1. To investigate the effect of dietary fat source on host resistance to intracellular pathogens, weanling female C3H/Hen mice were fed one of three experimental diets containing, 20% by weight, lard, soybean oil or 17% menhaden fish oil plus 3% corn oil. After 4 weeks, survival of mice (n = 12/treatment group) injected intraperitoneally with 2 x 10(6) colony forming units of live Listeria monocytogenes was determined. In a second study, bacterial clearance from the liver and spleen at 2, 4 and 7 days post-challenge was determined (n = 8/treatment group). 2. We found that the survival of mice fed the diets with soybean oil or menhaden fish oil was significantly lower than those fed lard (P < 0.05). Survival rates were 58% (7/12), 33% (4/12) and 100% (12/12), respectively, for mice fed soybean oil, menhaden fish oil and lard. In the second study, mice fed menhaden fish oil had approximately 1 log10 greater bacteria in their spleens at day 4 than mice fed lard or soybean oil (P < 0.001). There were no significant treatment differences in the number of bacteria recovered from liver samples. 3. In summary, dietary fat source significantly affects murine resistance to Listeria, with diets rich in n-3 polyunsaturated fatty acids, such as from fish oil, having the most detrimental effect.

Broth cultures and washed cells of 13 of 24 bovine isolates of Fusobacterium necrophorum aggregated human platelets in platelet-rich plasma. The cell-free culture fluid was inactive. Bacteria stored at 4°C in saline remained active for at least 3 months, but they did not release activity into the storage solution. Aggregation typically began within 1 min after the addition of 103 bacteria to 103 platelets and was complete within 5.5 min. Assays for cytosolic lactic dehydrogenase revealed that platelet lysis did not occur. The release of ['4C]serotonin from platelets preincubated with this amine accompanied aggregation, indicating that this was a typical aggregation-degranulation reaction. Platelet aggregation was inhibited by EDTA (88% at 2.0 mM), aspirin (75% inhibition at 1.0 mM), and quinacrine (80% inhibition at 0.25 mM). Thus the reaction was an ion-dependent, cyclooxygenase-sensitive event. Gel-filtered platelets were less sensitive to aggregation than were platelets in plasma, but this sensitivity was fully restored by the addition of plasma and partially restored with fibrinogen. Biotyping of the cultures revealed that none of the avirulent, B-type strains of F. necrophorum could aggregate platelets, whereas 13 of 16 virulent A type strains were positive. These results suggest that platelet aggregation by F. necrophorum is related to the virulence of this organism.

Protective cultures can be used successfully as an additional hurdle together with phages to reduce growth of Listeria monocytogenes on sliced cooked ham. Addition of phages resulted in a rapid 10-fold reduction of L. monocytogenes. After 14 to 28 days of storage, a 100-fold reduction was observed in samples with phages and protective culture compared to results for samples with phages alone.

Four chlorhexidine diacetate (CHD) antiseptic wound lavage preparations were evaluated in vivo to determine their effects on second intention wound healing in the dog in vitro to determine their relative antibacterial activity against Staphylococcus intermedius. Chlorhexidine was diluted to 0.05% in sterile water, 0.9% sodium chloride, lactated Ringers solution (LRS), and LRS that was allowed to form a precipitate with CHD. Control solutions included sterile water and LRS. There were no significant differences in wound contraction or epithelialization. All 0.05% CHD preparations provided 100% bacterial kill.