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Previous studies have shown that indigenous bacteria isolated from cervical, vaginal, and urethral surfaces of healthy women are able to adhere to human uroepithelial cells in vitro. Furthermore, these organisms were found to block the adherence of uropathogenic bacteria to uroepithelial cells from women with and without a history of urinary tract infections. In the present study, complete or partial inhibition of the adherence of gram-negative uropathogens was achieved by preincubating the uroepithelial cells with bacterial cell wall fragments isolated from a Lactobacillus strain. Competitive exclusion was most effective with whole viable cells and less effective with cell wall fragments obtained by sonication, extraction with sodium dodecyl sulfate, and treatment with sodium dodecyl sulfate and acid. Analysis of the Lactobacillus cell wall preparations suggested that lipoteichoic acid was responsible for the adherence of the Lactobacillus cells to uroepithelial cells but that steric hindrance was the major factor in preventing the adherence of uropathogens. This conclusion was also supported by blockage studies with reconstituted lipoteichoic acid-peptidoglycan, which was more effective at blocking adherence than lipoteichoic acid or peptidoglycan alone. The results suggest that the normal flora of the urinary tract may be used to protect against the attachment of uropathogens to the surfaces of uroepithelial cells. The long-term implications of these findings may lead to alternative methods for the management and prevention of recurrent urinary tract infections in females.

The cell envelope of a marine pseudomonad as seen in thin section by electron microscopy has the double-membrane structure typical of other gram-negative bacteria. Cells washed with a solution containing Na+, K+, and Mg++ at their concentrations in the growth medium, when suspended briefly in 0.5 M sucrose, lost 13% of their hexosamine in a form nonsedimentable by centrifugation at 73,000 x g. Since the resulting cells in thin section appeared unchanged, it was concluded that the material released was derived from a nonstaining, loosely bound outer layer. This same layer could be removed from the cells by washing with 0.5 M NaCI. A second nonsedimentable fraction was released after successive suspension of the cells in 0.5 M sucrose. Since this material was released only when the outer doubletrack structure had broken, it was concluded that it arose from a layer immediately underlying the latter layer. The three layers differed in their content of hexosamine and protein. None of the layers released contained muramic or diaminopimelic acid. The cell form remaining was rod shaped and appeared in thin section to be bounded only by its cytoplasmic membrane. This form contained all the muramic and diaminopimelic acid in the cell. Treatment with lysozyme released the muramic and diaminopimelic acid and converted the rod form to a protoplast, indicating that in the rod form (mureinoplast) a thin layer of peptidoglycan is located on the outside surface of the cytoplasmic membrane. Thus, five separate layers have been detected in the cell envelope of this marine pseudomonad.

It has been widely accepted that there is an ascending route of bacterial infection of the biliary tract but there is a lack of direct evidence. This hypothesis was tested in an animal experiment using the cat as an animal model. The implantation of biliary stents and surgical sphincterotomy were performed in these animals, with sham controls. Stents bypassing the sphincter of Oddi with the tip in the duodenal micro-organisms and the biliary tract was heavily contaminated. Blockage of these stents resulted in biliary obstruction. Stents implanted within the common bile duct, proximal to the sphincter were largely unaffected by biofilm formation. After surgical sphincterotomy the biliary tract was also contaminated but, in the absence of obstruction, the animals did not develop any symptoms. It was concluded that ascending infection by duodenal biliary reflux, via the sphincter of Oddi, is an important route of infection in the biliary system.