethal secretory diarrheal disease caused by Vibrio cholerae. V. cholerae 0139 produce a diarrheal disease indistinguishable from cholera due to V. cholerae 01, however, the intestinal pathologies are different. V. cholerae 0139 infection is associated with intestinal inflammation and tissue destruction, which is not seen with V. cholerae 01. In addition, septicemia and bacteremia can occur with V. cholerae 0139 infection. V. cholerae 0139 isolates possess the same virulence factors as V. cholerae 01; however, they additionally express a capsule (CPS) and a distinct lipopolysaccharide (LPS). We have found that V. cholerae 0139 CPS (Vc CPS) induced the secretion of IL-8, G-CSF, IL-1beta, and to a lesser degree TNF-alpha and IL-6. Encapsulation of V. cholerae 0139 hindered phagocytosis and significantly decreased TNF-alpha secretion from human PBMCs. Purified VcCPS suppressed TNF-alpha secretion from PBMCs in response to unencapsulated V. cholerae 0139 bacterial cells as well as E. coli LPS (EcLPS). In contrast, VcCPS up-regulated IL-1beta secretion in response to EcLPS and VcLPS, but had no effect on IL-8 secretion. Using T84 intestinal monolayers, neither purified CPS nor LPS could induce significant IL-8 secretion from T84 intestinal monolayers. Surprisingly, no significant differences in IL-8 secretion in response to either acapsular or encapsulated V. cholerae 0139 were detected, and both strains were able to induce PMN transmigration across T84 monolayers. Using electron microscopy, V. cholerae 0139 infection was found to produce vacuolation of T84 monolayers, a phenomenon not observed with acapsular V. cholerae 0139. In the in vivo rabbit reversible intestinal tie adult rabbit diarrhea (RITARD) model, we did not find evidence of V. cholerae 0139 mucosal invasion, tissue damage, nor any significant inflammation as previously reported in ileal loop models. These results suggest that the capsule of V. cholerae 0139 may serve to down-regulate the acute inflammatory response in both the bloodstream as well as the intestines. Such a property increases the bacteria's ability to survive in the host environment and consequently is a significant component of pathogenesis. Understanding the role of the capsule in V. cholerae 0139 infection may potentially aid in vaccine development and the prevention of disease.
Recovery and characterization of high-level gentamicin resistant strains of enterococci from commercial poultryMcIntosh, Angela C.; Johnson, Judith A. (Judith Ann), 1957- (2001)Enterococci are normal enteric flora in humans and many animal species, and they are also opportunistic pathogens that have become increasingly responsible for many hospital-acquired infections. Antibiotic resistant enterococci have become an important public health concern; therefore, identifying potential sources of antibiotic resistant enterococci and/or factors contributing to their resistance has become a priority. During the raising of commercial poultry, chickens are often exposed to antibiotics in order to prevent infection and/or as growth-promoters. We have found that antibiotic exposure of chickens, even at subtherapeutic levels, encourages the growth of and selects for an antibiotic resistant enteric flora. To assess the level of antibiotic resistant enterococci in a typical commercial flock, we randomly sampled 1-, 2-, and 6-week old chickens of a large commercial poultry supplier. Antibiotic susceptibility assays of the recovered enterococcal isolates demonstrated that chickens harbor a multitude of multiply antibiotic resistant enterococcal species. It may be possible that enterococci are specially adapted for the intestinal tract of chickens and are not easily transmitted to humans. However, it may also be possible that there are subpopulations of enterococci that are more capable of transmission between animal species. Also, if enterococci from poultry are not capable of colonizing humans, they may still contribute to antibiotic resistance in humans by donating resistance genes to resident bacteria. Enterococci are model organisms to study antibiotic resistance because they readily acquire and transfer antibiotic resistance factors. Thus, the possibility that enterococci of human and chicken origin can exchange genetic elements coding for antibiotic resistance was addressed by filter-mating experiments to determine the transferability of gentamicin resistance. We found that transfer of gentamicin resistance (i) occurred between strains of enterococci derived from humans and chickens, (ii) was strain dependent, (iii) was most efficient when donor strains were of human origin, and (iv) was not enhanced with enterococci derived from like origins. Finally, the success of these in vitro transfer experiments prompted further experimentation of such transfers within an in vivo chicken model in which transfer of gentamicin resistance was observed but also appears to be strain dependent and fairly inefficient.