Submitted to: Federation of Animal Science Societies
Publication Type: Abstract Only
Publication Acceptance Date: 3/18/2004
Publication Date: 7/25/2004
Citation: Rasmussen, M.A., Franklin, S.L., Carlson, S.A. 2004. Predation survival in rumen protozoa enhances Salmonella virulence [abstract]. 2004 Joint Annual Meeting of the American Dairy Science Association, American Society of Animal Science, Poultry Science Association. p. 166.
Technical Abstract: The objective of this study was to determine if there is a relationship between predation by rumen protozoa and the enhancement of virulence in Salmonella. Previous research indicates that intracellular bacterial pathogens can become more pathogenic after engulfment, survival and release from free-living eukaryotic micro-organisms, such as amoeba. In order to investigate if such relationships exist within the rumen microbiota, we determined the virulence of Salmonella strains after recovery from lysed preparations of mixed rumen protozoa. Virulence was determined using a tissue culture invasion assay (HEp-2 human carcinoma cells) and by monitoring disease progression after oral inoculation of Salmonella into calves. Laboratory cultured Salmonella isostrains not exposed to protozoa served as controls. Of the strains of Salmonella investigated (n=30), only those possessing the DT104 gene cluster encoding antibiotic resistance were found to be hyperinvasive (5-10 times greater than controls) after recovery from lysed rumen protozoa. The hyperinvasive strains included S. typhimurium DT104, U302, and multiple antibiotic resistant S. infantis and S. agona. When inoculated into calves, S. typhimurium DT104 recovered from rumen protozoa caused a more rapid disease progression, including pyrexia (increased body temperature spikes), greater recovery of the bacteria from lymph nodes and spleen, and a more unfavorable prognosis resulting in earlier euthanasia. We conclude that intracellular bacterial/protozoal interactions in the rumen can enhance Salmonella virulence. The molecular mechanisms (and their relationship to antibiotic resistance) which contribute to intracellular survival and subsequent bacterial release from protozoa merit further investigation. These observations have implications for mechanisms of disease pathogenesis, rumen microbial ecology, fecal shedding of foodborne pathogens from ruminants, and pathogen reservoir status of the rumen.