The pathogenesis of Salmonella
diarrhea is unclear. Bacterial invasion of the ileal and colonic mucosa resulting in an intense
ileocolitis regularly occurs in concert with secretion of water and
sodium in jejunum, ileum, and colon. To examine the role of altered permeability in Salmonella
diarrhea we studied intestinal histology, water and
electrolyte transport, clearance of intravenously injected [14C]
erythritol and [3H]
mannitol, and changes in transmural electrical potential difference in normal and Salmonella-infected rhesus monkeys. In normal animals, absorption of water and
sodium occurred in jejunum, ileum, and colon and a gradient of diminishing permeability from jejunum to ileum to colon for both
erythritol and
mannitol was observed. Permeability as measured by determining permeability coefficients was not increased by
Salmonella infection and in fact was significantly reduced for
erythritol in the jejunum of infected animals. Perfusion with hypertonic
erythritol and
mannitol produced the same streaming potentials (deltaPD) in control and infected animals, indicating no differences in transmucosal permeability. As a positive control, perfusion with 25 mM
ethylenediaminetetraacetic acid in normal animals increased permeability, resulting in increased plasma-to-lumen
isotope flux and no deltaPD in response to hypertonic perfusates. These data show that despite severe alterations in intestinal histology, transmucosal permeability remains unchanged and thus is not a contributing factor in Salmonella
diarrhea.