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.

Forty Holstein and Jersey cattle were assigned to four groups by milk production of Dairy Herd Improvement Association records. Cattle were on pasture and free-choice roughage supplemented with a concentrate and mineral mixture that was mixed without iodine supplementation. Teats of cows in each group were dipped for 27 days with chlorhexidine (controls) or iodophor teat dips with 1, .25, or .1% concentrations of iodine. Individual milk samples were taken on days 0, 20, and 27 for determination of iodine in milk. Mean iodine remained fairly constant, although there was a transitory increase for 1 and .25% dips at day 20. Mean iodine in milk (microgram/liter) for days 0, 20, and 27 were control: 31.3, 19.8, 14.7; 1.0%: 21.8, 51.5, 23.7; .25%: 34.5, 46.9, 36.7; .1%: 13.6, 14.5, 14.9. Iodophor teat dips did not add appreciable amounts of iodine to the bulk milk.

The objective of this study was to investigate the impact of feeding mice a diet rich in n-3 polyunsaturated fatty acids (PUFA) from fish oil on the interferon-gamma (IFN-gamma) response during an active infection with Listeria monocytogenes. Weanling female C3H/Hen mice were fed experimental diets containing 20% by weight one of the following fats: soybean oil, lard, or a mixture of menhaden fish oil and corn oil (17:3, w/w). After 4 weeks, mice were injected with 10(5) live L. monocytogenes, and the concentration of IFN-gamma in serum and spleen was determined 0, 2, 4, and 7 days postinfection by enzyme-linked immunosorbent assay (ELISA). Fish oil-fed mice showed significantly higher IFN-gamma in their blood at 2 and 4 days postchallenge compared with mice fed the soybean oil-containing or lard-containing diets (p < 0.001). A higher concentration of IFN-gamma was also found in the spleen homogenate of fish oil-fed mice on day 4 postchallenge (p < 0.005). To examine in vitro IFN-gamma production, splenocytes were isolated from fish oil-fed and soybean oil-fed mice on day 4 postchallenge and cultured with concanavalin A (1 microgram/ml and 10 micrograms/ml) for 24 and 48 h. There were no significant differences in the IFN-gamma concentration in cell culture supernatants between these diet treatments. This study demonstrated that the elevation in the concentration of IFN-gamma in blood and spleen during murine listeriosis is accentuated and prolonged by dietary n-3 PUFA, and these effects may not be due to changes in IFN-gamma production.

Due to concerns about high I in milk, the dairy industry has proposed a voluntary standard of 500 micrograms of I/L as the maximum allowable I in milk sold for processing and human consumption. This study was undertaken to determine the amount of ethylenediamine dihydroiodide that could be fed to dairy cattle without exceeding this standard. Various amounts (0 to 45 mg/head per d) of the I compound were fed to a commercial dairy herd for 50 wk. Individual and bulk milk samples were analyzed for total iodine. Milk I in herd bulk milk was directly correlated (r = .92) with the amounts fed. However, the correlation of milk I of individual cows was not as high (r = .66), indicating some individual variation in metabolism and secretion of the I into the mammary gland. Milk production and number of lactations did not correlate with I in milk. Regression analysis indicated that 25 to 30 mg of ethylenediamine dihydroiodide per day can be fed to dairy cattle receiving a diet otherwise low in I without exceeding a 500 micrograms concentration in milk.

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