Effect of lipopolysaccharide mutations on the pathogenesis of experimental Salmonella gastroenteritis.

Lipopolysaccharide mutants of Salmonella typhimurium provoked diminished amounts of fluid in rabbit ileal loops as compared with the response to the wild type. The responses elicited by these mutants ranged from 0 to 60% of that caused by the parent strain. Two completely rough mutants and one leaky rough mutant were chosen for further study. Purified lipopolysaccharide from the parent and the mutant strains failed to stimulate fluid exsorption in ileal loop experiments. Histological studies revealed that the three lipopolysaccharide mutants were less invasive than wild type and were less able to generate an inflammatory reaction in the rabbit ileum. A Salmonella enterotoxin was present in culture filtrates from one rough mutant and the wild type; however, the rough mutant appeared to produce less toxin. Enterotoxic activity was absent in culture filtrates from the two other rough mutants. These results suggest that reductions in both invasiveness and the ability to produce Salmonella enterotoxin decreased the ability of these mutants to provoke fluid exsorption. Also, the results indicate that lipopolysaccharide mutations can have a profound effect on the enteropathogenic properties of S. typhimurium.